Volume 2 - Issue 3 (May-Jul)

487 Interferon IRF6 Gene Variants and the Risk of Isolated Cleft lip or Palate in South 

Indian Dravidian Population 

491 Role of ‘Live Microorganisms’ (Probiotics) in Prevention of Caries: Going on the 

Natural Way Towards Oral Health 

497 Oral Health and Wellness on Wheels!!! 

500 Programmed Self-cell Suicide (Apoptosis) – Current Review, Concepts and Future 

Prospects 

507 Oral Health Aspects of Cannabis Use 

512 Ayur Health for Dentist’s Wealth 

514 Pregnancy Epulis 

518 Ludwig’s Angina: A Rare Case Report 

522 Management of an Unusual Crown Root Fracture of Mandibular First Primary Molar 

526 Follicular Adenomatoid Odontogenic Tumor 

529 Sodium Hypochlorite Solution Enhances Healing of Periapical Lesion by Nonsurgical 

Method 

532 Vital Bleaching with Diode Laser 

535 Replantation of Avulsed Tooth after Trauma: A One Year Follow-up Study

Indian Journal of 

Multidisciplinary Dentistry 

Executive Editor 

S Bhuminathan 

IJMD’s Editorial Panel 

Editor-in-Chief 

KMK Masthan 

IJMD Advisory Board 

Volume 2, Issue 3 

May-July 2012 

Associate Editor 

N Aravindha Babu 

Prosthodontics 

Mahesh Verma 

Srinisha J 

Raghavendra Jayesh S 

Suresh V Nayar (UK) 

Sanjna Nayar 

Conservative Dentistry/ 

Endodontics 

Sukumaran VG 

Subbiya A 

Swaminathan S (Singapore) 

Implantology 

John W Thurmond (USA) 

Genetics 

Aravind Ramanathan 

Oncology 

Abraham Kuriakose M 

Oral and Maxillofacial 

Surgery 

Ramakrishna Shenoi 

Vijay Ebenezer 

Raj Kutta (USA) 

Oral Pathology and 

Microbiology 

Vinay K Hazarey 

Ipe Vargese V 

Puneet Ahuja 

Sangeeta P Wanjari 

Gouse Mohiddin 

Orthodontics 

Krishna Nayak US 

Dhandapani G 

Murali RV 

Deepak C 

Pharmacology 

Muthiah NS 

IJCP’s Editorial Panel 

Elumalai M 

General Medicine 

Rajendran SM 

Periodontics 

Chandrasekaran SC 

Ash Vasanthan (USA) 

Oral Medicine and 

Radiology 

Nalini Aswath 

Panjab V Wanjari 

Praveen BN 

Mubeen 

Pedodontics 

Krishan Gauba 

Ashima Gauba 

Biochemistry 

Julius A 

Microbiology 

Mahalakshmi K 

Dr Sanjiv Chopra 

Prof. of Medicine & Faculty Dean 

Harvard Medical School 

Group Consultant Editor 

Dr Deepak Chopra 

Chief Editorial Advisor 

Dr KK Aggarwal 

CMD, Publisher and Group 

Editor-in-Chief 

Dr Veena Aggarwal 

Joint MD & Group Executive Editor 

Anand Gopal Bhatnagar 

Editorial Anchor 

IJMD is included in the databases of Genamics Journal Seek, Ulrich International periodical directory, 

Index Copernicus International Ltd., HINARI, CINAHL, EBSCO Publishing, Proquest, Chemical Abstracts 

Service Source Index (CASSI) and Google Scholar. 

482 

Advisory Bodies 

Heart Care Foundation of India, Non-Resident Indians Chamber of Commerce & Industry, 

World Fellowship of Religions 

Indian Journal of Multidisciplinary Dentistry, Vol. 2, Issue 3, May-July 2012

From the Editor’s desk 

From the Editor-in-chief 

xxxxxxxxx 

Dr KMK Masthan 

Professor and Head, 

Department of Oral Pathology and Microbiology 

Sree Balaji Dental College and Hospital 

Chennai 

My editorial in the previous issue on academics and research elicited a mixed response ranging from 

strong criticisms to “You are stepping on my toes” to surprising applause. My only response to all of 

them is what Somerset Maugham once said “It is very hard to be a gentleman and a writer”. In this 

issue I write about palliative care since, I was a witness to one patient’s final moments last month. I felt his last 

days would have been better if he had received some form of palliative care instead of the well meaning deceit of 

his relatives who kept telling him that he was going to get better. Hence, I share what feel about such care with 

the readers. 

Palliative care is the care given to the dying, encompassing physical, psychological, social and spiritual 

dimensions. It is not the efforts of the medical profession alone, but includes the family members and the 

society. This is not some thing new and was practised by King Asoka twenty-four centuries back. He had 

installed several hospices to attend to the needs of the dying with special care and attention. All countries 

face the rapidly increasing burden of patients nearing their end due to cardiovascular disorders, cancers, 

diabetes, respiratory diseases, neurological disabilities and psychiatric ailments. In our country especially, certain 

factors like extreme changes in lifestyle during the past four decades have brought about higher incidence of 

hypertension, diabetes mellitus, cancers due to tobacco chewing and smoking and coronary artery disease due to 

junk/fatty food and hence more number of patients facing premature death. 

Whereas, we, as Indians, pride ourselves to be more spiritual and religious, the reality is our dying 

elders do not get the dignity due to them and the rightful care they deserve. Busy life, mind set, financial 

obligations, poverty, trend towards abolition of joint families all contribute to this insensitivity on the part of the 

family members and so the due palliative care is not provided to the dying. Another factor that must be mentioned 

is the present medical care system including paid hospitals is more geared to cures and alleviation rather than 

support and care. The governmental medical care is totally oblivious and frankly resistant to this palliation concept 

at all, the common instruction to the patient’s relative being “Take the patient home’’. 

In palliative care, most care givers are faced with situations that have obvious solutions, but unsuitable for the 

recipient. For example, whether to advise cardio-pulmonary resuscitation for a patient under palliative care. For 

a normal person whose heart has failed due to heart attack or electric shock, it is a life saving procedure. But for 

a person who is expected to succumb to his/her disease in a few days, is it justified to subject them to this? My 

opinion is a definite ‘No’. 

Indian Journal of Multidisciplinary Dentistry, Vol. 2, Issue 3, May-July 2012 

483

From the Editor-in-chief 

The solution is to train community volunteers and to empower them to avail the help of nurses, doctors and 

hospices. They can be trained by medical personnel and they can be given access to any other information through 

toll free numbers, free on-line training, open access websites and periodic free training at the cost of the NGOs 

and government. Even small things like daily visits, emotional support, spiritual counseling, basic patient care 

techniques like how to avoid bedsores, advising a suitable diet within the means of the patient, awareness of the 

difference between communicable and noncommunicable diseases can help the patient greatly during the last few 

days of their life. 

One question the care-giver has to face all the time from the patient is “How long will I live?’’. Let us leave all the 

mercy and mental agony issues aside and handle this question in a more pragmatic manner. No medical or nonmedical 

person can exactly specify when and at what time the patient is likely to die. But patients may have some 

goals like settling their properties in the way they choose or seeing their daughters or sons married before they die 

etc. Such expectations are not unreasonable and hence the palliative care-giver can clearly inform the patients to 

expedite matters on their wishes. Another issue that always hampers the palliative care giver is the pressure of the 

close relatives not to tell the patient that the end is nearing. A fair analogy is if I were to be given some money 

and am allowed to spend it, without being told only the last few rupees are remaining, will I consider that as fair? 

It is always better if we know when we are nearing the end of our resources. So it is more merciful if the patients 

were told that their end is nearing. Probably such information will cause a few upset moments.But everyone 

knows that when there is birth, there is death. So they will come to terms with it and handle it better.By not 

revealing that, we may actually do injustice to the patient. Because he/she might want to speak to certain friends 

and relatives, express his/her opinions, concerns and fears better before the end. Another aspect of this revelation 

is that the patients may choose not to waste their meagre resources any further on treatments and medicines. If 

a person has worked for 20 years earning money for the marriage of his/her daughter, then it is not logical to 

let them spend it when the care giver surely knows the outcome. The trouble with concealment is that one can 

quite easily drift into deception. I feel minimal levels of wisdom and massive doses of idealism probably lead the 

medical professional to adapt this well meaning deceit and frank injustice to the patient. That logic is as circular 

as a Mobius strip where an ant can traverse the entire strip without touching edge anywhere. I would welcome 

guidance on this multi-faceted issue from the well informed. It is the province of the knowledge to speak and it 

is the privilege of wisdom to listen. Now it is time for the readers to speak their mind. 

Best wishes. 

484 


From the Desk of IJCP Group Editor-in-Chief 

xxxxxxxxx 

American College of Radiology Five Things 

Physicians and Patients should Question 

Dr KK Aggarwal 

Padma Shri and Dr BC Roy National Awardee 

Sr. Physician and Cardiologist, Moolchand Medcity 

President, Heart Care Foundation of India 

Group Editor-in-Chief, IJCP Group 

Editor-in-Chief, eMedinewS 

Chairman Ethical Committee, Delhi Medical Council 

Director, IMA AKN Sinha Institute (08-09) 

Hony. Finance Secretary, IMA (07-08) 

Chairman, IMA AMS (06-07) 

President, Delhi Medical Association (05-06) 

emedinews@gmail.com 

http://twitter.com/DrKKAggarwal 

Krishan Kumar Aggarwal (Facebook) 

• Don’t do imaging for uncomplicated headache. Imaging headache patients without specific risk factors for 

structural disease is not likely to change management or improve outcome. Those patients with a significant 

likelihood of structural disease requiring immediate attention are detected by clinical screens that have been 

validated in many settings. Many studies and clinical practice guidelines concur. Also, incidental findings lead 

to additional medical procedures and expense that do not improve patient well-being. 

• Don’t image for suspected pulmonary embolism (PE) without moderate or high pre-test probability. While 

deep vein thrombosis (DVT) and PE are relatively common clinically, they are rare in the absence of elevated 

blood d-Dimer levels and certain specific risk factors. Imaging, particularly computed tomography (CT) 

pulmonary angiography, is a rapid, accurate and widely available test, but has limited value in patients who 

are very unlikely, based on serum and clinical criteria, to have significant value. Imaging is helpful to confirm 

or exclude PE only for such patients, not for patients with low pre-test probability of PE. 

• Avoid admission or preoperative chest X-rays for ambulatory patients with unremarkable history and physical 

exam. Performing routine admission or preoperative chest X-rays is not recommended for ambulatory patients 

without specific reasons suggested by the history and/or physical examination findings. Only 2% of such 

images lead to a change in management. Obtaining a chest radiograph is reasonable if acute cardiopulmonary 

disease is suspected or there is a history of chronic stable cardiopulmonary disease in a patient older than age 

70 who has not had chest radiography within six months. 

• Don’t do computed tomography (CT) for the evaluation of suspected appendicitis in children until 

ultrasound has been considered as an option. Although CT is accurate in the evaluation of suspected 

appendicitis in the pediatric population, ultrasound is nearly as good in experienced hands. Since ultrasound 

will reduce radiation exposure, ultrasound is the preferred initial consideration for imaging examination in 


485

From the Desk of IJCP Group Editor-in-Chief 

children. If the results of the ultrasound exam are equivocal, it may be followed by CT. This approach is costeffective, 

reduces potential radiation risks and has excellent accuracy, with reported sensitivity and specificity 

of 94%. 

• Don’t recommend follow-up imaging for clinically inconsequential adnexal cysts. Simple cysts and 

hemorrhagic cysts in women of reproductive age are almost always physiologic. Small simple cysts in 

postmenopausal women are common, and clinically inconsequential. Ovarian cancer, while typically cystic, 

does not arise from these benign-appearing cysts. After a good quality ultrasound in women of reproductive 

age, don’t recommend follow-up for a classic corpus luteum or simple cyst

ORIGINAL RESEARCH 

Interferon IRF6 Gene Variants and the Risk of Isolated Cleft lip or 

Palate in South Indian Dravidian Population 

S Kishore Kumar*, MR Sukumar*, B Saravanan**, Arvind Ramanathan † , M Boominathan ‡ 

Abstract 

Nonsyndromic clefts of the lip and palate (CL, CP, CL/P) are among the most common congenital defects caused by multifactorial 

etiological factors that include both environmental and genetic factors. There is sufficient evidence to hypothesize 

that disease locus for this condition can be identified by candidate genes. The purpose of this study is to investigate the 

prevalence of mutation in exon 7 of IRF6 gene to determine whether this mutation is implicated in the South Indian Dravidian 

population. Material and methods: Blood samples were collected with informed consent from 10 subjects with nonsyndromic 

cleft lip/palate and genomic DNA was extracted from the blood samples, polymerase chain reaction was performed and the 

products were subjected to direct sequencing. Results: There was a significant positive association between the occurrence of 

homozygous valine polymorphic variant and isolated CL, CP and CL or CP (90%, n = 9) relative to heterozygous valine and 

isoleucine variant (10%, n = 1) in the present study. Conclusion: The study is clinically significant because it has for the first 

time identified the genetic status of exon 7 of IRF6 in Tamil speaking Dravidian population. 

Key words: Nonsyndromic cleft lip and palate, IRF6 gene variant, polymerase chain reaction 

Development of the head and face comprises 

of one of the most complex events during 

embryonic development, coordinated by a 

network of gene expressions that include transcription 

factors and signaling molecules, which confer polarity 

of cells. Disturbance of this tightly regulated network 

of signaling events may interfere with otherwise normal 

cellular function and consequently may result in the 

failure of meeting and fusion of the developing facial 

primordia, thereby causing orofacial cleft. The extent 

of orofacial cleft phenotype varies among the affected 

children with some having cleft lip (CL) or cleft palate 

(CP) (isolated CL or CP), while the others have cleft lip 

with cleft palate (CL/P). Clefts may involve either onehalf 

of the oral cavity or both and accordingly they are 

classified as unilateral or bilateral clefts. Such orofacial 

cleft may either occur as an isolated event (designated as 

nonsyndromic) or as a part of complex malformations 

(designated as syndromic). Nonsyndromic cleft makes 

about 70% of all orofacial clefts, while the remaining 

* 

Professor 

** 

Reader, Dept. of Orthodontics 

† 

Principal, Investigator, Human Genetics Laboratory 

‡ 

Postgraduate Student, Dept. of Orthodontics 

Sree Balaji Dental College and Hospital, Chennai 

Address for correspondence 

Dr S Kishore kumar 

E-mail: spkishorekumar@yahoo.co.in 

30% are accounted for syndrome associated clefts. 1,26,29 

The etiology seems complex 2,,3,9,11,12,16 but genetics 

plays a major role. 1,4,6,8,15 Various candidate genes have 

been associated with nonsyndromal cleft lip/palate 

in different populations, but Interferon regulatory 

factor-6 (IRF6) is strongly related in various populations 

on a consistent basis. 19,20,23,25,27,28 Identification of 

etiologic explanation for clefting has included extensive 

evaluation of genes. 22 

IRF6 belongs to a family of nine transcription 

factors that share a highly-conserved helix-turn-helix 

DNA-binding domain. The DNA-binding domain 

is essential for IRF6 to bind the promoter region of 

the genes it regulates (activates). Mutations in IRF6 

were first reported in van der Woude syndrome 

(VWS). 13 Investigation of the genetic status of IRF6 

in nonsyndromic CL/P patients identified common 

polymorphic variant G>A at position 820 in the 

coding DNA of IRF6 gene. This causes the conversion 

of GTC to ATC and creates a valine→isoleucine 

substitution at amino acid 274 in the protein-binding 

domain of IRF6 gene. 29 GTC encoding valine amino 

acid has been found to be significantly associated with 

cleft in several populations. 

Material and Methods 


487

original research 

The sample consisted of 10 subjects reporting to the 

Dept. of Orthodontics and Dentofacial Orthopedics, 

Sree Balaji Dental College and Hospitals, Chennai, 

India. The study was carried out after approval from 

Institutional Ethical Committee and guidelines from 

Helinsiki declaration were followed. Written consents 

were obtained from all subjects. Patients with CL or 

CP (isolated CL or CP) associated with any history 

of developmental disabilities, including learning 

disabilities and attention deficits, hearing impairment 

and speech deficits or abnormalities were excluded 

from the study. Blood samples (1.5 ml) were obtained 

from subjects and genomic DNA was purified by 

conventional phenol: Chloroform extraction and 

ethanol precipitation procedure. A 100 ng DNA was 

used as a template to amplify the mutant region in 

exon 7 by polymerase chain reaction (PCR) with 

the primer sequences mentioned in Table 1. Twenty 

microliter l aliquots of amplified PCR products were 

subjected to agarose gel electrophoresis in a 1.5% 

agarose gel containing ethidium bromide at 100 V 

for 30 minutes with 1X TAE (Tris Acetate EDTA) 

buffer. The DNA bands were visualized in a long 

wavelength UV (364 nm) transilluminator and the 

exon 7 specific bands were cut with a clean surgical 

blade. Gel blocks containing the exon 7 specific bands 

were transferred to a fresh 1.5 ml microcentrifuge tube 

and three volumes of solubilization buffer was added. 

The tubes were incubated at 55°C for 10 minutes with 

intermittent agitation to solubilize the gel blocks. After 

the incubation period, 1 gel volume of isopropanol 

was added to each tube and mixed by vortex mixer, 

following which the contents were transferred to a spin 

column. The spin column tubes were centrifuged at 

10,000 rpm for one minute at room temperature to 

enable binding of the DNA (PCR product of exon 

7 of IRF6 gene) to the silica membrane in the spin 

columns. The bound DNA was eluted with 40 µl of 

elution buffer and 10 ng of the eluted product was 

Table 1. IRF6 Exon 7 Mutant Region Primers 

Set 1 

Sequence Length (T.M*) 

Left primer 19 57.35 

Aaccttgcagtgactgacc 

Right Primer 18 57.47 

Atcaggttgggagcaaca 

sequenced with sequencing grade primers (A*STAR 

facility, Singapore). 

Results 

DNA size marker 

Lane # 1 2 

500 bp 

400 bp 

300 bp 

200 bp 

100 bp 

Figure 1. Initial PCR product of IRF6 gene (353 bp). 

A 100 ng aliquot of the total genomic DNA was used 

as template to amplify the exon 7 of IRF6 gene, which 

is known to carry the genetic mutation in CP patients 

in other races. The mutation converts ‘GTC’, which 

is the genetic code for ‘valine’ amino acid to ‘ATC’ 

the genetic code for ‘isoleucine’ amino acid. In order 

to analyze for the presence of the above mutation, we 

downloaded the sequence of IRF6 coding region from 

the public domain database and designed the primers 

to specifically amplify exon 7 (Table 1). Amplifications 

in all the samples were of the expected size 

(353 bp) and a representative of two samples is shown in 

Figure 1 (lanes 1 and 2). 

Identification of Genetic Polymorphism in 

Exon 7 of IRF6 Gene 

A 2 µl aliquot of the eluted DNA was sequenced in 

a 20 µl reaction volume and the sequenced data was 

analyzed with BioEdit software. The genetic code GTC 

that encodes for valine amino acid was found in all the 

patients, while ATC that encodes for isoleucine was 

not found as an isolated event in any of the patients. 

However, ATC occurred in heterozygous state along 

with GTC in one of 10 samples (10% of samples) 

that were analyzed. There was a significant positive 

association between the occurrence of homozygous 

valine polymorphic variant and isolated CL, CP and 

CL/CP (90%, n = 9) relative to heterozygous valine and 

isoleucine variant (10%, n = 1). The data was further 

analyzed for the distribution pattern of homozygous 

488 



valine or valine and isoleucine in heterzygous state in 

each of the conditions - isolated CL or isolated CP 

or CL with CP. Valine/Valine homozygous vairant was 

found in 20% (n = 2) of isolated CL, 0% (n = 0) of 

isolated CP and 70% of CL with CP (n = 7), while 

valine/isoleucine heterozygous variant were found to 

be 10% (n = 1) in isolated CL, 0% (n = 0) in isolated 

CP and 0% (n = 0) in CL with CP. 

Taken together valine/valine homozygosity was 

significantly associated with clefting relative to valine/ 

isoleucine heterozygosity. This pattern is consistent with 

a recessive effect of the valine allele, which requires to 

be in homozygous condition to cause orofacial cleft. 

While in the heterozygous state, the valine allele being 

recessive may not be able to cause orofacial cleft in the 

presence of a normal isoleucine allele. 

Discussion 

A total of 10 patients of tamil speaking dravidian race, 

with isolated nonsyndromic CL, CP or CL/CP were 

screened for genetic polymorphism (silent mutation) 

in exon 7 of IRF6 gene. The polymorphism converts 

GTC that encodes for valine amino acid to ATC, 

which encodes for isoleucine amino acid. The screen 

identified valine (GTC) in 90% (n = 9) of patients 

with CL, CP or CL/CP and both valine (GTC) and 

isoleucine (ATC) in heterzygous state in 10% (n = 1) of 

them. None of them were found to carry homozygous 

isoleucine (ATC) variant. 

The IRF6 gene has been shown to be mutated in 

patients with VWS and/or Popliteal pterygium 

syndrome (PPS) in several populations. 13,17 VWS is 

a dominantly inherited disorder characterized by the 

presence of pits and/or sinuses on the lower lip in 85% 

of cases, CL/P in 50% of the patients and hypodontia 

in 20% of them. 7,14,18,21,24 PPS is a less frequent allelic 

orofacial clefting disorder. In addition to the signs of 

VWS, PPS includes webbing of the knee, syndactyly 

(or absence) of the toes and digits, ankyloblepharon, 

syngnathia and genital abnormalities. 5 More than 59 

different mutations in IRF6 gene have been reported, 

which includes silent mutations in protein-binding 

domain, frame-shift and nonsense mutations and 

deletions all of which either alter or render the protein 

functionless. 2,10 

IRF6 is expressed at key stages of facial development 

in mouse embryos. Specifically, a high level 

of IRF6 expression is detected in the ectoderm covering 

the facial processes during their fusion to form the 

lip and primary palate. Zucchero et al investigated 

the prevalence of mutations in IRF6 gene in patients 

with nonsyndromic CL, CP or CL/CP, by sequencing 

the entire coding region of the IRF6 gene. The study 

found strong evidence of overtransmission (67%) of 

the valine (GTC) variant at position 274 relative to 

isoleucine (ATC) variant in IRF6 protein in Japanese, 

Chinese, Vietnamese and Filipino populaiton but not 

in Europeans and Indians. 29 In the present study, we 

have analyzed a cohort of 10 patients of tamil speaking 

dravidian race with CL, CP or CL with CP and found 

valine variant to be transmitted in 90% of them 

(p ≤ 0.05). When the data was analyzed for stratified 

distribution of valine/valine alleles in isolated CL or CP 

or CL with CP, the association was found to be significant 

relative to valine/isoleucine heterozygous alleles. 

Summary and Conclusion 

The present study, however, has to be interpreted 

carefully since it did not involve analysis of IRF6 gene 

from normal individuals. The distribution of valine/ 

valine and valine/isoleucine alleles in normal individuals 

is required to arrive at a more affirmative conclusion. 

Nevertheless, the present study has helped us to 

understand the genetic status of exon 7 of IRF6 in the 

tamil speaking dravidian race. Besides we also made an 

interesting observation that 10% of the patients that 

we examined carried both valine/isoleucine alleles in 

heterozygous state, which is in contrary to Zucchero 

et al study 29 who reported this to be rare event in the 

Indian population. This may be explained by the fact 

that the patients that we investigated were from tamil 

speaking dravidian race, while those that were analyzed 

by Zucchero et al were from West Bengal. 

References 

1. 

2. 

3. 

Lidral AC, Moreno LM, Bullard SA. Genetic Factors and 

Orofacial Clefting. Semin Orthod 2008;14(2):103-114. 

Jugessur A, Murray JC. Orofacial clefting: recent 

insights into a complex trait. Curr Opin Genet Dev 

2005;15(3):270-8. 

Beaty TH, Maestri NE, Hetmanski JB, Wyszynski DF, 

Vanderkolk CA, Simpson JC, et al. Testing for interaction 

between maternal smoking and TGFA genotype among 

oral cleft cases born in Maryland 1992-1996. Cleft Palate 


489


4. 

5. 

6. 

7. 

8. 

9. 

10. 

11. 

12. 

13. 

14. 

15. 

16. 

Craniofac J 1997;34(5):447-54. 

Blanton SH, Cortez A, Stal S, Mulliken JB, Finnell 

RH, Hecht JT. Variation in IRF6 contributes to 

nonsyndromic cleft lip and palate. Am J Med Genet A 

2005;137A(3):259-62. 

Froster-Iskenius UG. Popliteal pterygium syndrome. J 

Med Genet 1990;27(5):320-6. 

Ghassibé M, Bayet B, Revencu N, Verellen-Dumoulin 

C, Gillerot Y, Vanwijck R, et al. Interferon regulatory 

factor-6: a gene predisposing to isolated cleft lip with 

or without cleft palate in the Belgian population. Eur J 

Hum Genet 2005;13(11):1239-42. 

Gorlin R, Cohen MJ, Hennekam R. Syndromes of 

the Head and Neck: Orofacial Clefting Syndromes: 

Common Syndromes. 4th edition, Oxford University 

Press: New York, 2001. 

Indian Genome Variation Consortium. Genetic 

landscape of the people of India: a canvas for disease gene 

exploration. J Genet2008;87(1):3-20. 

Murray JC. Face facts: genes, environment, and clefts. 

Am J Hum Genet 1995;57(2):227-32. 

Murray JC, Schutte BC. Cleft palate: players, pathways, 

and pursuits. J Clin Invest 2004;113(12):1676-8. 

Shi M, Wehby GL, Murray JC. Review on genetic variants 

and maternal smoking in the etiology of oral clefts and 

other birth defects. Birth Defects Res C Embryo Today 

2008;84(1):16-29. 

Rothman KJ, Moore LL, Singer MR, Nguyen US, 

Mannino S, Milunsky A. Teratogenicity of high vitamin 

A intake. N Engl J Med 1995;333(21):1369-73. 

Kondo S, Schutte BC, Richardson RJ, Bjork BC, Knight 

AS, Watanabe Y, et al. Mutations in IRF6 cause Van der 

Woude and popliteal pterygium syndromes. Nat Genet. 

2002;32(2):285-9. 

Lacombe D, Pedespan JM, Fontan D, Chateil JF, Verloes 

A. Phenotypic variability in van der Woude syndrome. 

Genet Couns 1995;6(3):221-6. 

Nemana LJ, Marazita ML, Melnick M. Genetic analysis 

of cleft lip with or without cleft palate in Madras, India. 

Am J Med Genet 1992;42(1):5-9. 

Lammer EJ, Shaw GM, Iovannisci DM, Finnell RH. 

Maternal smoking, genetic variation of glutathione s- 

transferases, and risk for orofacial clefts. Epidemiology 

2005;16(5):698-701. 

17. 

18. 

19. 

20. 

21. 

22. 

23. 

24. 

25. 

26. 

27. 

28. 

LMR parnalba Lack of association between IRF6 

polymorhisms and non syndromic cleft lip or palate in 

Brazilian population. 2008. 

Mossey PA, Little J, Munger RG, Dixon MJ, Shaw WC. 

Cleft lip and palate. Lancet 2009;374(9703):1773-85. 

Mossey P, Little J. Addressing the challenges of cleft lip 

and palate research in India. Indian J Plast Surg 2009;42 

Suppl:S9-S18. 

Park JW, McIntosh I, Hetmanski JB, Jabs EW, Vander 

Kolk CA, Wu-Chou YH, et al. Association between IRF6 

and nonsyndromic cleft lip with or without cleft palate 

in four populations. Genet Med 2007;9(4):219-27. 

Stottmann RW, Bjork BC, Doyle JB, Beier DR. 

Identification of a Van der Woude syndrome mutation 

in the cleft palate 1 mutant mouse. Genesis 2010;48(5): 

303-8. 

Romitti PA, Sun L, Honein MA, Reefhuis J, Correa 

A, Rasmussen SA. Maternal periconceptional alcohol 

consumption and risk of orofacial clefts. Am J Epidemiol 

2007;166(7):775-85. 

Scapoli L, Palmieri A, Martinelli M, Pezzetti F, Carinci 

P, Tognon M, Carinci F. Strong evidence of linkage 

disequilibrium between polymorphisms at the IRF6 

locus and nonsyndromic cleft lip with or without cleft 

palate, in an Italian population. Am J Hum Genet 

2005;76(1):180-3. 

Van der woude A. Fistula labii inferioris congenita and 

its association with cleft lip and palate. Am J Hum Genet 

1954;6(2):244-56. 

Vieira AR, Cooper ME, Marazita ML, Orioli IM, Castilla 

EE. Interferon regulatory factor 6 (IRF6) is associated 

with oral-facial cleft in individuals that originate in South 

America. Am J Med Genet A 2007;143A(17):2075-8. 

Wyszynski DF, Beaty TH, Maestri NE. Genetics of 

nonsyndromic oral clefts revisited. Cleft Palate Craniofac 

J 1996;33(5):406-17. 

Pan Y, Ma J, Zhang W, Du Y, Niu Y, Wang M, et al. 

IRF6 polymorphisms are associated with nonsyndromic 

orofacial clefts in a Chinese Han population. Am J Med 

Genet A 2010;152A(10):2505-11 

Zeiger JS, Beaty TH, Liang KY. Oral clefts, maternal 

smoking, and TGFA: a meta-analysis of gene-environment 

interaction. Cleft Palate Craniofac J 2005;42(1):58-63. 

29. Zucchero TM, Cooper ME, Maher BS, Daack-Hirsch S, 

490 


Role of ‘Live Microorganisms’ (Probiotics) in Prevention of 

Caries: Going on the Natural Way Towards Oral Health 

Vineet Agrawal*, Sonali Kapoor**, Nimisha Shah † 

*Senior Lecturer 

**Professor 

Dept. of Conservative and Endodontics, MP Dental College and Oral 

Research Institute, Vadodara 

† 

Professor, Dept. of Conservative and Endodontics, KM Shah Dental 

College, Vadodara 


Dr Vineet Agrawal 

E-mail: vineetdent@yahoo.co.in 

Abstract 

Science is providing us the tools to diagnose and treat an infection before it causes damage. For some decades now, bacteria 

known as probiotics have been added to various foods because of their beneficial effects for human health. Very encouraging 

studies have come up in recent past exploring probiotics in fields of caries, periodontal diseases and few other areas and the 

results tend to suggest beneficial effects of probiotics on oral health and on whole body in general. The application of probiotic 

strategies may, in near future, provide an end to many infections occurring in oral cavity. This article reviews the probiotic 

approaches, such as genetically modified Streptococcus mutans and targeted antimicrobials in the prevention of caries and 

discuss its future directions. 

Key words: Probiotics, dental caries, prevention, Bifidobacterium, Lactobacillus 

W 

D Miller first described dental caries as a 

bacterially-mediated process more than 

100 years ago. 1 Today, we know that dental 

caries is a multifaceted disease process. Several models 

have been put forward describing mechanism of caries 

formation. One of the earlier models that is familiar 

to most dentists was put forth by Fitzgerald and 

Keyes. 2 They used three overlapping circles describing 

the host, bacteria and nutrients required to foment 

the production of organic acids and the subsequent 

demineralization activity. The beauty of this model is 

that all three elements must be present for the disease 

to progress. Since all three are required for disease 

initiation and progression, removal of any one element 

ostensibly leads to the interception of the disease 

process. 

The surgical approach has been the predominate 

mode of caries management for the past 150 years. 

Dentistry has, however, in recent years moved 

toward an antibiotic/antimicrobial model of disease 

management. This approach, however, raises serious 

questions: 1) Do the antibiotic/antimicrobial agents 

Review article 

(chlorhexidine, povidone-iodine, fluoride, etc.) kill 

all offending organisms?; 2) if so, do the agents 

preclude the re-entry of the same organisms from 

external sources? and 3) if the agents do kill all the 

offending organisms, do any remaining pathogenic 

organisms have selective advantage in repopulating the 

tooth surfaces? To overcome the problems inherent 

in an antibiotic/antimicrobial approach, probiotic 

methods are currently under study as means of caries 

management. 

What are Probiotics, Prebiotics and 

Synbiotics 

The term ‘probiotic’ is derived from the Latin preposition 

pro (‘for’) and the Greek adjective (biotic), the latter 

deriving from the noun (bios, ‘life’). 3 It was first used 

by Lilly and Stillwell in 1965 to describe “substances 

secreted by one microorganism, which stimulates the 

growth of another” and thus was contrasted with the 

term antibiotic. 4 Today, two main definitions are used. 

According to a WHO/FAO report (2002), probiotics 

are “live microorganisms which, when administered in 

adequate amounts, confer a health benefit on the host”. 

International Life Science Institute (ILSI) Europe 

suggests a definition according to which a probiotic is 

“a live microbial food ingredient that, when ingested 

in sufficient quantities, exerts health benefits on the 

consumer”. Probiotics are microorganisms, basically 

bacteria, that when ingested would confer health 

benefit beyond the basic nutrition. 5 


491

Review Article 

The term prebiotic was introduced by Gibson and 

Roberfroid who exchanged ‘pro’ for ‘pre’ which 

means ‘before’ or ‘for’. They defined prebiotics as a 

“nondigestible food ingredient that beneficially affects 

the host by selectively stimulating the growth and/or 

activity of one or a limited number of bacteria in the 

colon.” 6 More specifically, prebiotics are short-length 

carbohydrates, such as fructooligosaccharides, that 

resist digestion in upper gastrointestinal tract or are 

fermented in the colon to produce short-chain fatty 

acids, such as acetate, butyrate and propionate, which 

have positive effects on colonic cell growth and stability, 

generate many of the same bacteria as provided in 

probiotics. 7 

The term synbiotic is used when a product contains 

both probiotics and prebiotics. According to this 

approach, a food or food supplement will include both 

the live cells of the beneficial bacteria and the selective 

substrate. The idea being that the beneficial bacterial 

cells can grow quickly and competitively because of 

the presence of selective substrate and establish their 

predominance. 6 

Table 1. Possible Mechanism of Probiotics in Oral 

Health 

Production of antimicrobial substances 

Organic acids 

Hydrogen peroxide 

Bacteriocins 

Binding in oral cavity 

Compete with pathogens for adhesion sites 

Involvement in metabolism of substrates (competing with 

oral microorganisms for substrates 

available) 

Immunomodulatory 

Stimulate nonspecific immunity 

Modulate humoral and cellular immune 

response 

Modify oral conditions 

Modulating pH 

Modification of oxidation reduction potential 

Mechanism of Probiotics 

Probiotics can help prevent and treat disease through 

several mechanisms. 8 

• Direct interaction: Probiotics interact directly 

with the disease-causing microbes, making it 

harder for them to cause the disease. 

• Competitive exclusion: Beneficial microbes 

directly compete with the disease, developing 

microbes for nutrition or enterocyte adhesion 

sites. 

• Modulation of host immune response: Probiotics 

interact with and strengthen the immune system 

and help prevent disease. 

In oral cavity, probiotics tend to create a biofilm, 

acting as a protective lining for oral tissues against oral 

diseases. Such a biofilm keeps bacterial pathogens off 

oral tissues by filling a space, which could have served 

as a niche for pathogens in future; and competing with 

cariogenic bacteria. Table 1 describes the mechanism 

of action of probiotics in oral health. 9 

Potential Benefits of Probiotics 

Probiotics have traditionally been used for prevention 

of colon cancer, 10 lowering cholesterol, 10 lowering blood 

pressure, 10 managing lactose intolerance, 11 Helicobacter 

pylori, 12 improving immune function and preventing 

infections, 13 antibiotic-associated diarrhea, 14 reducing 

inflammation, 15 improving mineral absorption, 15 

preventing harmful bacterial growth under stress, 16 

irritable bowel syndrome and colitis, 16 and managing 

urogenital health. 16 

Common Strains Used in Oral Probiotics 

The most commonly-used probiotic strains belong 

to the genera, Lactobacillus, Bifidobacterium, 17 and 

Streptococcus. 18 Streptococcus salivarius, Streptococcus 

mitis and Streptococcus sanguinis showed a significantly 

more pronounced reduction in total anerobic bacteria, 

black-pigmented bacteria and Campylobacter rectus. 

Probiotic strains of Lactobacillus species include 

L. salivarius, L. reuteri, L. acidophilus, L. fermentum, 

L. lactis, L. helveticus and L. rhamnosus. Lactobacilli 

produce different antimicrobial components, such as 

organic acids, hydrogen peroxide, low molecular weight 

antimicrobial substances, bacteriocins and adhesion 

inhibitors. Similarly, Bifidobacterium strains include 

B. bifidum, B. longum and B. infantis. 19 

492 



Administration of Probiotic 

Different means of probiotic administration for oral 

health purpose are: 20 

• A culture concentrate added to a beverage or food 

(such as a fruit juice) 

• Inoculated into prebiotic fibers 

• Inoculants into a milk-based food (dairy products 

such as milk, milk drink, yoghurt) 

• Yogurt drink, cheese, kefir, biodrink 

• As concentrated and dried cells packaged as dietary 

supplements (nondairy products) 

• Such as powder, capsule, gelatin tablets. 

Role of Probiotics in Dental Caries 

A number of researchers are developing ‘probiotic’ 

methods to treat the caries causing pathogens. ‘Probiotic’, 

as used here, means that mechanisms are employed to 

selectively remove only the (odonto) pathogen while 

leaving the remainder of the oral ecosystem intact. 21 

One of the replacement therapy options entails the 

application of a genetically engineered ‘effector strain’ 

of S. mutans that will replace the cariogenic or ‘wild 

strain’ to prevent or arrest caries and to promote optimal 

remineralization of tooth surfaces that have been 

demineralized but that have not become cavitated. 

In caries, there is an increase in acidogenic and acid 

tolerating species such as mutans streptococci and 

lactobacilli, although other bacteria with similar 

properties can also be found like Bifidobacteria, 

nonmutans streptococci, Actinomyces spp., 

Propionibacterium spp., Veillonella spp. and Atopobium 

spp. Use of probiotics and molecular genetics to replace 

and displace cariogenic bacteria with noncariogenic 

bacteria has shown promising results. These studies 

have employed different approaches: 22 

• Early studies concentrated on utilizing bacteria that 

expressed bacteriocins or bacteriocin-like inhibitory 

substances (BLIS) that specifically prevented the 

growth of cariogenic bacteria. 

• One approach has been to identify food grade and 

probiotic bacteria, which have ability to colonize 

teeth and influence the supragingival plaque. 

• Also, strains have been screened for suitable 

antagonistic activity against relevant oral bacteria. 

• Another approach utilized recombinant strain of 

S. mutans expressing urease, which was shown to 

reduce the cariogenicity of plaque in an animal 

model. 

• Similarly, genetically modified probiotics with 

enhanced properties can be developed (‘designer 

probiotics’). For example, a recombinant strain 

of Lactobacillus that expressed antibodies 

targeting one of the major adhesions of S. mutans 

(antigen I/II) was able to reduce both the viable 

counts of S. mutans and the caries score in a rat 

model. 

• A different way of accomplishing the removal of the 

pathogens is to develop ‘targeted antimicrobials’. 

The basic idea is to develop an inexpensive 

targeting molecule that will reliably attach to only 

the organism of interest, in this case S. mutans, 

S. sobrinus or other chosen pathogen. Once the 

targeting molecule is perfected, then a ‘killer’ 

molecule is optimized and chained to the targeting 

molecule. The combined unit then selectively 

eliminates the infection of interest. In the case 

of the oral cavity and dental caries, this system is 

attractive from the perspective of eliminating all 

the pathogens thereby precluding the regrowth 

of the original infection. There is also compelling 

evidence from clinical trials and laboratory efforts 

demonstrating that once the bacterial ecosystem 

is free of S. mutans, it is difficult to reintroduce 

the organisms (another competitive inhibition 

situation). 21,22 

Various Studies Involving Probiotics for 

Decreasing Dental Caries 

Considering the growing body of evidence about 

the role of probiotics on caries pathogens, however, 

it has been suggested that the operative approach in 

caries treatment might be challenged by probiotic 

implementation with subsequent less invasive 

intervention in clinical dentistry and thus, recently, 

many studies are been carried on probiotics. 

The first randomized, double-blind, placebo-controlled 

intervention study, 23 examining the effect of milk 

containing L. rhamnosus GG on caries and the risk 

of caries in children when compared with normal 

milk was completed in 2001; the study included 

594 children, 1-6 years old, who consumed milk 

for seven months. Probiotic milk was able to reduce 

S. mutans counts at the end of the trial and a 


493


significant reduction of caries risk was also observed. 

L. rhamnosus is one of the most extensively studied 

probiotic and of particular interest in oral biology 

since it does not readily ferment sucrose and is safer for 

teeth than lactic acid-producing bacteria. Controlled 

studies have shown the effectiveness of L. rhamnosus 

in reducing caries. L. rhamnosus was found to inhibit 

cariogenic S. mutans but colonization of oral cavity by 

L. rhamnosus seems improbable. 24 A study aimed at 

benefit of cheese containing L. rhamnosus showed that 

probiotic intervention helped in reducing the highest 

level of Streptococcus mutans. 25 

In order to assess whether naturally occurring oral 

lactobacilli have probiotic properties, lactobacilli were 

isolated from saliva and plaque from children and 

adolescents, with or without caries lesions. Twenty-three 

Lactobacillus spp. completely inhibited the growth of 

all mutans streptococci tested. Species with maximum 

interference capacity against mutans streptococci 

included Lactobacillus paracasei, Lactobacillus plantarum 

and L. rhamnosus. 26 

Calgar et al (2006) investigated the effect of probiotic 

bacterium L. reuteri on levels of mutans streptococci 

and lactobacilli, which was introduced by two different 

straw containing L. reuteri and lozenges containing 

L. reuteri and concluded that short-term daily ingestion 

of lactobacilli-derived probiotics delivered by prepared 

straws or lozenges reduced the levels of salivary mutans 

streptococci in young adults. 27 

Comelli et al (2002) studied 23 dairy bacterial strains 

for the prevention of dental caries and reported that 

only two strains namely Streptococcus thermophilus and 

L. lactis were able to adhere to saliva-coated 

hydroxyapatite and were further successfully 

incorporated into a biofilm similar to the dental 

plaque. Furthermore, they could grow together with 

five strains of oral bacterial species commonly found in 

supragingival plaque. In this system, L. lactis was able 

to modulate the growth of the oral bacteria, and in 

particular to diminish the colonization of Streptococcus 

oralis, Veillonella dispar, Actinomyces naeslundii and of 

the cariogenic S. sobrinus. 28 

Few studies have reported reduction in mutans 

streptococci levels in saliva following use of probiotic 

containing yoghurts but it is not clear whether this 

decrease is due to the bactericidal activity of yoghurt 

or other mechanisms. Petti et al (2008) investigated 

the differences in susceptibility of strains of viridians 

streptococci. In vitro, yoghurt with live bacteria showed 

selective antimutans activity, suggesting that the overall 

decrease in mutans streptococci in vivo could be due to 

a bactericidal effect on S. mutans. 29 

Calgar et al (2007) evaluated the effect of xylitol and 

probiotic chewing gums on salivary mutans streptococci 

and lactobacilli and concluded that daily chewing on 

gums containing probiotic bacteria or xylitol reduced 

the levels of salivary mutans streptococci in a significant 

way. However, a combination of probiotic and xylitol 

gums did not seem to enhance this effect. 30 

Kang et al (2006) did a study in which they found 

out that the water-soluble polymers produced from 

sucrose by the Weissella cibaria isolates inhibited the 

formation of S. mutans biofilm. In the clinical study, 

the subjects mouthrinsed with a solution containing 

W. cibaria CMS1 and exhibited plaque index reduction 

of approximately 20.7%. 31 

To study the effect of bifidobacteria a doubleblind, 

randomized crossover study was performed. 

A statistically significant reduction of salivary mutans 

streptococci was recorded after the probiotic yoghurt 

consumption containing Bifidobacterium, which 

was in contrast to the controls. A similar trend was 

seen for lactobacilli, but this decrease failed to reach 

statistical significance. Investigators concluded that 

probiotic bifidobacteria in yoghurt may reduce the 

levels of selected caries-associated microorganisms in 

saliva. 18 In a similar study using Bifidobacterium lactis a 

statistically significant reduction (p < 0.05) of salivary 

mutans streptococci was recorded after consumption 

of the probiotic ice-cream in adults. 32 

Conclusion 

Concept of probiotics is emerging as a fascinating 

field and it prompts a new horizon on the relationship 

between diet and oral health. Probiotic strategies are 

part of the continuing evolution of the treatment of 

oral infection that produces the clinical manifestations 

of dental caries. As a profession, we are slowly moving 

away from the purely surgical approach to treating this 

disease. Science is providing us the tools to diagnose 

and treat the infection before it causes damage. 

The application of probiotic strategies may, in the 

494 



not-distant future, provide the end of new cavities in 

treated populations. 

Future Directions 

Probiotics can be used as passive local immunization 

against dental caries. High titers of antibodies can 

also be directed against human cariogenic bacteria 

produced in bovine colostrum over the vehicle of 

fermented milk. 

Studies have been largely conducted in animals, and 

human studies have not been of sufficient duration to 

assess the impact on caries. Most studies on the effects of 

probiotics on caries prevention are aimed at decreasing 

the number of mutans streptococci. Primarily probiotic 

Lactobacillus and Bifidobacterium strains have been 

used along with few more strains. Unfortunately, in 

most cases, the study groups were relatively small, and 

the studies were fairly short. Preliminary data obtained 

has been encouraging, but numerous randomized 

clinical studies will be required to clearly establish the 

potential of probiotics in prevention of dental caries. 

Also complete understanding of the broad ecological 

changes induced in the mouth by probiotics or 

prebiotics will be essential to assess their long-term 

consequences for oral health and disease. 

References 

1. 

2. 

3. 

4. 

5. 

6. 

7. 

8. 

Miller W. Micro-organisms of the Human Mouth. SS 

White; Philadelphia, 1890. 

Keyes PH. Research in dental caries. J Am Dent Assoc 

1968;76(6):1357-73. 

Hamilton-Miller JM, Gibson GR, Bruck W. Some 

insights into the derivation and early uses of the word 

‘probiotic’. Br J Nutr 2003;90(4):845. 

Lilly DM, Stillwell RH. Probiotics: growth-promoting 

factors produced by microorganisms. Science 

1965;147(3659):747-8. 

de Vrese M, Schrezenmeir J. Probiotics, prebiotics, and 

synbiotics. Adv Biochem Eng Biotechnol 2008;111: 

1-66. 

Schrezenmeir J, de Vrese M. Probiotics, prebiotics, and 

synbiotics - approaching a definition. Am J Clin Nutr 

2001;73(2 Suppl):361S-364S. 

Isolauri E. Probiotics in human disease. Am J Clin Nutr 

2001;73(6):1142S-1146S. 

Meurman JH. Probiotics: do they have a role in oral 

medicine and dentistry? Eur J Oral Sci 2005;113(3): 

188-96. 

9. 

10. 

11. 

12. 

13. 

14. 

15. 

16. 

17. 

18. 

19. 

20. 

21. 

22. 

23. 

Haukioja A. Probiotics and oral health. Eur J Dent 

2010;4(3):348-55. 

Sanders ME. Considerations for use of probiotic 

bacteria to modulate human health. J Nutr 2000;130(2S 

Suppl):384S-390S. 

Brady LJ, Gallaher DD, Busta FF. The role of probiotic 

cultures in the prevention of colon cancer. J Nutr 

2000;130(2S Suppl):410S-414S. 

Reid G, Jass J, Sebulsky MT, McCormick JK. Potential 

uses of probiotics in clinical practice. Clin Microbiol Rev 

2003;16(4):658-72. 

Ouwehand AC, Salminen S, Isolauri E. Probiotics: an 

overview of beneficial effects. Antonie Van Leeuwenhoek 

2002;82(1-4):279-89. 

Szajewska H, Ruszczyński M, Radzikowski A. Probiotics 

in the prevention of antibiotic-associated diarrhea in 

children: a meta-analysis of randomized controlled trials. 

J Pediatr 2006;149(3):367-372. 

Famularo G, De Simone C, Pandey V, Sahu AR, 

Minisola G. Probiotic lactobacilli: an innovative tool to 

correct the malabsorption syndrome of vegetarians? Med 

Hypotheses 2005;65(6):1132-5. 

Reid G. Probiotic agents to protect the urogenital 

tract against infection. Am J Clin Nutr 2001;73(2 

Suppl):437S-443S. 

Comelli EM, Guggenheim B, Stingele F, Neeser JR. 

Selection of dairy bacterial strains as probiotics for oral 

health. Eur J Oral Sci 2002;110(3):218-24. 

Caglar E, Sandalli N, Twetman S, Kavaloglu S, 

Ergeneli S, Selvi S. Effect of yogurt with Bifidobacterium 

DN-173 010 on salivary mutans streptococci and 

lactobacilli in young adults. Acta Odontol Scand 

2005;63(6):317-20. 

Meurman JH, Stamatova I. Probiotics: contributions to 

oral health. Oral Dis 2007;13(5):443-51. 

Caglar E, Kargul B, Tanboga I. Bacteriotherapy and 

probiotics’ role on oral health. Oral Dis 2005;11(3): 

131-7. 

Anderson MH, Shi W. A probiotic approach to caries 

management. Pediatr Dent 2006;28(2):151-3; discussion 

192-8. 

Bhusan J, Chachra S. Probiotics: their role in prevention 

of dental caries. J Oral Health Commun Dent 

2010;4(3):78-82. 

Näse L, Hatakka K, Savilahti E, Saxelin M, Pönkä A, 

Poussa T, et al. Effect of long-term consumption of a 

probiotic bacterium, Lactobacillus rhamnosus GG, in 

milk on dental caries and caries risk in children. Caries 

Res 2001;35(6):412-20. 


495


24. 

25. 

26. 

27. 

28. 

Yli-Knuuttila H, Snäll J, Kari K, Meurman JH. 

Colonization of Lactobacillus rhamnosus GG in the oral 

cavity. Oral Microbiol Immunol 2006;21(2):129-31. 

Ahola AJ, Yli-Knuuttila H, Suomalainen T, Poussa T, 

Ahlström A, Meurman JH, et al. Short-term consumption 

of probiotic-containing cheese and its effect on dental 

caries risk factors. Arch Oral Biol 2002;47(11):799-804. 

Simark-Mattsson C, Emilson CG, Håkansson EG, 

Jacobsson C, Roos K, Holm S. Lactobacillus-mediated 

interference of mutans streptococci in caries-free vs. 

caries-active subjects. Eur J Oral Sci 2007;115(4): 

308-14. 

Caglar E, Cildir SK, Ergeneli S, Sandalli N, Twetman S. 

Salivary mutans streptococci and lactobacilli levels after 

ingestion of the probiotic bacterium Lactobacillus reuteri 

ATCC 55730 by straws or tablets. Acta Odontol Scand 

2006;64(5):314-8. 

Comelli EM, Guggenheim B, Stingele F, Neeser JR. 

29. 

30. 

31. 

32. 

Selection of dairy bacterial strains as probiotics for oral 

health. Eur J Oral Sci 2002;110(3):218-24. 

Petti S, Tarsitani G, Simonetti D’Arca A. Antibacterial 

activity of yoghurt against viridans streptococci in vitro. 

Arch Oral Biol 2008;53(10):985-90. 

Caglar E, Kavaloglu SC, Kuscu OO, Sandalli N, 

Holgerson PL, Twetman S. Effect of chewing gums 

containing xylitol or probiotic bacteria on salivary 

mutans streptococci and lactobacilli. Clin Oral Investig 

2007;11(4):425-9. 

Kang MS, Chung J, Kim SM, Yang KH, Oh JS. Effect of 

Weissella cibaria isolates on the formation of Streptococcus 

mutans biofilm. Caries Res 2006;40(5):418-25. 

Caglar E, Kuscu OO, Selvi Kuvvetli S, Kavaloglu Cildir 

S, Sandalli N, Twetman S. Short-term effect of ice-cream 

containing Bifidobacterium lactis Bb-12 on the number 

of salivary mutans streptococci and lactobacilli. Acta 

Odontol Scand 2008;66(3):154-8. 

496 


Oral Health and Wellness on Wheels!!! 


R Sushma*, D Nagabhushana** 

Abstract 

Fully equipped mobile dental clinics provide on-the-spot diagnostic, preventive, interceptive and curative services to the 

doorsteps of the underprivileged, rural population. It’s an innovative, on-site, dental outreach provider to bring state of 

the art, preventive dental care to those in need in the most comfortable and effective way possible. 

Key words: Mobile dental service, outreach program, mobile dental unit, portable dentistry 

The greatest equity of access is said to exist 

when need, rather than structural or individual 

factors determine who gains entry to the 

healthcare system. 

Healthcare is a right, not a privilege but is healthcare 

accessible? 

Basic oral care facilities should be accessible to every 

individual since oral health is an important and crucial 

part of one’s overall health and wellness. Over the ages, 

oral healthcare has been delivered to the community, 

in different ways. The horse back dentistry of olden 

days has evolved into the most modern painless dental 

procedures. 

All over the world, different countries have different 

healthcare delivery systems. In our country, different 

state governments have established the dental clinics 

at different levels from the state capitals to rural areas, 

where salaried dentists give dental treatment. In India 

70% of the dentists practice in urban areas and we 

seldom find dental clinics in rural areas except for a few 

government establishments, which lack the required 

infrastructure. 

Providing universal health insurance coverage and 

developing integrated delivery systems may fail to 

*Lecturer, Dept. of Public Health Dentistry 

**Reader, Dept of Oral Medicine and Radiology 

JSS Dental College and Hospital, JSS University, Mysore, Karnataka 


Dr R Sushma 

E-mail: hisushhere@yahoo.co.in 

provide universal access. Fully equipped mobile dental 

clinics to provide effective dental care to the doorsteps 

of the underprivileged, rural population is the need 

of the hour. A mobile dental clinic offers dentists 

the freedom to offer patients access to care whenever, 

wherever. 1 

The most persistent problems in healthcare, especially 

rural healthcare are: 

• Provider shortages 

• Fragmented delivery systems 

• Cultural and language barriers 

• Uninsured populations 

• Geographic isolation. 

These are just some of the challenges to be 

encountered. 2 

With the help of dedicated professionals, volunteers 

and community support ‘creative solutions’ can provide 

vital services to the communities through outreach 

programs. 

Need for Mobile Dental Service 

Areas where services do not exist and people are in real 

need of it: 

• Rural and frontier residents 

• The disabled 

• The frail elderly 

• At-risk pregnant women and their infants and 

children 

• The homeless, poor. 


497


How Mobile Services Started with 

Dentistry? 

In the early 1970s when dentistry was in its infancy, 

introduction of public health dentistry initiated the 

need for making dental students aware that there 

are people who are beyond the reach of available 

services. The objective was to expose students to work 

in rural setup of country, so that they will be able to 

work in rural areas after graduation. This was the act 

of reaching out. With this exposure, students enjoyed 

working for the needy people, saw more patients, felt 

like real dentists and came in contact with other health 

professionals. 

Mobile Dental Units are Used in many 

Ways and Many Places 

• School programs (children) 

• Retirement homes (elderly) 

• Small communities (rural) 

• Corporate (employees) 

• Community agencies 

• Organizations 

• Families in need of oral health services. 

The general concept is to drive the ‘clinic on wheels’ 

to residents of outlying communities where limited 

resources and travel are obstacles for receiving timely 

dental care. 3 

Mobile Dental Clinic is Involved in the 

Following Activities 4 

Community Programs 

• Training of dental students in community dental 

services 

• Community awareness and oral health promotion 

Dental Services 

• Dental check-up and treatment 

Research 

• Oral health surveys 

• Screening of oral diseases 

Mobile Dental Clinic 5,6 

Advantages 

• Moderate start up costs 

• It addresses the problem of transportation to the 

clinics 

• It decreases missed appointments when run in 

conjunction with schools 

• Services can be made available at multiple sites 

• Services are made available to the needy 

population 

• Excellent patient attendance 

• Treat child without parent 

• Transportation issues eliminated 

Disadvantages 

• High maintenance costs 

• Difficult to access and store patient records 

• Provides limited services and follow-up may be 

difficult 

• Requires permission for site use 

• High administrative needs 

• High productivity difficult 

• Location of appropriate parking 

• Patient record access/storage 

• Computer and phone access difficult 

• Multiple weather related problems 

Factors to be Considered to Pursue a 

Mobile Unit 

Purchasing a mobile unit to deliver healthcare services 

can be an expensive undertaking for anyone interested 

in pursuing this option. Yet, little information is found 

in the literature on planning or designing such vehicles. 

A set of guidelines could help administrators to make 

better decisions regarding this approach for delivering 

healthcare. 7 

The process of deciding to pursue a van purchase is 

complicated, and administrators may best be served by 

obtaining experienced consultants to help them fully 

comprehend the issues involved. After the decision to 

purchase a mobile unit is made, it is necessary to focus 

on van requirements and design. 8 

The mobile dental clinic should be equipped with two 

dental chairs with all attachments and seating space for 

15-20 people. 9 

• Equipments to be fitted inside the clinic. 10,11 

• Dental chair-Hydraulically operated dental chair 

with water connection, spittoon and tumbler. 

• Air ventury suction with flow control valve, auto 

drain and auto flush system. 

498 



• Aerotor, micromotor and scaler with three scaling 

tips. 

• 3-way-syringe. 

• Light cure unit with gun, eye protection shield. 

• Multifunctional foot control 

• Transparent water booster 

• Basin 

• Stainless steel instrument tray 

• X-ray viewer. 

• Dental operator’s stool 

• Operating light with two intensity, fixed with 

hinge on the top of the Van 

• Dental X-ray unit 70 KV, 8 mA with digital arm 

timer and day light manual developer. 

• Autoclave 

• High speed automatic instrument autoclave with 

digital timer for wet and cycles, which can achieve 

135°C, minimum capacity of 20 lt. Screw type 

handle for the door locking to prevent sudden 

opening of the door. 

• Glass bead sterilizer; Portable, easy to handle with 

a very low current consumption. Instruments may 

be kept only for 10-30 seconds and will be ready 

for use. 

• Metal cabinets with wash basin 

• Portable dental unit 

• Compact compressor: Built in 0.25 HP oil-free, 

medical grade Monobloc compressor fitted with 

auto head air release valve, safety release valve and 

over heat thermo cut off. 

• Stabilizer: Highly accurate stabilizer of 4 KV. 

It should have high correction speed with the 

input range of 170-270 V and output range of 

220/230 V. 

• Generator: It should be a portable generator with 

4 KVA capacity with petrol start and run 

• Water Tank: 400 lt capacity 

• Oxygen cylinder 

• Public address system 

• TV and DVD player 

• Health education models 

The mobile clinic requires a garage with proper security. 

The driver has to be full time and an integral part of 

the care delivery team. 

Conclusion 

The focus should be on reducing the major disparities 

in oral health status and inequities in access to oral 

healthcare, while providing the highest caliber of 

dentistry for patients in a highly efficient manner. Most 

developing countries cannot afford to build adequate 

modern healthcare infrastructures to be accessed by 

every citizen. The key to a successful dental practice is a 

cohesive dental team, which will create an atmosphere 

of cooperation resulting in the achievement of the goal 

of oral health. 

In order to provide dental health curative and 

restorative services along with primary prevention of 

dental diseases, it is proposed that there should be well 

equipped mobile dental clinics so that the services can 

be rendered to the rural masses at their doorsteps, more 

so in various remote and inaccessible areas. 12 

References 

1. 

2. 

3. 

4. 

5. 

6. 

7. 

8. 

9. 

10. 

11. 

12. 

Griffith J. Establishing a dental practice in a rural, lowincome 

county health department. J Public Health Manag 

Pract 2003;9(6):538-41. 

Lewis JH, Andersen RM, Gelberg L. Health care for 

homeless women. J Gen Intern Med 2003;18(11):921-8. 

Krust KS, Schuchman L. Out-of-office dentistry: 

an alternative delivery system. Spec Care Dentist 

1991;11(5):189-93. 

Auceda R. Outreach: big wheel surgery. Perspectives in 

health volume 1 – No. 2 1996. 

Morreale JP, Dimitry S, Morreale M, Fattore I. Setting up a 

mobile dental practice within your present office structure. 

J Can Dent Assoc 2005;71(2):91. 

Carr BR, Isong U, Weintraub JA. Identification 

and description of mobile dental programs - a brief 

communication. J Public Health Dent 2008;68(4):234-7. 

Lalumandier JA, Molkentin KF. Establishing, funding, and 

sustaining a university outreach program in oral health. 

Health Aff (Millwood) 2004;23(6):250-4. 

Moulavi D, Bushy A, Peterson J, Stullenbarger E. Thinking 

about a mobile health unit to deliver services? Things to 

consider before buying. Aust J Rural Health 2000;8(1): 

6-16. 

Lee EE, Thomas CA, Vu T. Mobile and portable dentistry: 

alternative treatment services for the elderly. Spec Care 

Dentist 2001;21(4):153-5. 

Doherty NJ, Crakes G. Estimating the costs of public 

dental programmes: mobile clinics. Community Dent 

Health 1987;4(2):151-6. 

Berkey DB, Ela KM, Berg RG. Advances in portable 

and mobile equipment systems. Int Dent J 1993;43(5): 

455-65. 

Douglass JM. Mobile dental vans: planning considerations 

and productivity. J Public Health Dent 2005;65(2):110-3. 


499


Programmed Self-cell Suicide (Apoptosis) – Current Review, 

Concepts and Future Prospects 

JP Rajguru*, KMK Masthan**, TS Thirugnanasambandan † , N Aravindha Babu ‡ 

Abstract 

Homeostasis of tissues depends upon cell division and proliferation. Well-organized or programmed cell death (apoptosis) is 

an intrinsic mechanism of our human body playing in various physiological and pathological processes during evolution. This 

type of programmed cell death (PCD) is essential for development of highly cellular organisms. Apoptosis plays a major role 

in embryogenesis and many diseases like neoplasia, necrosis, acquired-immunodeficiency syndrome (AIDS) and neurogenic 

disorders. It releases new essential activated death receptors and mitochondria, which are the beginning of the pathway proposed 

for initiating apoptosis. This process is regulated by intra-and extrasomatic signals. Damage of cell results in activation of 

a family of caspases (CASP). Caspases are released by inactivated proenzymes activating various organelles in cytosol and 

nucleus. This leads to cellular monopoly change and cell death. Uncontrolled mechanisms of signals lead to pathology in the 

body. Hence, clinically much pathology is the ultimate result of either increased or decreased apoptosis. 

Key words: Apoptosis, necrosis, clinical considerations 

Apoptosis (programmed cell death) is a Greek 

terminology, meaning “falling of leaves from 

tree”. Earlier, it was known as physiological cell 

death. Kerr and co-worker (1972), 1 coined the term 

Apoptosis. It is a well-organized regulated mechanism 

in eukaryotes during the process of embryogenesis. 

It is also known as cellular self-destruction; cell self 

suicide or programmed cell death (PCD). 2 Apoptosis 

is mandatory for normal physiological development 

and removal of transformed cells. 3,4 Genetically, it is 

a controlled process regulated by complex molecular 

signaling systems. In this system, cells undergo change 

an organized fashion, an energy-dependant enzymatic 

breakdown resulting in cellular fragments. DNA 

fragmentation, chromatin condensation, blebbing of 

cellular membrane, cell shrinkage and apoptotic bodies 

known as Councilman bodies are seen. These fragments 

* 

Senior Lecturer, Dept. of Oral Pathology 

Saraswati Dental College and Hospital, Lucknow 

** 

Professor and Head, Dept. of Oral Pathology and Microbiology 


† 

Professor, Dept. of Oral Pathology 

Rajah Muthiah Dental College and Hospital 

Annamalai University, Chidambaram 

‡ 

Professor, Dept. of Oral Pathology and Microbiology 



Dr JP Rajguru 

E-mail: drgurumdsop@gmail.com 

are degraded and phagocytosed. 5 Programmed 

cell death plays a central role in etiopathogenesis 

of human diseases. When apoptotic process is 

suppressed, overexpressed or mutated, the imbalanced 

or uncontrolled apoptosis leads to pathology of human 

diseases. Ischemic cell death can cause nuclear as well as 

cytoplasmic swelling and karyolysis. Normal stimulus 

are absent in apoptosis but can be seen in necrosis 

as shown in Table 1. This mechanism will also cause 

disordered apoptosis as shown in Table 2. 

Difference between Apoptosis and 

Necrosis 

Self-suicide is an organized program, through which 

unstipulated or destroyed cells undergo destruction with 

activated genes. 7 It results in shrinkage of cell, cellular 

detachment and fragmentation of bodies preserving 

the membrane. Glueksmann distinguished between 

apoptosis (physiologically natural cell death) and necrosis 

(accidental cell death due to injury or toxins) as shown 

in Table 2. 8 Ischemic cell death leads to cytoplasmic 

and nuclear swelling. Apoptosis process results in 

phagocytosis. 9-12 To overcome noxious stimulus (toxins/ 

ischemia) cells undergo cell aging and necrosis. 13 On 

the other hand, apoptosis refers to cell death occurring 

during normal embryogenesis of immature organs and 

the maturation of tissues or organs. 14 

500 



Table 1. Apoptosis vs Necrosis 

Apoptosis 

Late loss of membrane 

integrity 

Asynchronous process in 

single cells 

Genetically controlled 

Physiological and 

pathological 

No inflammatory reaction 

Cell shrinkage 

Condensation of nuclear 

contents 

Table 2. Apoptotic Genes 

Pro-apoptotic genes 

P 53 

Bcl-xl, Bax, Bak, Bad 

Ced-3 

Pathophysiology 

Necrosis 

Early loss of membrane integrity 

Occurs synchronously in multiple 

cells 

Caused by overwhelming 

noxious stimuli 

Always pathological 

Inflammatory reaction 

Generalized cell and nucleus 

swelling 

Nuclear chromatin disintegration 

Anti-apoptotic genes 

Bcl-2 

Abl 

Caspases family --- 

Ced-9 

Apoptotic Incentive 17,18 

Four group of stimuli are found, which includes group 

stimuli: I, II, III, IV. 

Group I stimuli includes ionizing and alkylating 

agents. They will further induce DNA damage. 

Group II stimuli cause apoptosis by stimulation of 

death receptors. Group III stimuli include biochemical 

agents, which will increase the downstream components 

of apoptotic pathway. (e.g.), (phosphatase and kinase 

inhibitors including calphotin C). Group IV stimuli 

may cause cell boundary damage either by heat, light 

and oxidizing agents. If the dose increases, then it may 

cause necrosis. 

PCD (apoptosis) is a multidirectional process. The 

genes activity and mediators influence the cell’s likelihood 

of activating it`s self-death programmers. If the 

decision phase is properly executed then cell death may 

occur. 

Mechanism 19-21 

Apoptosis is an unexplored highly complicated process. 

Decision of cell death is not a light mechanism. 

Apoptosis process involves two pathways. 

Pathway of Apoptosis 

It consists of two mechanisms: (Fig. 1) 

Apoptosis includes three phases. 

• In first phase, cells get detached from its 

substratum and adjacent cells. There will 

be absence of microvilli and desmosomes. 15 

Fragmentation of DNA by specific endonucleases 

gets packed into vesicles. We can observe strand 

breakage and nuclear chromatin condensation. 

The rough endoplasmic reduction (RER) and 

smooth endoplasmic reduction (SER) swells and 

cell becomes dense and shrinkage of cytoplasm 

is seen. 

• In second phase, cell produce cell buds by 

breaking into multiple membranes and result in 

apoptolic bodies. 

• In third phase, the permeability of cell membrane 

is increased to stain. Later, the apoptotic bodies are 

phagocytosed. 

The duration of this mechanism is around 15-25 

minutes. 16 

Figure 1. Pathway or mechanism of apoptosis. 


501


• Activation of cell surface death receptors - extrinsic 

phase. 

• Release of cytochrome C from mitochondria - 

intrinsic phase. 

Activated Cell Surface Death Receptorinduced 

Apoptosis: (Extrinsic Phase) 

Apoptosis-induced cell surface death receptors are 

Fas and tumor necrosis factor (TNF). Fas receptor 

is CD95 or APO-1. It is a cytoplasmic protein. It is 

activated by binding of Fas legend to cell membrane. 

This mechanism is very important in regulating 

immune response cytototoxic T lymphocytes and 

induces apoptosis. TNF receptor systems show some 

differentiation in biochemical pathway. TRIAL (TNFrelated 

apoptosis inducing legend) binds to TNF 

receptor system and form TRADD (TNF receptor 

associated death domain) by following two phases. 

Judgment Phase 

Important genes, which control apoptosis, are Bcl-2 

andp53. Bcl-2 is oncogene 22 and blocks apoptosis. 23 

It is also known as cell death suppressor gene. 

It directly regulates apoptosis. If the concentration 

of Bcl-2 is increased, it prevents apoptosis. Apoptosis 

induced death receptors are: 

• TNF receptors - TNF receptors system 

• FAS receptor 

Fas receptor is also known as CD95/APO-1. It is a 

transmembrane glycoprotein death receptor. It is 

activated by binding Fas legend (Fas-L) to cell molecule. 

FADD (Fas-associated death domain) is produced. 

These are necessary for controlling immune response 

of cytotoxic T lymphocytes and apoptosis. 

TNF receptors systems mediate another biochemical 

pathway. TNF-related apoptosis inducing legend 

(TRAIL) fix to TNF receptor system and create TRADD 

(TNF-receptor associated death domain) through two 

phases. Two genes are going to regulate the apoptosis 

(1) Bcl-2 (2) p53. Bcl-2 is an oncogene or cell death 

suppressor gene, because it may suppress apoptosis. 

Families of Bcl-2 are - Bcl XL 

, Bax, Bak and Bad. They 

promote Apoptotic - Proapoptotic proteins. 24 Bcl-2 and 

Bcl-XL, present apoptotic - proapoptotic proteins. All 

cells depend upon proapoptotic or else antiapoptosis 

prevails. P53 gene is a 53 Kda nuclear phosphoprotein, 

Table 3. Apoptosis-induced in Various Condition 

Decrease apoptosis 

Neoplasia 

Follicular lymphoma 

Carcinoma With P 53 Mutations 

Autoimmune disorders 

Viral disorders 

Herpes viruses 

Pox viruses 

Adenoviruses 

which is seen in chromosome mutation of P 53 . These 

genes are predominant in 50% of human cancers and 

are associated with resistance to treatment. 25 It is a 

proapoptotic mediator. If there is any DNA damage, 

then p53 restrict the replication and gives sufficient 

time for repairing of the cell. If cell repair can’t be done, 

apoptosis will be induced preventing multiplication 

of the damaged cell. Cell arrest is quite impossible in 

neoplastic cells in which p53 activity is mutated. 26 p53 

gene is an important cell growth regulator. Decrease 

in p53 in a cell also makes it resistant for radiation 

and chemotherapy and inhibiting cancer treatment 

(Table 3 Apoptotic supporting genes). 28,29 

Implementation Phase 

In this phase, proteolysis and mitochondrial inactivation 

occurs. Cellular distruption results from activation of 

a cystine proteases family known as caspases (CASP). 30 

Up to now, CASP 1-10 have been discovered. They are 

subclassified in to three subgroups. 

• Group - 1: CASP-1, 4 and 5. 

They are going to support proinflammatory cytokines. 

• Group - 2. CASP-2, 3 and 7. 

They are involved in cleavage of apoptotic substrates. 

• Group -3. CASP - 6, 8 and 9. 

They activate Group-2 caspases. 31 

increased Apoptosis 

AIDS 

Neurogenerative disorders 

Alzheimer’s disease 

Parkinson’s disease 

Amyotrophic lateral 

serosis 

Retinitis pigmentosa 

Few intermediate factors like oncogene C-myc 

transcription for E 2 

F-1 32 and Ras oncoprotein are 

involved in the internal regulation of apoptosis. E 2 

F-1 

is a positive regulator of C-myc protein. 

Release of Cytochrome C from Mitochondria 

(Intrinsic Phase) 33-38 

502 



Various stimulations induce binding of proapoptotic 

Bcl-2 family members to chief cell organelles 

Bcl-2 family members. This will cause release of 

cytochrome C and binds cytoplasmic protein Apaf-1. 

Apaf-1 activates procaspase-9 allosterically, which again 

activates procapase-3 and 7. Activation and activity 

is tightly regulated. Mitochondrial pathway signal is 

controlled as anti-apoptotic Bcl-2 family members 

who inhibit release of cytochrome C. 

Apoptosis Promoting Factors 

This is a flavoprotein, initiating the caspase independent 

pathway by causing fragmentation of DNA and 

chromatin condensation. This factor also participates 

in the regulation of apoptotic mitochondrial membrane 

peremeability and exhibits an NADH oxidase activity. 

Under normal physiological process, AIF is programmed 

behind the outer mitochondrial membrane. In case 

of apoptosis, AIF translocates to the cytoplasm and 

nucleus. Decrease in this factor results in resistance of 

embryonic stem cell to death following the withdrawal 

of GF. Caspase-independent effects can be contributed 

to AIF. 39 The mammalian AIF precursors contain 

an N-terminal mitochondrial localization sequence. 

In humans, one AIF sequence has been recently 

discovered, which promotes proapoptotic function. 

The redox reaction catalyze by AIF in mitochondrial 

in the living cell is in questioned. It has been proposed 

that AIF might interact with cytochrome Bcl complex 

and catalyze the electron transfer to the mitochondrial 

repertory chain. AIF can do a caspase-independent 

death receptor. When caspase activation occurs early 

during apoptosis activated caspases induced the caspaseactivated 

protein t-Bid, which can trigger the regulation 

of AIF from mitochondrial. So AIF is released from 

mitochondria before cell death occurs. It indicates that, 

AIF is required for cytochrome C40 dependent caspaseactivation 

cascade. MMP can operate apoptosis. AIF is 

an important factor in regulation of apoptosis. Bcl-2 

family regulates the release of AIF. 

Significance of Apoptosis 

Unregulated cell death can be a significant component 

of diseases such as cancer, Alzheimer’s disease and 

Hutingoton’s disease. Few of them are showing under 

expression as well as over expression. All diseases of 

human are associated with disordered apoptosis. 

In normal human physiology, apoptosis places a key 

role to maintain homeostasis. It has been estimated that 

around 10 billion cells/day are being made of which few 

are lost and few survive. 41 They balanced those dying 

by apoptosis. It is an essential mechanism, removing 

pathogens invaded cells and plays an important role in 

wound healing. 42 

apoptosis is also important to estimate aggressive 

immune cells. It is also mentioned that adaptive stress 

plays an important role in pathophysiology. 43,44 

Apoptosis in Various Disease and 

Conditions (Table 4 and 5) 

Immune System 

Autoimmunity is an important factor in apoptosis. 45 

Dysregulation of apoptosis cause critical autoimmune 

disease, immunodeficiency and lymphoid malignancy. 

Apoptosis dysregulation can also cause rheumatoid 

arthritis, systemic lupus erythematosus (SLE), bowel 

diseases and insulin-dependent diabetes mellitus 

(IDDM). 46,47 Increased apoptosis cause Aplastic-A, 

β thalassemia. 48 

Viral Disorders 

Virology also shows a major mode of cell death as 

in cytotoxic lymphocyte (CTF)-induced cell killing. 

Certain viruses show anti-apoptotic proteins that 

lead to development of cancer (e.g. HPV and 

adenovirus). 49 HIV can be regarded as a pathological 

imbalance between CD 4 

cell death rate and cell 

replacement. HIV shows depletion of CD 4 

T 

lymphocytes, which is to immunodeficiency 50 and 

lymphoma. In HIV infection, CD 4 

T cells are gradually 

lost due to increase apoptosis and leads to AIDS. 50 

Central Nervous System 

In embryogenesis, the nervous system produces 

a surplus of cells. apoptosis are programmed cell 

death that removes those neuron cells, which 

fail to reach the target. Cytokines (TNF-α) 

and reactive oxygen special (ROS) may induced 

PCD. 51 Increased apoptosis plays an important 

role in neurodegenerative diseases 52 and aging. It 

is commonly seen like Alzheimer’s and parkinson’s 

disease and malignancies of neuron. 53,54 


503


Table 4. Human Diseases associated with 

Disordered Apoptosis 6 

Decreased apoptosis 

• Epithelial tissue • Carcinogenesis 

• Blood vessels • Intimal hyperplasia 

• Lymphocytes • Autoimmune disorders 

• Hemopoeitic • Leukemia, lymphoma 

systems 

Increased apoptosis 

• Macrophages Bacillary dysentery, peri-infarct 

Border zone lymphocytes Depletion 

In HIV injections and sepsis 

• Myocardium neurodegenerative diseases like 

Alzheimer’s and Parkinson’s 

• Lymphocytes 

disease 

CNS 

Table 5. Apoptosis associated with Various Diseases 

Decreased 

apoptosis 

Cancer 

• Viral disorders 

• Herpesviruses 

• Poxviruses 

• Adenoviruses 

Follicular lymphomas 

Carcinomas with 

P53 mutations 

Cardiovascular System 

Myocytic degeneration occurs in apoptosis as well as 

necrosis. In case of necrosis it occurs due to hypoxia and 

ischemia. apoptosis is seen in myocardial infarction, 

reperfusion, increases free radical production and 

intercellular calcium, which are main inducer of 

apoptosis. In cardiac development, apoptosis plays a 

major role. Increased apoptosis leads to bradycradia 

and sudden death. 

Neoplasia 

Increased apoptosis 

Aids 

• Neurodegenerative disorders 

• Alzheimer’s disease 

• Parkinson’s disease 

• Amyotrophic lateral sclerosis 

• Retinitis pigmentosa 

• Cerebellar degeneration 

Myelodysplastic syndromes/ Aplastic 

anemia 

Ischemic injury/Myocardial infarction/ 

Stroke/ Reperfusion injury 

It is associated with accumulation of neoplastic cells 

due to enhanced cell proliferation, decrease cell turn 

over or both. Decrease apoptosis plays an important 

role in carcinogenic process. 55-57 

Gastrointestinal Disorders 

We can appreciate decreased or increased apoptosis in 

gastrointestinal diseases. Colorectal cancer is associated 

with inhibition of apoptosis; Mutated gene may be 

seen in case of colonic and gastric cancer. Hepatitis 

shows decreased apoptosis. 58 

Renal Disorders 

In case of renal malignancy, the apoptotic level is 

increased. 59 

Reproductive System 

Due to presence of trophic hormone, apoptosis is 

properly regulated. 60 

Future Prospects 

Since last few years,’ many of advances have been made 

to exploit mutated expression of “inhibitors of apoptotic 

proteins (IAPs)” for detection and treatment of human 

diseases. Many preclinical studies have provided end 

line of evidence, that IAPs can be cross-checked by 

antisense oligonucleotides, RNA interference or small 

molecule compounds. This leads to a new line of 

treatment of cancer. But still the question of using 

these strategies as diagnostic or therapeutic tools in 

clinical management of cancer, autoimmune disorders 

or neurodegenerative diseases is to be answered. 

References 

1. 

2. 

3. 

4. 

5. 

6. 

Kerr JF, Wyllie AH, Currie AR. Apoptosis: a basic 

biological phenomenon with wide-ranging implications 

in tissue kinetics. Br J Cancer 1972;26(4):239-57. 

Savitz SI, Rosenbaum DM. Apoptosis in neurological 

disease. Neurosurgery 1998;42(3):555-72; discussion 

573-4. 

White E. Life, death, and the pursuit of apoptosis. Genes 

Dev 1996;10(1):1-15. 

Weil M, Jacobson MD, Coles HS, Davies TJ, Gardner 

RL, Raff KD, et al. Constitutive expression of the 

machinery for programmed cell death. J Cell Biol 

1996;133(5):1053-9. 

Wyllie AH, Kerr JF, Currie AR. Cell death: the significance 

of apoptosis. Int Rev Cytol 1980;68:251-306. 

Pritchard DM, Watson AJ. Apoptosis and gastrointestinal 

pharmacology. Pharmacol Ther 1996;72(2):149-69. 

504 



7. 

8. 

9. 

10. 

11. 

12. 

13. 

14. 

15. 

16. 

17. 

18. 

19. 

20. 

21. 

22. 

23. 

24. 

25. 

Martin SJ. Apoptosis: suicide, execution or murder? 

Trends Cell Biol 1993;3(5):141-4. 

Kam PC, Ferch NI. Apoptosis: mechanisms and clinical 

implications. Anaesthesia 2000;55(11):1081-93. 

Majno G, Joris I. Apoptosis, oncosis, and necrosis. An 

overview of cell death. Am J Pathol 1995;146(1):3-15. 

Farber E. Programmed cell death: necrosis versus 

apoptosis. Mod Pathol 1994;7(5):605-9. 

Farber E. Chemical carcinogenesis. N Engl J Med 

1981;305(23):1379-89. 

Hockenbery D. Defining apoptosis. Am J Pathol 

1995;146(1):16-9. 

Lennon SV, Martin SJ, Cotter TG. Dose-dependent 

induction of apoptosis in human tumour cell lines by 

widely diverging stimuli. Cell Prolif 1991;24(2):203-14. 

Cobb JP, Hotchkiss RS, Karl IE, Buchman TG. 

Mechanisms of cell injury and death. Br J Anaesth 

1996;77(1):3-10. 

Wyllie AH. Apoptosis: an overview. Br Med Bull 

1997;53(3):451-65. 

Weedon D, Searle J, Kerr JF. Apoptosis. Its nature and 

implications for dermatopathology. Am J Dermatopathol 

1979;1(2):133-44. 

Rudin CM, Thompson CB. Apoptosis and disease: 

regulation and clinical relevance of programmed cell 

death. Annu Rev Med 1997;48:267-81. 

MacLellan WR, Schneider MD. Death by design. 

Programmed cell death in cardiovascular biology and 

disease. Circ Res 1997;81(2):137-44. 

Haimovitz-Friedman A, Kan CC, Ehleiter D, Persaud 

RS, McLoughlin M, Fuks Z, et al. Ionizing radiation acts 

on cellular membranes to generate ceramide and initiate 

apoptosis. J Exp Med 1994;180(2):525-35. 

Santana P, Peña LA, Haimovitz-Friedman A, Martin S, 

Green D, McLoughlin M, et al. Acid sphingomyelinasedeficient 

human lymphoblasts and mice are defective in 

radiation-induced apoptosis. Cell 1996;86(2):189-99. 

Narula J, Kharbanda S, Khaw BA. Apoptosis and the 

heart. Chest 1997;112(5):1358-62. 

Hockenbery D, Nuñez G, Milliman C, Schreiber 

RD, Korsmeyer SJ. Bcl-2 is an inner mitochondrial 

membrane protein that blocks programmed cell death. 

Nature 1990;348(6299):334-6. 

Korsmeyer SJ. Bcl-2: an antidote to programmed cell 

death. Cancer Surv 1992;15:105-18. 

Steller H. Mechanisms and genes of cellular suicide. 

Science. 1995 Mar 10;267(5203):1445-9. 

Donehower LA, Harvey M, Slagle BL, McArthur MJ, 

Montgomery CA Jr, Butel JS, et al. Mice deficient for 

26. 

27. 

28. 

29. 

30. 

31. 

32. 

33. 

34. 

35. 

36. 

37. 

38. 

39. 

40. 

p53 are developmentally normal but susceptible to 

spontaneous tumours. Nature 1992;356(6366):215-21. 

Lane DP. Cancer. p53, guardian of the genome. Nature 

1992;358(6381):15-6. 

Clarke AR, Maandag ER, van Roon M, van der Lugt 

NM, van der Valk M, et al. Requirement for a functional 

Rb-1 gene in murine development. Nature. 1992 Sep 

24;359(6393):328-30. 

Yuan J, Shaham S, Ledoux S, Ellis HM, Horvitz HR. 

The C. elegans cell death gene ced-3 encodes a protein 

similar to mammalian interleukin-1 beta-converting 

enzyme. Cell 1993;75(4):641-52. 

Nicholson DW, Thornberry NA. Caspases: killer 

proteases. Trends Biochem Sci 1997;22(8):299-306. 

Oberhammer F, Wilson JW, Dive C, Morris ID, 

Hickman JA, Wakeling AE, et al. Apoptotic death in 

epithelial cells: cleavage of DNA to 300 and/or 50 kb 

fragments prior to or in the absence of internucleosomal 

fragmentation. EMBO J 1993;12(9):3679-84. 

Green D, Kroemer G. The central executioners of 

apoptosis: caspases or mitochondria? Trends Cell Biol 

1998;8(7):267-71. 

Wu X, Levine AJ. p53 and E2F-1 cooperate to mediate 

apoptosis. Proc Natl Acad Sci U S A 1994;91(9): 

3602-6. 

Gross A, McDonnell JM, Korsmeyer SJ. BCL-2 family 

members and the mitochondria in apoptosis. Genes Dev 

1999;13(15):1899-911. 

Earnshaw WC, Martins LM, Kaufmann SH. Mammalian 

caspases: structure, activation, substrates, and functions 

during apoptosis. Annu Rev Biochem 1999;68:383- 

424. 

Rodriguez J, Lazebnik Y. Caspase-9 and APAF-1 form an 

active holoenzyme. Genes Dev 1999;13(24):3179-84. 

Henkart PA. ICE family proteases: mediators of all 

apoptotic cell death? Immunity 1996;4(3):195-201. 

Schulze-Osthoff K, Ferrari D, Los M, Wesselborg S, 

Peter ME. Apoptosis signaling by death receptors. Eur J 

Biochem 1998;254(3):439-59. 

Reed JC. Bcl-2 family proteins. Oncogene 

1998;17(25):3225-36. 

Miramar MD, Costantini P, Ravagnan L, Saraiva LM, 

Haouzi D, Brothers G, et al. NADH oxidase activity of 

mitochondrial apoptosis-inducing factor. J Biol Chem 

2001;276(19):16391-8. 

Cregan SP, Fortin A, MacLaurin JG, Callaghan SM, 

Cecconi F, Yu SW, et al. Apoptosis-inducing factor 

is involved in the regulation of caspase-independent 

neuronal cell death. J Cell Biol 2002;158(3):507-17. 


505


41. 

42. 

43. 

44. 

45. 

46. 

47. 

48. 

49. 

50. 

51. 

Renehan AG, Booth C, Potten CS. What is apoptosis, 

and why is it important? BMJ 2001;322(7301): 

1536-8. 

Greenhalgh DG. The role of apoptosis in wound healing. 

Int J Biochem Cell Biol 1998;30(9):1019-30. 

Harman D. Role of free radicals in aging and disease. 

Ann N Y Acad Sci 1992;673:126-41. 

Ozawa T. Mechanism of somatic mitochondrial DNA 

mutations associated with age and diseases. Biochim 

Biophys Acta 1995;1271(1):177-89. 

Shortman K, Egerton M, Spangrude GJ, Scollay R. The 

generation and fate of thymocytes. Semin Immunol 

1990;2(1):3-12. 

Elkon KB. Mechanisms of autoantibody production and 

their role in disease. Mt Sinai J Med 1994;61(4):283- 

90. 

Emlen W, Niebur J, Kadera R. Accelerated in vitro 

apoptosis of lymphocytes from patients with systemic 

lupus erythematosus. J Immunol 1994;152(7):3685-92. 

Solary E, Dubrez L, Eymin B. The role of apoptosis in 

the pathogenesis and treatment of diseases. Eur Respir J 

1996;9(6):1293-305. 

Young LS, Dawson CW, Eliopoulos AG. Viruses and 

apoptosis. Br Med Bull 1997;53(3):509-21. 

Terai C, Kornbluth RS, Pauza CD, Richman DD, 

Carson DA. Apoptosis as a mechanism of cell death in 

cultured T lymphoblasts acutely infected with HIV-1. J 

Clin Invest 1991;87(5):1710-5. 

Louis JC, Magal E, Takayama S, Varon S. CNTF 

protection of oligodendrocytes against natural 

and tumor necrosis factor-induced death. Science 

1993;259(5095):689-92. 

52. 

53. 

54. 

55. 

56. 

57. 

58. 

59. 

60. 

61. 

Loo DT, Copani A, Pike CJ, Whittemore ER, 

Walencewicz AJ, Cotman CW. Apoptosis is induced by 

beta-amyloid in cultured central nervous system neurons. 

Proc Natl Acad Sci U S A 1993;90(17):7951-5. 

Wu JK, Ye Z, Darras BT. Frequency of p53 tumor 

suppressor gene mutations in human primary brain 

tumors. Neurosurgery 1993;33(5):824-30; discussion 

830-1. 

Bögler O, Huang HJ, Kleihues P, Cavenee WK. The 

p53 gene and its role in human brain tumors. Glia 

1995;15(3):308-27. 

Evan GI, Wyllie AH, Gilbert CS, Littlewood TD, Land 

H, Brooks M, et al. Induction of apoptosis in fibroblasts 

by c-myc protein. Cell 1992;69(1):119-28. 

Reed JC. Bcl-2 and the regulation of programmed cell 

death. J Cell Biol 1994;124(1-2):1-6. 

Allsop TE, Wyatt S, Paterson HF, Davies AM. The photooncogene 

BCL-2 can selectivity rescue neurotrophic 

factor-dependant neurons from apoptosis. Cell 1993;73: 

293-307. 

Hiramatsu N, Hayashi N, Katayama K, Mochizuki K, 

Kawanishi Y, Kasahara A, et al. Immunohistochemical 

detection of Fas antigen in liver tissue of patients with 

chronic hepatitis C. Hepatology 1994;19(6):1354-9. 

Veis DJ, Sorenson CM, Shutter JR, Korsmeyer SJ. 

Bcl-2-deficient mice demonstrate fulminant lymphoid 

apoptosis, polycystic kidneys, and hypopigmented hair. 

Cell 1993;75(2):229-40. 

Gosden R, Spears N. Programmed cell death in the 

reproductive system. Br Med Bull 1997;53(3):644-61. 

Ishizaki Y, Burne JF, Raff MC. Autocrine signals 

enable chondrocytes to survive in culture. J Cell Biol 

1994;126(4):1069-77. 

506 


Oral Health Aspects of Cannabis Use 


Ramandeep Singh Gambhir*, Prabhleen Brar**, Sameer Anand † , Amaninder Ranhawa ‡ , Heena Kakar # 

Abstract 

The use of cannabis, both medicinal and recreational, is growing. There are three main forms of cannabis: Marijuana, hash 

and hash oil, all of which contain the main psychoactive constituent THC. Many people are getting addicted to Marijuana, 

ignorant of its harmful effects on health. Today, cannabis abuse is a major concern because of its negative effects on general 

and oral health. Cannabis users are more prone to develop dental caries, xerostomia, alveolar bone loss, pre-cancerous oral 

lesions and other oral infections. The debate over the personal use of marijuana in around the world is extremely contentious 

with supporters for decriminalization and legalization, and others who assert the importance of strict prohibition. Public 

should have the best information at their disposal about the harms and risks associated with using cannabis in any form. 

The present review will throw a spot light on the global prevalence of cannabis use and some of the important oral health 

effects of cannabis abuse, which are an important concern to a dental professional. 

Key words: Cannabis, oral health, oral cancer, legislation 

Cannabis is the generic term used for the 

psychoactive substance derived from the three 

species of the cannabis plant. The cannabis 

plant, cannabis sativa, originated in central Asia and 

was introduced into India in the 8th century BC, 

where it was used for religious ceremonies and medical 

purposes. Subsequently, cannabis was widely used 

to treat gastric complaints, headaches, coughing, 

hepatitis, gout, ‘hard tumors’, tetanus and rabies. 1 

Cannabis contains a unique group of chemicals, 

namely cannabinoids, some of which are psychoactive. 

Cannabis contains 66 cannabinoids. The most potent 

psychoactive substance is delta-9-tetrahydrocannabinol 

(THC). However, despite the potential benefits, the 

nonmedical use of cannabis can have adverse effects on 

the general, mental and oral health of users particularly 

when used regularly for an extended period of time. 2 

There are three main forms of cannabis: Marijuana, 

hash and hash oil. Cannabis has become more closely 

*Senior Lecturer, Dept. of Public Health Dentistry 

Gian Sagar Dental College and Hospital, Rajpura, Punjab 

**Assistant Professor, Dept. of Conservative Dentistry and Endodontics 

Punjab University Dental College, Chandigarh 

† 

Senior Lecturer, Dept. of Periodontics 

Rayat and Bahra Dental College, Punjab 

‡ 

Senior Lecturer, Dept. of Public Health Dentistry 

Sri Guru Ram Dass Dental College, Amritsar 

# 

Consultant, Apollo Dental Centre, Chandigarh 


Dr Ramandeep Singh Gambhir 

E-mail: raman1g@yahoo.co.in 

linked to youth culture and the age of initiation is 

usually lower than for other drugs. Cannabis, in the 

form of hash and marijuana is thought to be the most 

frequently used drug in the United States. 3,4 There 

has been a documented link shown between cannabis 

smoking and many intraoral disturbances. 5 The present 

paper focuses on some of the major implications on 

oral health regarding the use of cannabis by people 

worldwide. 

Global Prevalence of Cannabis Use 

Cannabis is the most widely used illicit drug in Europe, 

Australia and throughout the western world. About 

147 million people, 2.5% of the world population, 

consume cannabis (annual prevalence) compared 

with 0.2% consuming cocaine and 0.2% consuming 

opiates. Nearly, 40% of Australian population aged 14 

and above (over 5 million people) have tried cannabis, 

and 18% have used it in the last 12 months. As many 

as 45% of 14-19 years old and 64% of 20-29 years old 

have used cannabis at least once in their life. Estimates 

suggest that by the age of 21, 80% of young people 

in New Zealand will have used cannabis on at least 

one occasion with 10% developing a pattern of heavy 

dependent use. 6 In Europe, one out of 5 adults has used 

cannabis at least once in his or her lifetime. Estimates 

of the actual use of cannabis (use during the past 12 

months) in 15-34 years old in Europe vary from 5% 

to 20%. On a global basis, regular use of cannabis is 


507


highest in Canada and Spain (>15%) and Switzerland 

(18.3%) (European Monitoring Centre for Drugs and 

Drug Addiction [EMCDDA]. 1 During the past decade, 

regular cannabis use by young people (15-24 years old) 

has increased in Switzerland. Cannabis consumption 

has also increased in the developing world during the 

past few years. 7 An estimated 38,200,000 African adults 

(or 7.7% of the adult population) consume the drug 

each year - far higher than the 3.8% of cannabis users 

among the world population aged 15-64. 8 According 

to a study reports, smoking, drinking and cannabis 

use are common and clustered among adolescents in 

Seychelles, a rapidly developing country in the Indian 

Ocean. 9 Results of a survey conducted among students 

in northern Thailand showed that, at some time in 

their lives, 30-40% of the male respondents and 3-6% 

of the female respondents had used cannabis. 10 

Routes of Cannabis Intake 

Smoking marijuana is the most common and efficient 

way of using cannabis as it is easy to prepare and 

its effects are rapid. Marijuana is smoked in a handrolled 

cigarette, which may contain varying amounts 

of tobacco to assist burning and, on average, 0.5-l g 

of leaves, stalks, flowers or seeds. 2,6 A typical joint 

contains 0.5-1 g of leaves. A variety of pipes are also 

used to smoke marijuana, the most common being a 

water pipe (‘a bong’); smoke is sucked through a layer 

of water, which cools it and removes some of the tar 

and irritants. Smokers inhale deeply and hold their 

breath to maximize absorption. 

Hashish can be baked and eaten in foods such as cookies 

and cakes because it is soluble in fats and alcohol. It 

may also be mixed with tobacco and smoked, or heated 

and the vapours inhaled. More commonly, hash oil is 

spread on the tip or paper wrapping of a cigarette and 

smoked. 6 

Pharmacology of Cannabis 

About 50% of the THC in a joint of herbal cannabis 

is inhaled in the mainstream smoke; nearly all of this 

absorbed through the lungs, rapidly enters the bloodstream 

and reaches the brain within minutes. Effects 

are perceptible within seconds and fully apparent in 

a few minutes. 2 Peak levels of THC occur within 

10 minutes of smoking and decline to 5-10% of initial 

levels within an hour. THC is metabolized in the liver 

and forms the major metabolite 11-hydroxy-THC, 

which is also a psychoactive agent. 2,11 Because THC is 

extremely lipid soluble, it accumulates in fatty tissues, 

reaching peak concentrations in 4-5 days. It is then 

slowly released back into other body compartments, 

including the brain. 2 The tissue elimination half-life of 

THC is approximately seven days, and total elimination 

may take upto 30 days. When ingested, the amount of 

cannabis absorbed is 25-30% less than that of smoking 

the same amount due to the first-pass metabolism by 

the liver. Therefore, the onset of the effects is delayed 

by about 30 minutes to two hours, but the duration of 

effects is prolonged. 6 

Cannabis exerts its effects on the body by interaction 

with specific endogenous receptors, CB 1 

and CB 2 

. 12 

These receptors normally modulate neuronal activity by 

affecting second messenger and ion transport systems. 

CB 1 

receptors are located in the central nervous 

system (cerebellum, cerebrum and hippocampus). CB 2 

receptors are found in cells in the immune system, 

predominantly the macrophages. As there are very few 

CB 1 

receptors in the brainstem, vital functions are not 

affected by the use of cannabis. 2 

Cannabis Abuse and Oral Health 

Cannabis users are prone to oral infections. Generally, 

Cannabis abusers have poorer oral health than nonusers, 

with higher decayed, missing and filled (DMF) 

teeth scores, 1 higher plaque scores and less healthy 

teeth gums. 13 An important side effect of cannabis 

abuse is xerostomia (dryness of the mouth caused by 

malfunctioning salivary glands). According to a study 

report, cannabis smoking and chewing causes changes 

in the oral epithelium, termed ‘cannabis stomatitis’. Its 

symptoms include irritation and superficial anesthesia 

of the oral membranous tissue covering internal organs. 

With chronic use, this may progress to neoplasia (growth 

of a tumor). 14 Dental treatment on intoxicated patients 

can result in the patient experiencing acute anxiety, 

dysphoria and psychotic-like paranoiac thoughts. The 

use of local anesthetic solutions containing epinephrine 

may seriously prolong tachycardia already induced by 

an acute dose of cannabis. 

Cannabis Abuse Causes Oral Cancer 

Chronic smokers of cannabis have an increased risk 

of developing oral leukoplakia (thick white patches on 

508 



mucous membranes of the oral cavity, including the 

tongue. It often occurs as a pre-cancerous growth), oral 

cancer and other oral infections. Oral cancer related 

to cannabis usually occurs on the anterior floor of 

the mouth and the tongue. 14,15 Marijuana smoke is 

associated with dysplastic changes within the epithelium 

of the buccal mucosa (anucleated squamous cells, 

immature cell forms, increased nuclear pleomorphism 

and increased mitotic activity and abnormalities). 

Although smoking marijuana is associated with oral 

premalignant lesions, including leukoplakia and 

erythroplakia but results of a large population based 

study found no association between marijuana use 

and development of oral squamous cell carcinoma. 16 

The increased incidence of intraoral candidiais in 

persons who smoke cannabis may be because of the 

hydrocarbons present in marijuana, which act as an 

energy source for certain types of Candida species. 

Additional factors such as compromised immune 

response due to chronic use of marijuana, poor 

denture hygiene and nutritional factors should also be 

considered. 17 

Cannabis Use and Dental Caries 

The hypothesis that cannabis increases the risk of 

caries was not confirmed according to a study report. 1 

However, the difference between groups in the 

incidence of decayed surfaces was highly significant. 

Cannabis users had considerably more open carious 

lesions than those who did not use cannabis. Shortterm 

xerostomia and consumption of cariogenic food 

and beverages after using cannabis may be responsible 

for the high incidence of caries on smooth surfaces. 

The cariogenic diet, reduced frequency of oral hygiene 

and rare dental control visits indicate that the lifestyle 

of cannabis users makes an important contribution to 

the incidence of caries. Therefore, the combination of 

cannabis use and an unhealthy lifestyle increases the 

risk of caries on smooth surfaces. 1,13 

Cannabis and Periodontal Disease 

Smoking cannabis can affect the nerve endings in the 

mouth, masking any sensitivity that may be occurring. 

Various effects like fiery-red gingivitis, alveolar 

bone loss, gingival inflammation and hyperplastic 

gingiva are reported in cannabis smokers. 13,18 Current 

knowledge on the effects of cannabis on periodontal 

health is inadequate. Controlled epidemiologic studies 

are difficult to undertake as the frequency, amount, 

duration and mode of administration of cannabis 

differ amongst individuals. Personal risk factors 

including age, oral hygiene, general health, concurrent 

tobacco smoking and poly drug use make it difficult 

to identify the specific influence of cannabis abuse on 

susceptibility to periodontitis. 

The Legal Regulation of Cannabis Use 

Cannabis is a controversial drug; debate continues 

over its illegal nature and whether or not it should be 

legalized. This has become more problematic in recent 

years with the emergence of cannabis as a potential 

therapeutic agent for some medical problems (such as 

multiple sclerosis). Significantly, the issue of the longterm 

health effects of cannabis use remains unresolved. 

Much of the scientific debate has become entangled 

with the wider social question of whether its use should 

remain illegal or not. 19 The difficulties with cannabis 

prohibition have been noted in a number of reviews, 

which have pointed to the difficulties and injustices of 

attempting to criminalize the use of a substance, which 

is widely used. 20,21 

An important legislative issue that requires attention 

is the issue of the supply of cannabis to young people 

under the age of 18. There is increasing evidence to 

suggest that this age group is the most vulnerable to 

the effects of cannabis 22,23 and accordingly there are 

grounds for suggesting that sentencing in cases of the 

supply of cannabis should take into account the ages 

of the individuals to whom cannabis is being supplied 

with supply to adolescent populations attracting more 

severe penalties. 

Drug Education in Schools 

One approach that has been widely advocated has been 

the use of drug education in schools. In particular it 

has been argued that by educating young people about 

the harms of drugs including cannabis, risks of future 

drug use and abuse may be reduced. 24,25 However, the 

evidence in support of school-based drug education 

is not strong. In general, studies of drug education 

programs have found these programs to be most 

effective in increasing knowledge about the risks of 

drug abuse. 26 Evaluations have found that the program 

is effective in increasing student knowledge but that 


509


the effects decrease with time and do not appear to 

alter later risks of drug abuse. 

Treatment of Cannabis Abuse and 

Dependence 

There is a need to develop effective clinical services 

for the treatment and management of cannabis abuse 

and dependence. There are now an increasing number 

of studies that have examined the use of a number of 

therapeutic approaches to the treatment of cannabis 

abuse and dependence. 27,28 These approaches include 

cognitive behavioral therapy, motivational enhancement 

and contingency management training. While these 

treatments have been found in randomized controlled 

trials to have some efficacy, 29 their major benefits appear 

to be a reduction in levels of cannabis use rather than 

ensuring complete abstinence from cannabis. These 

results raise issues about the extent to which such 

therapy should focus on moderation of cannabis use 

rather than complete abstinence. 

Conclusion and Recommendations 

Cannabis abuse causes a wide array of physical, 

psychological, economic and legal issues for the user. 

It can lead to serious general as well as oral health 

problems. Despite the controversy that surrounds 

marijuana use, clinicians will encounter patients who 

use it either medicinally or recreationally, and the 

oral side effects that accompany its use. The dentist 

must use certain precautions while dealing with a 

patient who is known to use cannabis in any form in 

order to avoid any possible contraindications during 

dental treatment and be able to refer such patients, if 

so desired by the patient, to the proper professionals 

for counseling. Beverages and mouthrinses containing 

alcohol should not be prescribed to the patients because 

of their drying effects on the oral cavity. Adhering to 

a low cariogenic diet and following an effective oral 

healthcare regimen that includes fluoride exposure are 

also key to inhibiting caries in patients experiencing 

xerostomia because of cannabis use. The increasing 

prevalence of cannabis use demands awareness of the 

diverse adverse effects of cannabis abuse. People should 

know about these effects and take timely action in 

order to stay away from its negative implications. Laws 

should be enforced to regulate cannabis use in different 

parts of the world to protect young people from using 

cannabis. 

References 

1. 

2. 

3. 

4. 

5. 

6. 

7. 

8. 

9. 

10. 

11. 

12. 

13. 

14. 

15. 

16. 

Schulz-Katterbach M, Imfeld T, Imfeld C. Cannabis and 

caries--does regular cannabis use increase the risk of caries 

in cigarette smokers? Schweiz Monatsschr Zahnmed 

2009;119(6):576-83. 

Ashton CH. Pharmacology and effects of cannabis: a 

brief review. Br J Psychiatry 2001;178:101-6. 

Rees TD. Oral effects of drug abuse. Crit Rev Oral Biol 

Med 1992;3(3):163-84. 

Grotenhermen F. Pharmacokinetics and 

pharmacodynamics of cannabinoids. Clin Pharmacokinet 

2003;42(4):327-60. 

Darling MR. Cannabis abuse and oral health care: review 

and suggestions for management. SADJ 2003;58(5): 

189-90. 

Cho CM, Hirsch R, Johnstone S. General and oral health 

implications of cannabis use. Aust Dent J 2005;50(2): 

70-4. 

Hall W, Degenhardt L. Prevalence and correlates of 

cannabis use in developed and developing countries. 

Curr Opin Psychiatry 2007;20(4):393-7. 

United Nations Office on Drugs and Crime. Cannabis 

in Africa (Monograph on the Internet). United Nations; 

2007. (Cited 2012 sept. 1). Available from: www.unodc. 

org. 

Faeh D, Viswanathan B, Chiolero A, Warren W, Bovet 

P. Clustering of smoking, alcohol drinking and cannabis 

use in adolescents in a rapidly developing country. BMC 

Public Health 2006;6:169. 

Suwanwela C, Poshyachinda V. Drug abuse in Asia. Bull 

Narc 1986;38(1-2):41-53. 

Kumar RN, Chambers WA, Pertwee RG. Pharmacological 

actions and therapeutic uses of cannabis and cannabinoids. 

Anaesthesia 2001;56(11):1059-68. 

Iversen L. Cannabis and the brain. Brain. 2003;126(Pt 

6):1252-70. 

Darling MR, Arendorf TM. Review of the effects 

of cannabis smoking on oral health. Int Dent J 

1992;42(1):19-22. 

Negative Implications of Cannabis Abuse on General 

and Oral Health. Effect on the Oral Health (Monograph 

of the Internet). 2012 (Cited Sept. 3, 2012). Available 

from: www.worldwidehealth.com. 

Firth NA. Marijuana use and oral cancer: a review. Oral 

Oncol 1997;33(6):398-401. 

Rosenblatt KA, Daling JR, Chen C, Sherman 

KJ, Schwartz SM. Marijuana use and risk of oral 

squamous cell carcinoma. Cancer Res 2004;64(11): 

4049-54. 

510 



17. 

18. 

19. 

20. 

21. 

22. 

23. 

Darling MR, Arendorf TM, Coldrey NA. Effect of 

cannabis use on oral candidal carriage. J Oral Pathol 

Med 1990;19(7):319-21. 

Versteeg PA, Slot DE, van der Velden U, van der Weijden 

GA. Effect of cannabis usage on the oral environment: a 

review. Int J Dent Hyg 2008;6(4):315-20. 

Australian Transport Safety Bureau. Cannabis and 

its Effects on Pilot Performance and Flight Safety 

(Monograph on the Internet). Civic Square (ACT): 

Austtralian Government; 2004 (Cited Sept. 3, 2012). 

Available from: http://www.skybrary.aero/books//1108. 

pdf. 

Lenton S. Cannabis policy and the burden of proof: is it 

now beyond reasonable doubt that cannabis prohibition 

is not working? Drug Alcohol Rev2000;19(1): 95-100. 

Fergusson DM, Swain-Campbell NR, Horwood LJ. 

Arrests and convictions for cannabis related offences 

in a New Zealand birth cohort. Drug Alcohol Depend 

2003;70(1):53-63. 

Hall WD. Cannabis use and the mental health of young 

people. Aust N Z J Psychiatry 2006;40(2):105-13. 

Kelly E, Darke S, Ross J. A review of drug use and 

24. 

25. 

26. 

27. 

28. 

29. 

driving: epidemiology, impairment, risk factors and risk 

perceptions. Drug Alcohol Rev 2004;23(3):319-44. 

Botvin GJ. Preventing drug abuse in schools: social 

and competence enhancement approaches targeting 

individual-level etiologic factors. Addict Behav 

2000;25(6):887-97. 

Botvin GJ, Griffin KW. School-based programmes to 

prevent alcohol, tobacco and other drug use. Int Rev 

Psychiatry 2007;19(6):607-15. 

Faggiano F, Vigna-Taglianti FD, Versino E, Zambon 

A, Borraccino A, Lemma P. School-based prevention 

for illicit drugs use: a systematic review. Prev Med 

2008;46(5):385-96. 

Nordstrom BR, Levin FR. Treatment of cannabis 

use disorders: a review of the literature. Am J Addict 

2007;16(5):331-42. 

Denis C, Lavie E, Fatséas M, Auriacombe M. 

Psychotherapeutic interventions for cannabis abuse and/ 

or dependence in outpatient settings. Cochrane Database 

Syst Rev 2006;(3):CD005336. 

Budney AJ, Roffman R, Stephens RS, Walker D. 

Marijuana dependence and its treatment. Addict Sci 

Clin Pract 2007;4(1):4-16. 


511


Ayur Health for Dentist’s Wealth 

Pramod S Prasad*, R Jonathan**, Arvind Kumar † 

Abstract 

This review reminds us about nature’s hand in healing and relieving some of the cumulative trauma disorders commonly 

associated with dentists in general and endodontists in particular. This depicts the problems we face in our day-to-day practice 

like backache, carpal tunnel syndrome, cervical spondylitis, chronic bronchitis, hand arm vibration syndrome and the different 

natural therapies available to gain relief from the associated symptoms. 

Key words: Ergonomics, cumulative trauma disorders, hand arm vibration syndrome, carpal tunnel syndrome 

There is always a quest for fame and money 

among humans as a race. Dentists as 

professionals are not an exception to this, as a 

result most dentists practice beyond their physiologic 

and psycological limits. Whereby, there is always a 

tendency among most of the dentists to violate the 

principles of ergonomics, which is the study of man in 

relation to his working environment, the adaptation of 

machines and general conditions to fit the individual, so 

that he may work with maximum efficiency. Where will 

this culminate in? They fall as victims to one of the 

many occupational related diseases, to be more precise 

cumulative trauma disorders (CTD). The common 

cumulative trauma disorders encountered by dental 

surgeons are cervical spondylitis, chronic bronchitis, 

carpal tunnel syndrome, hand arm vibration syndrome 

and backache. In this present world of complementary 

medicine where both allopathic and ayurvedic forms 

combined are gaining in popularity, herbal treatment 

modalities are gaining acceptance as safe and effective 

adjuncts. 

Considering the availability, safeness 1 and affordability 

of herbal medicines, these can be used to heal or gain 

relief from many of the cumulative trauma disorders. 

*Postgraduate Student 

**Professor and Head 

† 

Reader 

Dept. of Conservative Dentistry and Endodontics 

Rajas Dental College and Hospital, Tirunelveli, Tamil Nadu 


Dr Pramod S Prasad 

Postgraduate Student 

E-mail: drpspkollam@gmail.com 

Some of the commonly encountered cumulative 

trauma disorders among dental surgeons and their 

herbal remedies are reviewed in brief. 

Cervical Spondylitis 

This is an inflammatory condition affecting the vertebral 

and paravertebral structures in the neck and shoulder 

region. Two herbs which are very effective for this 

condition are ginger and pineapple. Ginger (Zingiber 

officinale) 2,3 contains a proteolytic enzyme called 

zingibain, which is a powerful anti-inflammatory agent. 

Moreover, ginger contains >12 antioxidants. Increase 

of ginger content in our side dishes can be of immense 

help. Another most important herb is the pineapple. 

Pineapple (Ananas comosus) 2 contains a proteolytic 

enzyme called bromelain which is a powerful antiinflammatory 

agent. A very famous ayurvedic topical 

medicine called ‘Kedaki mooladhi’ 4 is prepared from 

pineapple. Pineapple is also very effective when taken 

as a diet supplement. 

Chronic Bronchitis 

It is the chronic inflammation of bronchi in the 

lungs caused mainly by cross-contamination from 

patients and inhalation of aerosols. Most common 

herbal remedy for this are eucalyptus and peppermint. 

Eucalyptus (Eucalyptus globulus) 2 and peppermint 

(Mentha piperita) 2 oil can be used as steam inhalation. 

It helps in loosening the phlegm. Tea can be made 

with the leaves of these herbs. Roots of Indian 

ginseng (Withania somnifera) commonly called as the 

‘ashwagandha’ 5 can be used to improve the immunity 

by activating the white blood cells. 

512 



Hand Arm Vibration Syndrome 

Previously, this was known as ‘white finger’- a part of 

Raynaud’s phenomenon. This occurs due to decreased 

blood flow and is commonly seen in persons who 

continuously use high frequency vibrating machines. 

Studies reveal that the dentists are more prone for this 

disorder than rock drillers. Garlic (Allium sativum) 5 

and ginkgo are effective in increasing the circulation. 

Systemic garlic consumption can be increased through 

our diet. Ginkgo (Ginkgo biloba) 2 leaf extract contains 

flavonoids, glycosides, terpenic lactones (ginkgolides), 

which increases the elasticity of vessel walls and 

rheologic properties of blood. 

Backache 

This is a very common disorder seen among dentists, 

which usually originates from the muscles, nerves, 

bones or joints. Red pepper and devils claw are 

very effective in alleviating back ache. Red pepper 

(Capsicum annuum) 6 contains capsaicin, which is a 

powerful anti-inflammatory and analgesic agent. It 

can be mashed and applied directly over the affected 

region. The secondary storage root of devils claw 

(Harpagophytum procumbens) commonly called as ‘puli 

nakham’ 3 contains glycosides, phenols and flavinoids 

and is found to be an effective anti-inflammatory and 

analgesic. The harpagosides inhibits the lipooxygenase 

and cyclooxygenase pathways of inflammation. 

Carpal Tunnel Syndrome 

It is considered as a repetitive stress injury more prone to 

endodontists caused by frequent flexion and extension 

as in a filing motion. Numbness, tinkling or burning 

sensation in the thumb and fingers, particularly the 

index and middle fingers are the common symptoms 

associated with this syndrome. The tunnel formed 

by the carpal bones of the wrist houses the median 

nerve which gets compressed by inflammation of the 

tendons, which pass through it. Resin from bark of 

boswellia (Boswellia serrata) 2 is an anti-inflammatory 

(lipooxygenase inhibitor) and analgesic agent. Tea 

made from the bark of willow (Salix babylonica) 5 

provides anti-inflammatory action by inhibiting the 

cyclooxygenase pathway. It is called as ‘natural asprin’ 

as it contains salicin, which has the chemical structure 

similar to aspirin. Another most important herb is 

turmeric (Curcuma longa) 6 which contains curcumin. 

It is a powerful anti-inflammatory agent. Turmeric 

inhibits both cyclooxygenase and lipooxygenase 

pathway of inflammation. 

Conclusion 

Hope this review can go a long way in encountering and 

preventing most of the cumulative trauma disorders in 

a more acceptable way and in accordance with nature. 

Thereby, helping the dental surgeon to maintain a 

healthy professional life - the ayur way. 

References 

1. 

2. 

3. 

4. 

5. 

6. 

Ashtanga Hridayam (Vagbhata Published by Chaukhamba 

Sanskrit pratishthana). 

Bhaishajya Ratnavali (Govinda Dasa; Published by 

Motilal Banarasi Das). 

Charaka Samhita (Charaka; Published by Chaukhamba 

Sanskrit Pratishthana). 

www.herbalremediesworld.com 

www.herbalremedypro.com 

www.who.int (WHO Geneva 2004; Guidelines on 

Herbal Pharmacovigilance). 


513

case report 

Pregnancy Epulis 

T Saravanan*, KR Shakila*, K Shanthini* 

Abstract 

Pregnancy epulis is a pyogenic granuloma of the gingiva, which develops rarely during pregnancy in women. Here, we report 

an unusual case of pregnancy epulis in a 20-year-old pregnant woman, which was surgically excised and give a review of the 

literature. 

Key words: Pregnancy epulis, pregnancy tumor, pyogenic granuloma 

Pyogenic granuloma (PG) is one of the 

inflammatory hyperplasia seen in the oral cavity 

as a tissue response to irritation. The first case 

was reported in 1844 by Hullihen 1 and term pyogenic 

granuloma or granuloma pyogenicum was coined in 

1904 by Hartzell. 2 It is common in skin and oral 

cavity especially gingivae, which is keratinized. 3 

Currently preferred histologic term is lobular capillary 

hemangioma as it represents a benign neoplasm, a 

form of capillary hemangioma, rather than a reactive 

infectious or traumatic process. Pyogenic granuloma 

has a diagnostic, lobular arrangement of capillaries at 

its base. 3 

Females are slightly more affected than males and 

the age at presentation ranges from 18 months to 

93 years. The pathogenesis of this benign lesion is 

not well-understood. Trauma is felt to be the most 

common initiating event but is not always present in 

the history. The occasional presence of microorganisms 

has led to speculation of an infectious cause. This 

has not been proven. There is a higher incidence of 

pyogenic granuloma in women during pregnancy. 4 

Pyogenic granuloma of the gingiva develops in upto 

5% of pregnancies and hence terms like ‘granuloma 

gravidaram’ and ‘pregnancy tumor’ are commonly 

used. 5 

Case Report 

A 20-year-old female patient reported to the OPD of 

Karpaga Vinayaga Institute of Dental Sciences, with a 

chief complaint of painful mass on the gingiva over a 

period of four months (Fig. 1). The history revealed 

that the growth had gradually increasing in size to 

the present size with ulceration and bleeding from 

the growth. Clinical examination of the oral cavity 

revealed two lobulated hemorrhagic masses one in 

palate, of size measuring about 3 × 2 cm and other in 

gingiva, 2 × 2 cm in the region of left molars (27, 28) 

(Fig. 2 and 3). On examination, the molar teeth (27, 

28) were mobile. Radiographic evidence could not be 

provided as the patient was in her third trimester of 

pregnancy and not cooperative. Routine hemogram 

was done. A provisional diagnosis of pregnancy epulis 

was given. 

The patient was then subjected to excisional biopsy 

under local anesthesia and the excised mass was 

*Senior Lecturer 

Dept. of Oral Medicine and Radiology 

Karpaga Vinayaga Institute of Dental Sciences 

Chinna Kolampakkam, Kanchipuram, Tamil Nadu 


Dr T Saravanan 

E-mail: sharvy79@gmail.com 

Figure 1 and 2. Photograph showing intraoral view of two 

lobulated masses. 

514 


Case Report 

Figure 3. Photograph of intraoperative excisional biopsy. 

Figure 4. Photograph of excisional biopsy with extracted 

tooth. 

Figure 5. Photomicrograph (40x) showing parakeratinized 

stratified squamous epithelium associated with fibrovascular 

connective tissue. 

Figure 6. Postoperative photograph shows good healing 

after one day. 

sent for histopathological examination (Fig. 4). 

Histopathological examination revealed parakeratinized 

stratified squamous epithelium associated with 

fibrovascular connective tissue. In most of the areas 

epithelium was ulcerated. The underlying connective 

tissue exhibited numerous dilated blood vessels, 

proliferating endothelial cells and extravasated red blood 

cells (RBCs). There was diffuse chronic inflammatory 

cell infiltration throughout the tissue (Fig.5). Thus, the 

final diagnosis of ‘pyogenic granuloma’ was confirmed. 

There was a uneventful healing on next day (Fig. 6). 

Discussion 

Gingiva is often the site of localized growths that are 

considered to be reactive rather than neoplastic in 

nature. Most of the lesions in the gingiva are reactive 

chronic inflammatory hyperplasia’s with minor trauma 

and chronic irritation being the main etiologic factors. 

They found an almost equal distribution of lesions 

between the maxilla and mandible, with the anterior 

maxilla the most prevalent site. 6 It predominantly 

occurs in young females in their 2nd and 3rd decades 

due to hormonal influences on vasculature. 

There is a higher incidence of pyogenic granuloma 

in women during pregnancy termed as pregnancy 

epulis. Clinically, the pregnancy epulis appears as a 

smooth or lobulated and ulcerated mass that is usually 

pedunculated or sometimes sessile. Younger tumors are 

soft in consistency, progressing to a rubbery texture 

on maturation. The color may range from pink to 

bright red to purple or brown. 4 Such lesions begin to 

develop in first trimester and their incidence increases 


515

Case Report 

upto 7th month of pregnancy. The cause for the 

pyogenic granuloma in pregnancy is the raised levels 

of progesterone and estrogen and it is seen that the 

tumor usually regresses postparturition. 4 

The hormonal imbalance coincident with pregnancy 

heightens the organism’s response to irritation 7 

however, bacterial plaque and gingival inflammation 

are necessary for subclinical hormone alterations 

leading to gingivitis. 8 The development of this 

particular kind of gingivitis, typical in pregnancy, not 

different from that appearing in nonpregnant women, 

suggests the existence of a relationship between the 

gingival lesion and the hormonal condition observed in 

pregnancy. Sometimes pregnancy gingivitis can show a 

tendency towards localized hyperplasia, which is called 

pregnancy granuloma. Generally, it appears in the 

2nd - 3rd month of pregnancy, the persistent influence 

of plaque induces catarrhal inflammation of the gingiva 

that serves as a base for development of hyperplastic 

gingivitis during the last months, modulated by the 

cumulating hormonal stimuli. In uncontrolled cases, 

pyogenic granuloma may arise. This lesion is rarely 

observed in women with poor oral hygiene in areas 

with local irritating factors such as improperly fitting 

restorations or dental calculus. During pregnancy, 

pyogenic grenuloma when treated by surgical excision 

may reappear due to incomplete excision or inadequate 

oral hygiene. 9 

The molecular mechanism behind the development and 

regression of pyogenic granuloma during pregnancy 

is due to changes associated with the functions and 

structure of the blood and lymph microvasculature 

of the skin and mucosa due to profound endocrine 

upheaval. 10 Recent studies have revealed that sex 

hormones manifest a variety of biological and 

immunological effects. Estrogen accelerates wound 

healing by stimulating nerve growth factor (NGF) 

production in macrophages, granulocyte-macrophagecolony 

stimulating factor (GM-CSF) production in 

keratinocytes and basic fibroblast growth factor (bFGF) 

and transforming growth factor beta 1 (TGF-β1) 

production in fibroblasts, leading to granulation tissue 

formation. Estrogen enhances vascular endothelial 

growth factor (VEGF) production in macrophages, an 

effect that is antagonized by androgens and which may 

be related to the development of pyogenic grenuloma 

during pregnancy. The molecular mechanism for the 

regression of pyogenic granuloma after the pregnancy 

is not clear. It is proposed that in the absence of VEGF, 

the Angiopoietin (Ang-2) causes the blood vessels to 

regress and VEGF, which was found high in pregnancy 

was found undetectable after parturition. 

There are two histological types of pyogenic 

granuloma. One type is characterized by proliferating 

blood vessels that are organized in lobular aggregates 

although superficially the lesion frequently undergoes 

no specific change like edema, capillary dilation or 

inflammatory granulation tissue reaction. This is 

known as lobular capillary hemangioma type, whereas 

the second type nonlobular capillary hemangioma 

type consists of highly vascular proliferation that 

resembles granulation tissue. In the case presented, the 

histological picture was that of chronic inflammatory 

cell infiltration, which showed that it was nonlobular 

capillary hemangioma. 

Differential diagnosis includes pyogenic granuloma, 

peripheral giant cell granuloma, peripheral ossifying 

fibroma and metastatic cancer. The clinical features 

of growth with ulceration and bleeding present 

interdentally during the period of pregnancy made us 

give a provisional diagnosis of pregnancy epulis. 

Possible treatment modalities are excision, curettage, 

cryotherapy, chemical and electric cauterization, 

and the use of lasers. The lasers commonly used are 

argon lasers, continuous wave (CW) Nd:YAG laser, 

pulsed dye laser and CW carbon dioxide laser, which 

permits rapid, minimally invasive surgical treatment, 

but the nonspecific coagulation may lead to scars. 11 

The management of pyogenic granuloma depends 

on the severity of symptoms. Excisional biopsy is 

indicated for treatment of pyogenic granuloma, 

except when the procedure would produce marked 

deformity. 12 Recurrence rate after excision ranges from 

0% to 16%. Pyogenic granuloma of pregnancy often 

regresses postparturition, they need not be excised 

unless symptomatic. 4 As the patient presented with 

huge painful mass, which was ulcerated and bleeding 

we decided to excise completely. 

Treatment considerations during pregnancy are very 

important as it is considered that there is a biological 

plausibility that periodontal diseases in pregnancy are 

associated with pregnancy complications like preterm 

births, preterm low birth weight (LBW) babies or even 

516 


Case Report 

pre-eclampsia. 13 Surgical and periodontal treatment 

should be completed, when possible. 

Precautions to be taken for teeth and gums during 

pregnancy are: 

• More frequent visits to your dentist are advisable. 

• Try to reduce snacking on food high in sugar 

content. 

References 

1. 

2. 

3. 

4. 

5. 

6. 

Hullihen SP. Case of aneurysm by anastomosis of the 

superior maxillae. Am J Dent Sc 1844;4:160-2. 

Hartzell MB. Granuloma pyogenicum. J Cutan Dis 

Symph 1904;22:520-5. 

Willies-Jacobo LJ, Isaacs H Jr, Stein MT. Pyogenic 

granuloma presenting as a congenital epulis. Arch Pediatr 

Adolesc Med 2000;154(6):603-5. 

Sheth SN, Gomez C, Josephson GD. Pathological 

case of the month: diagnosis and discussion; pyogenic 

granuloma of the tongue. Arch Pediatr Adolesc Med 

2001;155:1065-6. 

Sills ES, Zegarelli DJ, Hoschander MM, Strider WE. 

Clinical diagnosis and management of hormonally 

responsive oral pregnancy tumor (pyogenic granuloma). 

J Reprod Med 1996;41(7):467-70. 

Buchner A, Shnaiderman-Shapiro A, Vered M. Relative 

frequency of localized reactive hyperplastic lesions of the 

7. 

8. 

9. 

10. 

11. 

12. 

13. 

gingiva: a retrospective study of 1675 cases from Israel. 

J Oral Pathol Med 2010;39(8):631-8. 

Eversole LR. Clinical outline of oral pathology: diagnosis 

and treatment. 3rd edition, Decker BC (Ed.), Hamilton 

2002:p.141-2. 

Sooriyamoorthy M, Gower DB. Hormonal influences 

on gingival tissue: relationship to periodontal disease. 

J Clin Periodontol 1989;16(4):201-8. 

Boyarova TV, Dryankova MM, Bobeva AI, Genadiev GI. 

Pregnancy and gingival hyperplasia. Folia Med (Plovdiv) 

2001;43(1-2):53-6. 

Henry F, Quatresooz P, Valverde-Lopez JC, Piérard GE. 

Blood vessel changes during pregnancy: a review. Am J 

Clin Dermatol 2006;7(1):65-9. 

Raulin C, Greve B, Hammes S. The combined continuouswave/pulsed 

carbon dioxide laser for treatment of 

pyogenic granuloma. Arch Dermatol 2002;138(1):33-7. 

Jafarzadeh H, Sanatkhani M, Mohtasham N. Oral 

pyogenic granuloma: a review. J Oral Sci 2006;48(4): 

167-75. 

Bobetsis YA, Barros SP, Offenbacher S. Exploring the 

relationship between periodontal disease and pregnancy 

complications. J Am Dent Assoc 2006;137 Suppl: 

7S-13S. 


517

case report 

Ludwig’s Angina: A Rare Case Report 

S Vijay Parthiban*, R Sathish Muthukumar**, M Alagappan † , M Karthi ‡ 

Abstract 

Ludwig’s angina is a rapidly progressing cellulitis characterized by the bilateral involvement of the submandibular, sublingual 

and submental spaces. It typically originates from an infected or recently extracted tooth, commonly the lower second and 

third molars. We present a case of Ludwig’s angina in a 50-year-old man. 

Key words: Induration, airway obstruction, incision and drainage 

Ludwig’s angina is a potentially life-threatening 

infection of the neck and floor of the mouth. 

It is a rapidly progressing cellulitis of the 

floor of the mouth characterized by firm induration 

and elevation of the tongue leading to severe airway 

obstruction. This was described by William Frederick 

Von Ludwig in 1836, 1 when he presented a clinical 

observation and necropsy finding of a patient with the 

same clinical condition. He described a firm connective 

tissue tumefaction that extends uniformly about 

the periphery of the neck, under the chin region of the 

jaw and beyond to involve the tissues between larynx 

and floor of the mouth. 

Criteria for accurate diagnosis of Ludwig’s angina 

have been described by Ludwig and Grodinsky. They 

describe Ludwig’s angina as cellulitic infection of 

submandibular space, usually involving more than 

one neck space, producing firm induration of floor 

of mouth and posterior displacement of tongue. It 

spreads by continuity along the fascial planes, then 

by lymphatics and rarely involves the glandular 

structures. The condition is known for its aggressive 

course, airway compromise and high mortality when 

not treated promptly. 2-6 We report a case of Ludwig’s 

*Senior Lecturer, Dept. of Oral and Maxillofacial Surgery 

**Professor, Dept. of Oral and Maxillofacial Pathology 

† 

Reader, Dept. of Oral and Maxillofacial Surgery 

‡ 

Reader, Dept. of Oral and Maxillofacial Pathology 

Chettinad Dental College and Research Institute, Chennai 


Dr S Vijay Parthiban 

E-mail: drvijayparthiban79@gmail.com 

angina in a 50-year-old and review the presentation 

and management of this disease. 

Case Presentation 

A 50-year-old man weighing 60 kg and 165 cm in 

height, presented with complaints of swelling of lowerhalf 

of face and neck with difficulty in breathing and 

swallowing and inability to open the mouth for the 

past three days, and had been spitting out saliva. 

He had pain in the right back tooth region one week 

before swelling appeared. He was nil by mouth for more 

than eight hours. On physical examination, he had no 

respiratory distress, but was uncomfortable because of 

pain and intraoral drainage of pus. Patient was febrile 

(38.8 0 C) with the pulse rate of 106 beats/minute, blood 

pressure of 140/90 mmHg and a respiratory rate of 

25 breaths/minute. The mouth opening was restricted 

with inter-incisal gap of 1 cm. There was a diffuse, 

tender and indurated neck swelling, warm on palpation 

particularly in submandibular and submental space. 

Neck extension was painful and limited. On intraoral 

examination, floor of the mouth was erythematous and 

indurated. Tongue was elevated from the floor of the 

mouth and he was not able to protrude the tongue 

beyond the corner of mouth, which is characteristics 

of Ludwig’s angina. 

A diagnosis of Ludwig’s angina was made and he 

was scheduled for emergency drainage of abscess. He 

was admitted and observed for 10 days in the ward. 

Submental and sublingual incision and drainage was 

done and the pus was sent for culture and antibiotic 

sensitivity. Corrugated rubber drain was placed through 

518 


Case Report 

Figure 1. Photograph showing submandibular, submental 

swelling. 

Figure 2. Restricted mouth opening, tongue protrusion. 

Figure 3 and 4. Photograph showing submental incision and drain in place. 

Figure 5 and 6. Photograph showing improved tongue protrusion and mouth opening, respectively. 


519

Case Report 

muscle into to submaxillary space below and 

sublingual space above. The infection spreads among 

both the spaces via the posterior edge of mylohyoid 

muscle. Further progression occurs superiorly from 

submaxillary space to the sublingual space producing 

firm induration of floor of the mouth, elevation and 

posterior displacement of tongue leading to airway 

compromise. If untreated, it can spread posteriorly 

along the intrinsic tongue muscles to parapharyngeal 

and retropharyngeal spaces, which may progress to the 

mediastinum. 

Figure 7. Photograph of the patient on the day of 

discharge. 

a submental incision. Periodontally affected 44, 47 

and 48 were extracted. Empirical antibiotic regimen 

IV cefotaxime 1 g b.i.d., metronidazole 500 mg b.i.d, 

IV dexamethasone 8 mg was started immediately. 

The culture and antibiotic sensitivity test reported a 

predominant growth of Staphylococcus aureus that was 

sensitive to amikacin and ofloxacin. Based on the 

antibiotic sensitivity test, the drug regimen was altered. 

The patient was kept under observation for 10 days 

and discharged following complete recovery. 

Discussion 

While described as far back as the writings of 

Hippocrates and Galen, necrotizing fasciitis Ludwig’s 

angina was first detailed by Wilhelm Frederick 

Von Ludwig in 1836. 7 Ludwig’s angina is a rapidly 

progressing cellulitis involving the submandibular, 

sublingual and submental space. 8 Ludwig’s angina is 

odontogenic in origin in 90% of cases. Various other 

causes are oral lacerations, mandible fracture and 

infection of oral malignant tumor. Recent infection 

or extraction of lower 2 nd or 3 rd molar are the most 

common cause for Ludwig’s angina as their roots 

extend below the mylohyoid line of the mandible. 

To understand the pathophysiology of Ludwig’s angina 

requires the knowledge of anatomy of submandibular 

space. This space is bounded superiorly by the mucosa 

of floor of the mouth and inferiorly by superficial layer 

of deep cervical fascia as it extends from hyoid bone 

to mandible. This space is subdivided by mylohyoid 

Ludwig’s angina originates from infected or recently 

extracted tooth, most commonly mandibular second 

and third molars. 8 Various other causes reported 

are mandible fracture, submandibular sialadenitis, 

peritonsillar abscess, epiglottitis and oral malignancy. 

It begins as a moderate infection and can progress 

rapidly to brawny bilateral swelling of upper neck with 

pain, trismus and tongue elevation accompanied with 

dysphagia and fever. The most serious complication of 

Ludwig’s angina is asphyxia due to expanding edema 

of soft tissues of neck. 9 Another common cause of 

death is acute loss of airway during intervention to 

control the condition. 10 Stridors, anxiety, cyanosis, 

sitting posture are late signs of impending airway 

obstruction and indicate the need for immediate airway 

management. 3 Spread of infection to mediastinum, 

carotid sheath, skull base and meninges are other 

complications. Ludwig’s angina was formerly fatal, but 

now with adequate medical and surgical treatment, has 

a reduced rate of mortality. 11 Even after the advent of 

newer antibiotics Ludwig’s still remains a potentially 

life-threatening infection because of the impending 

airway crisis. 5 So, the early recognition, diagnosis 

and treatment of Ludwig’s angina is very important. 

The cornerstone of medical management is the use of 

antibiotics active against streptococci, staphylococci and 

anaerobic species. Steroid therapy has been suggested 

as an adjunct to halt the progression of edema and 

prevent the need for artificial airway. 

Conclusion 

Ludwig’s angina is a life-threatening infection of floor 

of the mouth and neck. Early diagnosis and immediate 

treatment is the key for successful management of 

Ludwig’s angina. In advanced cases, securing the airway, 

surgical drainage and antibiotics following culture and 

sensitivity test are important. 

520 


Case Report 

References 

1. 

2. 

3. 

4. 

5. 

6. 

Murphy SC. The person behind the eponym: Wilhelm 

Frederick von Ludwig (1790-1865). J Oral Pathol Med 

1996;25(9):513-5. 

Kurien M, Mathew J, Job A, Zachariah N. Ludwig’s angina. 

Clin Otolaryngol Allied Sci 1997;22(3):263-5. 

Marple BF. Ludwig angina: a review of current airway 

management. Arch Otolaryngol Head Neck Surg 

1999;125(5):596-9. 

Neff SP, Merry AF, Anderson B. Airway management 

in Ludwig’s angina. Anaesth Intensive Care 1999;27(6): 

659-61. 

Barakate MS, Jensen MJ, Hemli JM, Graham AR. Ludwig’s 

angina: report of a case and review of management issues. 

Ann Otol Rhinol Laryngol 2001;110(5 Pt 1):453-6. 

Nguyen VD, Potter JL, Hersh-Schick MR. Ludwig angina: 

an uncommon and potentially lethal neck infection. AJNR 

7. 

8. 

9. 

10. 

11. 

Am J Neuroradiol 1992;13(1):215-9. 

Tshiassny K. Ludwig’s angina: an anatomic study of the 

lower molar teeth in its pathogenesis. Arch Otolaryngol 

Head Neck Surg 1943;38:485-96. 

Durand M, Joseph M. Infections of the upper respiratory 

tract. In: Harrison’s Principles of Internal Medicine. Volume 

1. 16th edition, Braunwald E, Fauci AS, Kasper DL, et al 

(Eds.), McGraw-Hill: New York 2001:p.191. 

Spitalnic SJ, Sucov A. Ludwig’s angina: case report and 

review. J Emerg Med 1995;13(4):499-503. 

Ovassapian A, Tuncbilek M, Weitzel EK, Joshi CW. Airway 

management in adult patients with deep neck infections: 

a case series and review of the literature. Anesth Analg 

2005;100(2):585-9. 

Iwu CO. Ludwig’s angina: report of seven cases and review 

of current concepts in management. Br J Oral Maxillofac 

Surg 1990;28(3):189-93. 


521

case report 

Management of an Unusual Crown Root Fracture of 

Mandibular First Primary Molar 

A Vasanthakumari*, R Bharathan** 

Abstract 

Crown root fractures are seldom observed in the primary molars. The extensive involvement of the pulp dictates the treatment 

of such teeth for extraction. Early extraction of primary molars can lead to transient or permanent malocclusion, esthetic, 

phonetic and functional problems. The aim of this case report is to describe the diagnosis of an unusual complicated crownroot 

fracture involving the primary molars of a 4-year-old girl child as well as to describe its management in order to preserve 

them as a functional unit of the dentition. 

Key words: Crown-root fracture, primary molar 

The frequency of traumatic dental injuries in 

children and teenagers varies considerably 

because of the influence of factors such as 

gender, age and dentition. Their prevalence in early 

ages varies from 4.6% to 30.2% and more specifically 

it is about 15% in primary dentition. The peak of 

incidence of dentoalveolar trauma in primary dentition 

occurs between the age of 2-4 and 8-11 years in mixed 

dentition. 1,2 

Commonly reported causes for dental injuries are 

motor vehicle accidents, contact sports and fall. Boys 

are more prone to dental trauma than girls. Increased 

overjet and incomplete lip closure are predisposing 

factors for trauma. 7 

The crown and root fracture is defined as fractures 

involving enamel, dentin and cementum and also 

classified as complicated and uncomplicated according 

to the pulpal involvement. 3 About 86.5% of dental 

trauma suffered by preschool children cause injury to 

primary incisors, whereas only 0.5% of these cause 

injury to primary molars. The incidence of crown and 

root fracture in primary molars had been reported to 

be only 0.8%. The purpose of the present paper is to 

describe the management of an unusual crown root 

fracture of mandibular first primary molars. 10 

Case Report 

A 4-year-old girl came accompanied by her parents, 

with the chief complaint of pain in the lower left back 

tooth for past two days. History as given by mother 

revealed patient had a fall one week back while playing 

at home. Patient got laceration to the chin region 

(Fig. 1) and consulted a nearby private physician and 

suture was placed in the chin region. Broken lower 

teeth were asymptomatic due to medication and so 

no dental treatment was carried out that time. After 

two days the patient developed pain while taking food 

and water and her sleep was disturbed. On extraoral 

* Professor and Head 

**Postgraduate Student 

Dept. of Pedodontics and Preventive Dentistry 

Sri Ramachandra University, Porur, Chennai 


Dr A Vasanthakumari 

Professor and Head, Dept. of Pedodontics and Preventive Dentistry 

Faculty Dental Sciences 

Sri Ramachandra University, Porur, Chennai - 600 116 

E-mail: vkpedo@gmail.com 

Figure 1. Skin of chin exposing scar. 

522 


Case Report 

Figure 2. Fracture evident in 74. 

Figure 6. Access opening in 74. 

Figure 3. OPG 

Figure 7. Pulp therapy with entrance filling in 74. 

Figure 4. Preoperative IOPA. 

Figure 5. Reattaching fragment in 74. 

Figure 8. Placement of SSC in 74. 


523

Case Report 

the length of time that has passed between the accident 

and treatment. 12 Treatment may also depend on the 

ability of the child to co-operate with the treatment 

and number of teeth involved. 6 The increased incidence 

of traumatic injuries to anterior teeth is a consequence 

of modern leisure activities and the most common 

injuries are crown fractures. 11 

The following cases were reported in the literature 

wherein the fractured teeth were extracted owing 

to either a delay in the treatment instituted or the 

inability to provide a secure post-endodontic restoration 

and only two cases were reported for preserving 

the teeth. 8 

Figure 9. Postoperative IOPA. 

examination wound dressing in the chin region was 

observed, no gross asymmetry; no deviation and 

no extraoral swelling were observed. On intraoral 

examination revealed a vertical fracture of 74, fracture 

line extending mesiodistaly and occluso-gingivally 

towards the lingual side in 74 (Fig. 2). 

Extraoral examination showed a healing laceration on 

the chin. Mouth opening was normal and there was 

no pain on examination of temporomandibular joints. 

Orthopantomogram (OPG) (Fig. 3) and intraoral 

periapical (IOPA) (Fig. 4) confirmed the fracture line 

extension to pulpal region in 74. Extraction is usually 

the treatment of choice. But, the child being be too 

young to lose her teeth, an attempt was made to save 

the tooth 74 by attaching fragment with glass ionomer 

cement (GIC) type 1X (Fig. 5) followed by pulpectomy 

using metapex (Figs. 6 and 7), with placement of 

stainless steel crown (Figs. 8 and 9). 

Discussion 

Crown root fractures of primary molars are extremely 

rare and usually occur as a result of trauma to the 

chin, as occurred in this case. Although anterior teeth 

are more prone to trauma than the posterior teeth, it 

is essential that the posterior teeth are also carefully 

examined to ensure an accurate diagnosis, especially 

when there has been an injury to the chin. 9 

Treatment of the fractured tooth or teeth depends on 

the severity and position of the fracture line as well as 

The literature reports several different treatments 

for this kind of problem, ranging from the 

maintenance and use of the tooth fragment either as 

a temporary or permanent crown, definitive crown 

after an orthodontic or surgical extrusion or a crown 

lengthening to an extraction of the residual tooth 

followed by an immediate or delayed implant surgery, 

or fixed partial denture. 13 There have been reports of 

fractured primary molars being successfully treated by 

pulp therapy and restoration with preformed metal 

crowns but in many cases extraction will be the 

necessary treatment. 4 

The need for a multidisciplinary approach in the 

treatment of routine dental problems has been 

recognized for some time, especially for dental traumas 

that require comprehensive treatment and an accurate 

diagnosis and treatment plan, respecting the biological, 

functional and esthetic aspects as well as the patient’s 

will. 5 

In the present case report, we have attempted to save 

the teeth by pulpectomy with placement of stainless 

steel crown in order to maintain the masticatory 

function and thereby prevented the complicated 

clinical problems that may arise after extraction of the 

primary molars in such a very young patient. 

Conclusion 

Treatment of the dental trauma is complex and requires 

a comprehensive and accurate diagnosis and suitable 

treatment plan. It is also important to consider the 

biological, functional, esthetic and economic aspects 

as well as the patient’s desire. 

524 


Case Report 

In aiming to minimize the developmental disturbances 

in the permanent dentition, the most effective methods 

are firstly to obtain an exact diagnosis to provide correct 

first aid treatments and lastly to perform regular followup 

until the permanent successor has erupted. 

References 

1. 

2. 

3. 

4. 

5. 

6. 

Andreasen JO. Etiology and pathogenesis of traumatic 

dental injuries. A clinical study of 1,298 cases. Scand J 

Dent Res 1970;78(4):329-42. 

Andreasen JO, Andreasen FM. Textbook and Colour 

Atlas of Traumatic Injuries to the Teeth. 3rd edition, 

Copenhagen, Munksgaard: Denmark; 1994. 

Kenny DJ, Barrett EJ. Recent developments in dental 

traumatology. Pediatr Dent 200;23(6):464-8. 

Götze Gda R, Barreira AK, Maia LC. Crown-root fracture 

of a lower first primary molar: report of an unusual case. 

Dent Traumatol 2008;24(3):e377-80. 

Abdelnur JP, da Rosa Götze G, Barreira AK, Maia LC. 

Parasymphyseal fracture associated with fracture of a 

maxillary primary molar in a child: case report. Dent 

Traumatol 2009;25(2):e21-4. 

Klein H, Bimstein E. Conservative treatment of multiple 

accidental fractures of primary molars and bilateral 

7. 

8. 

9. 

10. 

11. 

12. 

13. 

fractures of the condyles: report of case. ASDC J Dent 

Child 1977;44(3):234-6. 

Maréchaux SC. Chin trauma as a cause of primary 

molar fracture: report of case. ASDC J Dent Child 

1985;52(6):452-4. 

Sockalingam SNMP, Mahyuddin A. Complicated crown 

root fracture treatment option: a case report. Arch Orofac 

Sci 2009;4(1):25-8. 

Needleman HL, Wolfman MS. Traumatic posterior 

dental fractures: report of a case. ASDC J Dent Child 

1976;43(4):262-4. 

Sasaki H, Ogawa T, Kawaguchi M, Sobue S, Ooshima T. 

Multiple fractures of primary molars caused by injuries 

to the chin: report of two cases. Endod Dent Traumatol 

2000;16(1):43-6. 

Croll TP. Primary molar shattered by a BB: clinical 

report. Pediatr Dent 1985;7(2):145-7. 

Soviero VM, Guimarães L, Miasato JM, Ramos ME, 

Alto LA. Traumatic fractures of primary molars: a case 

report. Int J Paediatr Dent 1997;7(4):255-8. 

Tejani Z, Johnson A, Mason C, Goodman J. Multiple 

crown-root fractures in primary molars and a suspected 

subcondylar fracture following trauma: a report of a case. 

Dent Traumatol 2008;24(2):253-6. 


525

case report 

Follicular Adenomatoid Odontogenic Tumor 

S Loganathan*, H Srinvasan**, R Veerakumar † , M Arul Pari ‡ 

Abstract 

Adenomatoid odontogenic tumor is an uncommon odontogenic lesion, composed of odontogenic epithelium, characterized 

histologically by duct like structures with amyloid like deposits, noninvasive lesion with slow but progressive growth. Here 

we are reporting a case of adenomatoid odontogenic tumor in a 16-year-old female patient in the maxillary region. This 

paper provides the controversies regarding its origin and management in light of recent findings, clinical, radiographic, 

histopathologic and therapeutic features of the adenomatoid odontogenic tumor. 

Key words: Adenomatoid odontogenic tumor, dentigerous cyst, impacted teeth 

Adenomatoid odontogenic tumor, is an 

uncommon benign epithelial lesion of 

odontogenic origin, accounting for 3-7% 

of odontogenic tumors, and was first described 

by Drieibaldt in 1907. 1 According to the second 

edition of the World Health Organization (WHO) 

“Histological typing of odontogenic tumors”, 2 

adenomatoid odontogenic tumor is defined as “A tumor 

of odontogenic epithelium with duct-like structures 

and with varying degrees of inductive change in the 

connective tissue. The tumor may be partly cystic, and 

in some cases the solid lesion may be present only as 

masses in the wall of a large cyst.” 

The epithelial lining of the odontogenic cyst may 

transform into an odontogenic neoplasm like 

ameloblastoma. There are three variants of adenomatoid 

odontogenic tumor, follicular variant (73%), which has 

a central lesion associated with an embedded tooth, the 

extrafollicular variant (24%), which has a central lesion 

and no connection with the tooth and the peripheral 

variety (3%). 3 The report describes a intraosseous 

follicular adenomatoid odontogenic tumor in the 

maxilla illustrating the clinical, histopathological and 

biological features of the tumor and emphasizes the 

importance of the relation between the dental follicle 

and the tumor tissue. 

Case Report 

A 16-year-old female patient reported with a chief 

complaint of unerupted tooth and pain in the upper 

anterior left maxillary region. The medical history 

was insignificant. Intraoral examination disclosed 

a nontender, expansible lesion of the left maxilla, 

surrounded by normal mucosa and retained deciduous 

canine and missing left permanent canine (Fig. 1). 

Orthopantomogram (OPG) and maxillary occlusal 

view revealed the presence of a significant unilocular 

radiolucent area with well-defined sclerotic borders, 

*Senior Lecturer, Dept. of Oral and Maxillofacial Surgery, Priyadarshini 

Dental College, Pandur, Thiruvallur 

**Reader, Dept. of Oral Surgery 

† 

Reader 

‡ 

Senior Lecturer, Dept. of Pedodontia 


Dr S Loganathan 

Priyadarshini Dental College - Pandur, Thiruvallur, Tamil Nadu 

E-mail: drloganathans@gmail.com, srini11@hotmail.com 

Figure 1. Intraoral picture showing asymmetry on the left 

maxillary region and missing left permanent canine, retained 

deciduous canine and malpositioned left lateral incisor. 

526 


Case Report 

involving an impacted upper left permanent canine 

(Figs. 2 and 3). According to the clinical and radiological 

findings, the lesion was diagnosed as an adenomatoid 

odontogenic tumor. Under local anesthesia, excisional 

biopsy was performed with excavation of upper left 

canine (Fig. 4). 

The differential diagnosis was dentigerous cyst, calcified 

epithelial odontogenic tumor and odontogenic 

keratocyst. 

Histopathological Features 

Figure 2. Panoramic radiograph reveals radiolucency 

surrounding the impacted left permanent canine, retained 

deciduous canine and displaced lateral incisor. 

Figure 3. Occlusal radiograph reveals radiolucency 

surrounding the impacted left permanent canine, retained 

deciduous canine and displaced lateral incisor. 

Figure 4. Picture showing the tumor and the impacted 

canine. 

Odontogenic epithelium is arranged in the form of 

sheets, rods and few odontogenic cells, arranged in 

duct like structures with eosinophilic material in the 

center. A well-defined firm thick fibrous tissue capsule 

is seen at the periphery, which confirms the diagnosis 

of adenomatoid odontogenic tumor. 

Discussion 

Adenomatoid odontogenic tumor is a slow growing 

lesion, constituting only 3% of all odontogenic tumors 

with a predilection for the anterior maxilla (ratio 2:1) 4 

Rick et al have reported adenomatoid odontogenic 

tumor to occur with many types of cysts and neoplasm’s 

including dentigerous cyst, calcifying odontogenic 

cyst, odontoma and ameloblastoma, etc. 5 In relation 

with a dentigerous cyst the adenomatoid odontogenic 

tumor may demonstrate, grossly and microscopically, 

one or more associated cystic cavities. Some of these 

cysts are lined by nonkeratinized stratified squamous 

epithelium, which is similar to the lining of the 

dentigerous cyst or lined by less structured membrane 

that may demonstrate bud like extensions into the 

connective tissue. In our case, a moderate amount 

of the inflammatory component was evident in the 

sections, which could cause the cystic epithelium to 

lose its characteristic features and hence restrict the 

typing to an odontogenic cyst alone. 

Odontogenesis is a complex process wherein neoplastic 

or hamartomatous lesions can occur at any stage of 

odontogenesis. The secondary development of an 

ameloblastic proliferation, whether hyperplastic or 

neoplastic is well-known, but remains controversial. 

In the present case, the multifocal cellular proliferation 

had the structure of an AOT although larger lesions 

reported in the literature are usually in the dimensions 

of 2-3 cm. Radiographically they usually appear as 


527

Case Report 

unilocular lesion, may contain fine calcifications with 

or without root resorption. 6,7 This appearance must be 

differentiated from various types of disease, such as 

calcifying odontogenic tumor or cysts. The differential 

diagnosis can also be made with ameloblastoma, 

ameloblastic fibroma and ameloblastic fibro-odontoma. 

The tumor is well-encapsulated and shows an identical 

benign behavior. Therefore, conservative surgical 

enucleation produces excellent outcome without 

recurrence. 8,9 Our patient has been under follow-up 

for eight months. 

Conclusion 

Our case report supports the general description of 

adenomatoid odontogenic tumor in the previous 

studies. We conclude that the rarity of adenomatoid 

odontogenic tumor may be associated with its slowly 

growing pattern and symptomless behavior. Therefore, 

it should be distinguished from more common 

lesions of odontogenic origin in routine dental 

examinations. 

References 

1. 

Neville BW, Damm DD, Allen CM, Bouquot JE. Oral 

and maxillofacial pathology. In: Odontogenic Cysts and 

Tumors. Warldon CA (Ed.), WB Saunders: Philadelphia, 

Pa, USA 2002:p.589-642. 

2. 

3. 

4. 

5. 

6. 

7. 

8. 

9. 

Jing W, Xuan M, Lin Y, Wu L, Liu L, Zheng X, et al. 

Odontogenic tumours: a retrospective study of 1642 

cases in a Chinese population. Int J Oral Maxillofac Surg 

2007;36(1):20-5. 

Bravo M, White D, Miles L, Cotton R. Adenomatoid 

odontogenic tumor mimicking a dentigerous cyst. Int J 

Pediatr Otorhinolaryngol 2005;69(12):1685-8. 

Swasdison S, Dhanuthai K, Jainkittivong A, Philipsen 

HP. Adenomatoid odontogenic tumors: an analysis of 67 

cases in a Thai population. Oral Surg Oral Med Oral 

Pathol Oral Radiol Endod 2008;105(2):210-5. 

Nigam S, Gupta SK, Chaturvedi KU. Adenomatoid 

odontogenic tumor - a rare cause of jaw swelling. Braz 

Dent J 2005;16(3):251-3. 

Larsson A, Swartz K, Heikinheimo K. A case of multiple 

AOT-like jawbone lesions in a young patient - a new 

odontogenic entity? J Oral Pathol Med 2003;32(1): 

55-62. 

Dayi E, Gürbüz G, Bilge OM, Ciftcioğlu MA. Adenomatoid 

odontogenic tumour (adenoameloblastoma). Case report 

and review of the literature. Aust Dent J 1997;42(5): 

315-8. 

Philipsen HP, Reichart PA, Nikai H. The adenomatoid 

odontogenic tumor (AOT): an update. J Oral Pathol 

Med 1997;2:55-60. 

Motamedi MH, Shafeie HA, Azizi T. Salvage of an 

impacted canine associated with an adenomatoid 

odontogenic tumour: a case report. Br Dent J 2005; 

199(2):89-90. 

528 


Sodium Hypochlorite Solution Enhances Healing of Periapical 

Lesion by Nonsurgical Method 

Subrata Sarkar *, Soumyabrata Sarkar**, Badruddin Ahmed Bazmi † , Sarbani Ghosh ‡ 

case report 

Abstract 

Sodium hypochlorite (NaOC1) is a broad-spectrum antimicrobial agent effective against bacteria, spores, yeast and viruses. 

It provides 100% bacterial reduction as it contains 50 ppm available chlorine at 6.7-10.7 pH at 20 0 C in one minute. 5.25% 

NaOCl solution has a pH 11-12 and it provides immediate antibacterial action during root canal irrigation. 2.5-3% solution 

has a pH of 11-12, which also gives good results. Grossman (1978) and others observed healing of large periapical lesions 

by nonsurgical methods using NaOC1 solution, though the exact mechanism of healing is not clear but it is proved that 

NaOC1 has good action against bacteria. 

Key words: Sodium hypochlorite, root canal irrigation, nonsurgical method 

Periapical infection of tooth/teeth is one of the 

common problems in young children. Various 

factors are responsible for this, of which caries and 

trauma are the prime causes. Neglected trauma causes 

apical swelling, pain and swallowing problem, which 

are the common signs. 1-5 Radiologic examination shows 

large radiolucent areas in relation to affected tooth, 

which may be an apical abscess, granuloma or cyst. 

Gram-positive anaerobic bacteria are cultured and gramnegetive 

anaerobic bacteria cause pathological change 

in the apical region. This lesion has a connection with 

root canals of the tooth. Various types of treatments 

have been advocated to overcome this problem such as 

root canal treatment along with surgical curettage in 

the apical region. 6 

Recently, various investigators 7-13 suggested a 

nonsurgical treatment procedure, which will control 

apical infection and promote healing of large periapical 

lesions. Present paper reflects the management of 

a periapical lesion of a young boy by a nonsurgical 

method. 

*Professor and Head, Dept. of Pedo-Preventive Dentistry 

**Senior Lecturer, Dept. of Oral Diagnosis 

Oral Medicine and Oral Radiology 

† 

Senior Lecturer, Dept. of Pedo-Preventive Dentistry 

‡ 

Clinical Tutor, Dept. of Community Dentistry 

Guru Nanak Institute of Dental Sciences and Research, Panihati, Kolkata 


Dr Subrata Sarkar 

7, PC Ghosh Road Kolkata - 700 048 

E-mail: drssarkar44@yahoo.com 

Case Report 

A 12-year-young boy came with complaints of pain 

and swelling in 41, 42 region for last seven days. 

He gave history of trauma in 41, 42 region one year 

back. Recently, he developed sudden apical swelling 

along with pain, fever, lymphadenitis. After proper 

antibiotics, anti-inflammatory and mouth rinse history 

of pain and fever subsided. 

Investigation: Intraoral periapical X-ray in 41, 42 

region was advised. Which showed large radiolucent 

area in the region (Fig. 1). 

Provisional diagnosis: Chronic periapical abscess in 

41, 42 region. 

Treatment plan: Nonsurgical endodontic treatment 

approach. 

Treatment procedure: Thermal and electrical pulp 

testing was done in 41, 42 region, which failed to 

respond indicating nonvital teeth. The access cavity 

was prepared with the help of Round-end Fissure 

Bur. Canal was kept open for 24 hours to drain out 

pus from the canal. After 24 hours, 5.25% sodium 

hypochlorite (NaOC1) irrigation was done drop by 

drop slowly (Fig. 2). 

After 48 hours, with the help of protaper, enlargement 

and removal of root canal debris was done. Then again 

irrigation was done with 5.25% NaOCl. Access cavity 

was sealed with Cavit cement (3M). Same procedure 


529

Case Report 

Patient was recalled after one month and intraoral 

periapical X-ray was taken, which showed absence of 

radiolucent zone in apical region of 41, 42. Healing 

had taken place. Radio-opaque root canal fillings were 

seen in 41, 42 (Fig. 3). 

Figure 1. Intraoral periapical X-ray of 41, 42 region showing 

large radiolucency in periapical region. 

Figure 2. Sodium hypochlorite irrigation with side vented 

needle drop by drop slowly. 

Figure 3. Healing of the periapical region in relation to 

41, 42 with radio-opaque gutta-percha in root canals. 

was repeated after 48 hours intervals for five times. 

Canals were debrided and dried and obturated with 

gutta-percha and zinc oxide eugenol. 

Discussion 

Treatment of effected pulp restore normal physiological 

function of tooth. Dental caries, trauma, attrition, 

abrasion, erosion, etc., all cause change of pulpal status 

and ultimately cause loss of vitality and house various 

bacterial growth. Long-standing pathological change of 

pulpal status leads to pathologic changes in periapical 

region of tooth like granuloma, apical abscess and 

radicular cyst. 

First evidence of endodontic treatment was reported in 

Israel in 2 nd and 3 rd century (BC). After that throughout 

the world endodontic treatment was performed by 

various investigators in deciduous and permanent 

teeth. Various endodontists believe proper and adequate 

biochemical preparation can control pulpal infection 

and restore normal physiological functions of tooth. 

In the year 1978, Grossman stated only biochemical 

instrumentation and cleaning of root canal would 

not lead to healing of apical region of nonvital tooth. 

Root canal irrigation during endodontic treatment 

was first introduced in the year 1859. 14 Various 

irrigating solutions like normal saline, hydrogen 

peroxide (20%vol), povidone-iodine, calcium 

hydroxide, mixture of tetracycline, acid detergent, 

[MTAD], ethylenediaminetetraacetic acid (EDTA), 

soluble terramycin tablet, neem leaves and other 

herbal solution) were used by endodontists for proper 

debridement of canals by dissolving organic matter. 

Ingle and Beveridge 1976, 7 Nicholls 1977, 8 Grossman 

1978 were of this opinions that NaOCl was the 

best irrigating solutions because NaOC1 has good 

antimicrobial property, property of dissolving pulpal 

remnants and debris material and heals large periapical 

lesions. Shih et al 1970, 9 Ayhan et al (1999), 10 

Ercan et al (2004), 11 Abdullah et al (2005), 12 Berber 

(2006), 13 and others are of same opinion that NaOC1 

is a broad-spectrum antimicrobial irrigating solution 

effective against bacteria, spores, yeast and virus. Ingle 

and Beveridge (1976), 7 Nicholls (1997) 8 and others 

suggested that NaOC1 helps in healing of apical lesions 

and debridement of root canal. 

530 


Case Report 

Various endodontists observed NaOC1 has good 

bacterial killing efficiency. Thus large apical healing 

can be obtained by a nonsurgical method. Present 

study supports the above views. 

Conclusion 

Dental pulpal infection can cause periapical lesion. 

Initially endodontists advocated proper root canal 

treatment with apical surgical curettage. Other group 

of investigators suggested that NaOC1 is broadspectrum 

antimicrobial irrigating solution, which can 

kill various microorganisms. Proper healing of apical 

region by NaOC1 is a nonsurgical method, which can 

control pulpal pathology. 

References 

1. 

2. 

3. 

4. 

Lalonde ER. A new rationale for the management of periapical 

granulomas and cysts: an evaluation of histopathological 

and radiographic findings. J Am Dent Assoc 1970;80 

(5):1056-9. 

Baskar SN. Periapical lesions - types, incidence and clinical 

features. Oral Surg Oral Med Oral Pathol 1966;21:657-71. 

Calişkan MK. Prognosis of large cyst-like periapical lesions 

following nonsurgical root canal treatment: a clinical review. 

Int Endod J 2004;37(6):408-16. 

Simon JH. Incidence of periapical cysts in relation to the 

root canal. J Endod 1980;6(11):845-8. 

5. 

6. 

7. 

8. 

9. 

10. 

11. 

12. 

13. 

14. 

Nair PN. New perspectives on radicular cysts: do they heal? 

Int Endod J 1998;31(3):155-60. 

Grossman LI. Endodontic practice. 9th edition, Lea & 

Febiger: Philadelphia 1978:p.191. 

Ingle JL, Beveridge EE. Endodontics. 2nd edition, Lea & 

Febiger: Philadelphia 1977:p.138. 

Nicholls E. Endodontics. 2nd edition, John Wright & Sons 

Ltd., Bristol 1977:p.138. 

Shih M, Marshall FJ, Rosen S. The bacterial efficacy of 

sodium hypochlorite as an endodontic irrigant. Oral Surg 

Oral Med Oral Pathol 1970;29:613-9. 

Ayhan H, Sultan N, Cirak M, Ruhi MZ, Bodur H. 

Antimicrobial effects of various endodontic irrigants on 

selected microorganisms. Int Endod J 1999;32(2):99-102. 

Ercan E, Ozekinci T, Atakul F, Gül K. Antibacterial 

activity of 2% chlorhexidine gluconate and 5.25% sodium 

hypochlorite in infected root canal: in vivo study. J Endod 

2004;30(2):84-7. 

Abdullah M, Ng YL, Gulabivala K, Moles DR, Spratt DA. 

Susceptibilties of two Enterococcus faecalis phenotypes to root 

canal medications. J Endod 2005;31(1):30-6. 

Berber VB, Gomes BP, Sena NT, Vianna ME, Ferraz CC, 

Zaia AA, et al. Efficacy of various concentrations of NaOCl 

and instrumentation techniques in reducing Enterococcus 

faecalis within root canals and dentinal tubules. Int Endod 

J 2006;39(1):10-7. 

Miller WD. An introduction to the study of the bacteriopathology 

of the dental pulp. Dent Cosmos 1894;36: 

505-27. 


531

case report 

Vital Bleaching with Diode Laser 

Sharath Pare*, SC Loganathan** 

Abstract 

Every individual with discolored teeth desires to have whiter teeth. Bleaching corrects or improves the color of teeth, and 

it is also the least expensive esthetic treatment option. Introduction of Lasers in dentistry has led to a new era of dental 

bleaching. 

Key words: Discolored teeth, Laser, bleaching 

Discolored anterior teeth are often perceived as an 

esthetic detraction. Because of the growing need 

for beautiful, white teeth and the establishment 

of esthetic treatment methods, the bleaching of discolored 

teeth has become increasingly important in recent years. 

The objective of laser bleaching is to achieve the ultimate 

power bleaching process using the most efficient energy 

source, while avoiding any adverse effect. 1 Bleaching is 

defined as the lightening of the color of a tooth through 

the application of a chemical agent to oxidize the organic 

pigmentation in the tooth. 2 

The release of hydroxyl-radicals from peroxide is 

accelerated by a rise in temperature according to the 

following equation: 

H 2 

O 2 

+ 211kJ/mol→2HO. 

This is in accordance with an increase in speed of 

decomposition of a factor of 2.2 for each temperature 

rise of 10 0 C. 3 

Hydrogen peroxide bleaching proceeds via perhydroxyl 

anion and a hydroxyl radical is formed. Use of light source 

such as Light Amplification by Stimulated Emission of 

Radiation (LASER) increases the formation of hydroxyl 

radicals. 4 

Classification: 5 

• Nonvital bleaching 

• In office bleaching 

*PG Student 

**Professor 

Dept. of Conservative Dentistry and Endodontics 

Thai Moogambigai Dental College and Hospital, Chennai 


Dr Sharath Pare 

E-mail: sharathpare@gmail.com 

• Walking bleach 

• Vital bleaching 

• In office (power bleaching) 

• Night guard bleaching 

Etiology of intrinsic discolorations 6 

• Pre-eruptive causes 

• Medications (tetracycline) 

• Metabolism (fluorosis) 

• Genetics (hyperbilirubinemia, amelogenesis 

imperfecta, cystic fibrosis of the pancreas) 

• Dental trauma 

• Post-eruptive causes 

• Pulpal necrosis 

• Intrapulpal hemorrhage 

• Residual pulp tissue after endodontic 

treatment 

• Endodontic materials 

• Filling materials 

• Root resorption 

• Aging process 

Redox reaction: 7 The reaction by which bleaching 

occurs. 

Tooth + Bleaching agent 

Hydroxyl radicals react with unsaturated bonds 

Simpler molecules are formed 

Reflects less light or becomes colorless 

Larger stain molecules are converted into smaller ones 

532 


Case Report 

Case 1 

A 22-year-old female patient reported to the Dept. 

of Conservative Dentistry and Endodontics, Thai 

Moogambigai Dental College, Chennai with chief 

complaint of color change in her left upper front tooth 

region. There was relevant medical history and patient 

gave no history of trauma. Oral examination showed that 

21 was slightly discolored 36, 37, 46 were restored. Soft 

tissue around the tooth was normal. RVG and thermal 

testing were used as diagnostic aids. RVG revealed no 

periapical changes and coronal portion was calcified 

in 21. Thermal test revealed tooth was vital. 

Oral prophylaxis was done and bleaching was carried 

out using 35% hydrogen peroxide gel and diode 

laser. Gingival barrier was applied and light cured for 

20 seconds. Then hydrogen peroxide gel is applied over 

the affected tooth and laser beam is used at 3 watts 

Postoperative (Case 1) 

for 20 seconds per tooth in pulse mode. Then the gel 

was left on the tooth for 20 minutes. The peroxide 

gel was wiped with cotton and the gingival barrier was 

removed. Immediately after the treatment, the patient 

was happy with the degree of color change. The patient 

reported after six months and one year. No change in 

the color was seen. 

Case 2 

Preoperative (Case 1) 

A 23-year-old female patient reported to the Dept. 

of Conservative Dentistry and Endodontics, Thai 

Moogambigai Dental College, Chennai, with chief 

complaint of color change in her front teeth. Patient 

gave no relevant medical history and no history of 

trauma. Oral examination revealed all anteriors were 

slightly discolored and soft tissue around the teeth 

were normal. 

Laser activation (Case1) 

Preoperative (Case 2) 


533

Case Report 

of ‘photo initiator’ in the gel. Mechanisms of tooth 

whitening by peroxide occur by the diffusion of 

peroxide through enamel to cause oxidation and hence 

lightening the colored species, particularly within the 

dentinal regions. The efficacy of light activated systems 

of bleaching has better effect on whitening procedure. 

In addition, it has been speculated that the light 

source can energise the tooth stain to aid the overall 

acceleration of the bleaching process. 8 

Conclusion 

Postoperative (Case 2) 

Oral prophylaxis was done and bleaching was carried 

out using 35% hydrogen peroxide gel and diode laser. 

Gingival barrier was applied and light cured for 20 

seconds. Then hydrogen peroxide gel was applied over 

the affected teeth and laser beam was used at 3 watts 

for 20 seconds per tooth in pulse mode. Then the gel 

was left on the tooth for 20 minutes. The peroxide 

gel was wiped with cotton and the gingival barrier was 

removed. Patient was reviewed after six months with 

no change in color. 

Discussion 

The use of high-intensity light, for raising the 

temperature of the hydrogen peroxide and accelerating 

the rate of chemical bleaching of teeth was reported in 

1918 by Abbot. 4 If heat or light activation is applied, it 

is strongly advised to follow manufacturer’s instructions 

with limited duration of heat activation to a short period 

of time, in order to avoid undesired pulpal responses. 

The light source can be laser (argon, CO 2 

), halogen, 

plasma arc, light emitting diodes (LED). Light activated 

tooth whitening systems such as ‘Brite smile’ system 

(400-500 nm) ‘Zoom’ system (350-400 nm). These 

systems use light, which matches the wavelength 

The light source can activate peroxide to accelerate the 

chemical redox reactions of the bleaching process. 9 But 

if proper regimens are not undertaken pulpal reactions 

can occur. Care should be taken during laser bleaching 

with a use of pulse mode, which prevents the increase 

of intrapulpal temperature. Therefore, application of 

activated bleaching procedures should be critically 

assessed considering the physical, physiological and 

pathophysiological implications. 

References 

1. 

2. 

3. 

4. 

5. 

6. 

7. 

8. 

9. 

Dostalova T, Jelinkova H, Housova D, Sulc J, Nemec M, 

Miyagi M, et al. Diode laser-activated bleaching. Braz 

Dent J 2004;15 Spec No:SI3-8. 

Sturdevant’s Art and Science of Operative Dentistry. 5th 

edition. Edited by Roberson, Heyman and Swift, 2009. 

Buchalla W, Attin T. External bleaching therapy with 

activation by heat, light or laser - a systematic review. 

Dent Mater 2007;23(5):586-96. 

Joiner A. The bleaching of teeth: a review of the literature. 

J Dent 2006;34(7):412-9. 

Ingle’s Endodontics. 6th edition by Ingle, Bakland and 

Baumgartner, 2008. 

Plotino G, Buono L, Grande NM, Pameijer CH, Somma 

F. Nonvital tooth bleaching: a review of the literature and 

clinical procedures. J Endod 2008;34(4):394-407. 

Text Book of Endodontics. Edited by Anil Kohli, 2010. 

Smigel I. Laser tooth whitening. Dent Today 

1996;15(8):32-6. 

Sun G. The role of lasers in cosmetic dentistry. Dent Clin 

North Am 2000;44(4):831-50. 

534 


Replantation of Avulsed Tooth after Trauma: A 

One Year Follow-up Study 

Swaty Jhamb*, Lalit Bida** 

case report 

Abstract 

Clinical practice has shown that it avulsed teeth are replanted after a delayed extra-alveolar time it compromises the prognosis 

of replantation. In case of delayed replantation, the use of adequate media for storage and transportation of avulsed teeth may 

improve the prognosis considerably. The case reported in the study is of an accidentally avulsed maxillary right central incisor 

that was kept in milk from the moment of trauma until its replantation, 30 minutes later. One year follow-up revealed absence 

of root resorption, ankylosis or abnormal mobility, which demonstrates the feasibility of keeping avulsed teeth in milk. 

Key words: Replantation, root resorption, ankylosis, prognosis, avulsion 

Dentoalveolar traumas are most commonly 

observed in children and adolescents, 

particularly boys but may affect individuals of 

any age. 1,2 Studies have demonstrated that replantation 

of avulsed teeth occurs most frequently between one 

and 4 hours after avulsion. 1,2 Despite the recognized 

therapeutic value of immediate tooth replantation, 

clinical practice has shown that most avulsed teeth are 

replanted after an extrabuccal time that extrapolates the 

adequate conditions for maintenance of the integrity of 

periodontal ligament cells. 3 In such cases, wet storage is 

considered the best way to store avulsed teeth. 3,4 Some 

characteristics of storage medium i.e. pH, osmolarity 5,6 

and temperature should be compatible with the survival 

of periodontal ligament cells. 4,6 Storage media as Milk, 

Hanks balanced salt solution and Viaspan have been 

proved to maintain cell viability after long periods. 7 

Case Report 

A 20-year-old male patient was referred to Dept. 

of Conservative Dentistry and Endodontics after 

falling from a motorbike and sustaining dental 

trauma. 

Routine protocol for management of trauma patients 

was carried out. On arrival, the patient was examined 

for extraoral signs of injury, including swelling and 

asymmetry of face and head. Inspection of facial bones 

revealed normal mouth opening. No area of ecchymosis, 

crepitus or pain on palpation was observed, which 

removed the suspicion of underlying fractures. 

Intraoral examination revealed avulsion of maxillary 

right central incisor (Fig. 1). The patient had difficulty 

This article reports, the case of an accidentally avulsed 

right permanent maxillary central incisor that was 

kept in milk from the moment of trauma until its 

replantation, 30 minutes later. The successful clinical 

and radiographic findings observed after 1-year followup 

are described. 

*Senior Lecturer, Dept. of Conservative and Endodontics 

**Senior Lecturer, Dept. of Prosthodontics 

Dr. HS Institute of Dental Sciences and Hospital, Chandigarh 


Dr Swaty Jhamb 

H.No. 70/1, Sec-38A, Chandigarh 

E-mail: drswaty2007@yahoo.co.in 

Figure 1. Preoperative photograph. 


535

Case Report 

Figure 2. Tooth stored in milk. 

Figure 4. Working length radiograph. 

Figure 3a. Replanted tooth in socket. 

Figure 5. Post-obturation radiograph. 

Figure 3b. Preoperative radiograph with splinted tooth. 

Figure 6. Postoperative radiograph after 1-year of 

restoration. 

in keeping the tooth in the oral cavity so was instructed 

to keep the tooth in milk (Fig. 2). The total time elapsed 

from the moment of trauma until tooth replantation 

was half an hour. 

The treatment consisted of replantation of 11 into 

socket after meticulous inspection and irrigation of the 

avulsed tooth with saline (Fig. 3a). Splinting was carried 

from tooth 12 to 11 using resin composite (Fig. 3b).’ 

536 


Case Report 

Antibiotics were administered for 7 days and 0.12% 

chlorhexidine mouth rinses daily were prescribed for 

7 days. One week after replantation, the root canal 

of 11 was biomechanically prepared using step back 

technique (Fig. 4). A Calcium Hydroxide paste was 

used as an intracanal dressing and was changed 14 days 

later, when splinting was removed. Radiographs were 

taken and intracanal medication was changed at 30 and 

60 days after replantation. The root canal of the tooth 

was obturated at 90 days with Gutta-percha points 

and Sealapex that is a Calcium Hydroxide based sealer 

(Fig 5). The patient wanted restoration of aesthetics so, 

a fixed bridge of metal –ceramic was given. The patient 

was kept on continuous recall. 

The clinical and radiographic findings after 1-year 

follow-up revealed absence of root radiolucency, 

absence of root resorption, ankylosis and abnormal 

mobility of the replanted tooth (Fig. 6). 

Discussion 

Milk is mostly used as a storage medium for accidentally 

avulsed teeth and therefore, the case reported is 

important in the clinical routine or management of 

tooth replantation. 

Lack of knowledge and possibility of immediate 

replantation and unawareness of ideal conditions and 

storage media for exarticulated teeth have contributed 

to a poor prognosis. Both, the length of extra-alveolar 

time and type of storage are significant factors that 

can affect the long-term survival of replanted teeth. 

Immersion of avulsed teeth in milk at room temperature 

preserves the viability of periodontal ligament cells 

for upto one hour; whereas, storage in refrigerated 

milk is reported to maintain cell viability for additional 

45 minutes. 4,8 

Irrespective of the type of root surface treatment, 

there is consensus in the literature that replanted teeth 

should be endodontically treated because the necrotic 

pulp and its toxins affect the periodontal ligament 

cells through the dentinal tubules and play a decisive 

role in the resorption process. 3,9,10 In this case, calcium 

hydroxide is the most recommended material for root 

canal filling of teeth to be replanted because of its 

well-known capacity of controlling the progression of 

inflammatory resorption. 11,12 

Another aspect of dental replantation is the preparation 

of socket, which consists of removal of destructions as 

blood clots and bone fragments in order to facilitate 

the replantation. 12-15 

Contention of replanted teeth is another variable 

that might affect the prognosis of tooth replantation. 

Basically, it should not interfere with oral hygiene, 

allow physiological mobility and remain for a short 

time in order to reduce the incidence of ankylosis. 2,16 

The goal of antibiotic therapy is to avoid bacterial 

proliferation in the area of ongoing process and 

contribute to the prevention of inflammatory 

resorption. Ideally a broad-spectrum antibiotic should 

be administered for seven days. 17 

Nevertheless, in the case presented in this paper, 

the 1-year clinical and radiographic controls showed 

maintainence of root integrity, intact Lamina dura 

periradicularly and absence of abnormal mobility, 

which are indicative of successful replantation. 

Certain precautions were taken while planning the 

replantation procedure. The tooth was immersed 

in saline prior to replantation to eliminate cell lysis 

products resulting from traumatic injury on root 

surface, as well as debris and bacteria from saliva. 18-20 

Systemic antibiotic therapy was administered and tooth 

was endodontically treated to prevent inflammatory 

resorption. 21 

Root resorption and ankylosis are frequently observed 

complications post-replantation. Therefore, despite 

the positive results observed after 1-year, clinical and 

radiographic follow-up of tooth replanted under the 

condition hereby described should be carried for a 

longer period. 

References 

1. 

2. 

3. 

4. 

Grossman LI, Ship II. Survival rate of replanted teeth. 

Oral Surg Oral Med Oral Pathol 1970;29(6):899-906. 

Andreasan JO, Andreason FM. Textbook and Color Atlas 

of Traumatic Injuries to Teeth. 3rd edition, Munksgaard: 

Copenhagen 1994:p.771. 

Andreasen JO, Borum MK, Jacobsen HL, Andreasen 

FM. Replantation of 400 avulsed permanent incisors. 4. 

Factors related to periodontal ligament healing. Endod 


Lekic P, Kenny D, Moe HK, Barretti E, McCulloch CA. 

Relationship of clonogenic capacity to plating efficiency 

and vital dye staining of human periodontal ligament 

cells: implications for tooth replantation. J Periodontal 

Res 1996;31(4):294-300. 


537

Case Report 

5. 

6. 

7. 

8. 

9. 

10. 

11. 

12. 

Blomlöf L, Otteskog P, Hammarström L. Effect of storage 

in media with different ion strengths and osmolalities on 

human periodontal ligament cells. Scand J Dent Res 

1981;89(2):180-7. 

Sigalas E, Regan JD, Kramer PR, Witherspoon DE, 

Opperman LA. Survival of human periodontal ligament 

cells in media proposed for transport of avulsed teeth. 


Hiltz J, Trope M. Vitality of human lip fibroblasts in 

milk, Hanks balanced salt solution and Viaspan storage 

media. Endod Dent Traumatol 1991;7(2):69-72. 

Blomlöf L, Lindskog S, Hammarström L. Periodontal 

healing of exarticulated monkey teeth stored in milk or 

saliva. Scand J Dent Res 1981;89(3):251-9. 

Andreasen JO. Relationship between cell damage in the 

periodontal ligament after replantation and subsequent 

development of root resorption. A time-related study in 

monkeys. Acta Odontol Scand 1981;39(1):15-25. 

Ehnevid H, Jansson L, Lindskog S, Weintraub A, 

Blomlöf L. Endodontic pathogens: propagation of 

infection through patent dentinal tubules in traumatized 

monkey teeth. Endod Dent Traumatol 1995;11(5): 

229-34. 

Trope M, Moshonov J, Nissan R, Buxt P, Yesilsoy C. 

Short vs. long-term calcium hydroxide treatment of 

established inflammatory root resorption in replanted 

dog teeth. Endod Dent Traumatol 1995;11(3):124-8. 

Flores MT, Andreasen JO, Bakland LK, Feiglin B, 

Gutmann JL, Oikarinen K, et al; International 

Association of Dental Traumatology. Guidelines for the 

evaluation and management of traumatic dental injuries. 


13. 

14. 

15. 

16. 

17. 

18. 

19. 

20. 

21. 

Trope M, Hupp JG, Mesaros SV. The role of the socket 

in the periodontal healing of replanted dogs’ teeth stored 

in ViaSpan for extended periods. Endod Dent Traumatol 

1997;13(4):171-5. 

Trope M. Clinical management of the avulsed tooth: 

present strategies and future directions. Dent Traumatol 

2002;18(1):1-11. 

Andreasen JO. The effect of removal of the coagulum 

in the alveolus before replantation upon periodontal and 

pulpal healing of mature permanent incisors in monkeys. 

Int J Oral Surg 1980;9(6):458-61. 

von Arx T, Filippi A, Buser D. Splinting of traumatized 

teeth with a new device: TTS (Titanium Trauma Splint). 


Sae-Lim V, Wang CY, Trope M. Effect of systemic 

tetracycline and amoxicillin on inflammatory root 

resorption of replanted dogs’ teeth. Endod Dent 

Traumatol 1998;14(5):216-20. 

Andreasen JO. Effect of extra-alveolar period and 

storage media upon periodontal and pulpal healing after 

replantation of mature permanent incisors in monkeys. 

Int J Oral Surg 1981;10(1):43-53. 

Loe H, Waerhaug J. Experimental replantation of teeth 

in dogs and monkeys. Arch Oral Biol 1961;3:176-84. 

Cvek M, Granath LE, Hollender L. Treatment of nonvital 

permanent incisors with calcium hydroxide. 3. 

Variation of occurrence of ankylosis of reimplanted 

teeth with duration of extra-alveolar period and storage 

environment. Odontol Revy 1974;25(1):43-56. 

Hammarström L, Blomlöf L, Feiglin B, Andersson 

L, Lindskog S. Replantation of teeth and antibiotic 

treatment. Endod Dent Traumatol 1986;2(2):51-7. 

538 


Indian Journal of 

Multidisciplinary Dentistry 

Information for Authors 

Manuscripts should be prepared in accordance with the ‘Uniform 

requirements for manuscripts submitted to biomedical journals’ compiled 

by the International Committee of Medical Journal Editors (Ann. Intern. 

Med. 1992;96:766-767). The Journal strongly disapproves of the submission 

of the same articles simultaneously to different journals for consideration as 

well as duplicate publication and will decline to accept fresh manuscripts 

submitted by authors who have done so. 

The boxed checklist will help authors in preparing their manuscript 

according to our requirements. Improperly prepared manuscripts may be 

returned to the author without review. The checklists should accompany 

each manuscript. 

Covering Letter: The covering letter should explain if there is any 

deviation from the standard IMRAD format (Introduction, Methods, 

Results and Discussion) and should outline the importance of the 

paper. Principal/Senior author must sign the covering letter indicating 

full responsibility for the paper submitted, preferably with signatures of 

all the authors. Articles must be accompanied by a declaration by all 

authors stating that the article has not been published in any Journal/ 

Book. Authors should mention complete designation and departments, 

etc., on the manuscript. 

Manuscript: Three complete sets of the manuscript should be submitted 

and preferably with a CD; typed double spaced throughout (including 

references, table and legends to figures). The manuscript should be 

arranged as follow: Covering letter, Checklist, Title page, Abstract, 

Keywords (for indexing, if required), introduction, Methods, Results, 

Discussion, References, Tables, Legends to Figures and Figures. All pages 

should be numbered consecutively beginning with the title page. 

Types of Submission: Original Research articles, Review articles, Case 

reports and Clinical study 

Title Page: Should contain the title, short title, names of all the authors 

(without degrees of diplomas), names and full location of the departments 

and institutions where the work was performed, name of the corresponding 

authors, acknowledgement of financial support and abbreviations used. The 

title should be of no more than 80 characters and should represent the 

major theme of the manuscript. A subtitle can be added if necessary. 

A short title of not more than 50 characters (including inter-word spaces) 

for use as a running head should be included. The name, telephone 

and fax numbers, e-mail and postal addresses of the author to whom 

communications are to be sent should be typed in the lower right corner 

of the title page. 

Abstract: The abstract of not more than 200 words. It must convey the 

essential features of the paper. It should not contain abbreviations, footnotes 

or references. 

Introduction: The introduction should state why the study was carried out 

and what were its specific aims/objectives were. 

Material and Methods: Theses should be described in sufficient details to 

permit evaluation and duplication of the work by others. Ethical guidelines 

followed by the investigations should be described. 

Results: These should be concise and include only the tables and figures 

necessary to enhance the understanding of the text. 

Discussion: This should consist of a review of the literature and relate 

the major findings of the article to other publications on the subject. The 

particular relevance of the results to healthcare in India should be stressed, 

e.g., practically and cost. 

References: These should conform to the Vancouver style. References 

should be numbered in the order in which they appear in the texts and 

these numbers should be inserted above the lines on each occasion the 

author is cited. 

Tables: These should be typed double spaces on a separate sheet and 

figure number (in Roman Arabic numerals) and title above the table and 

explanatory notes below the table. 

Legends: These should be typed double spaces on a separate sheet and 

figure numbers (in Arabic numerals) corresponding with the order in which 

the figures are presented in the text. The legend must include enough 

information to permit interpretation of the figure without reference to the 

text. 

Figures: Two complete sets of glossy prints of high quality should be 

submitted. The labeling must be clear and neat. All photomicrographs 

should indicate the magnification of the print. Special features should be 

indicated by arrows or letters which contrast with the background. The 

back of each illustration should bear the first author’s last name, figure 

number and an arrow indicating the top. This should be written lightly 

in pencil only. Please do not use a hard pencil, ball point or felt pen. 

Color illustrations will be accepted if they make a contribution to the 

understanding of the article. Do not use clips/staples on photographs and 

artwork. Illustrations must be drawn neatly by an artist and photographs 

must be sent on glossy paper. No captions should be written directly on 

the photographs or illustration. Legends to all photographs and illustrations 

should be typed on a separate sheet of paper. All illustrations and figures 

must be referred to in text and abbreviated as ‘Fig’. 

Please complete the following checklist and attach to the manuscript: 

1. Classification (e.g. original article, review, etc.)_________________ 

2. Total number of pages____________________________________ 

3. Number of tables________________________________________ 

4. Number of figures_______________________________________ 

5. Special requests_________________________________________ 

6. Suggestions for reviewers (name and postal address) 

Indian 1.______________ Foreign 1. _______________ 

2._____________________ 2._______________ 

7. All author’s signatures____________________________________ 

8. Corresponding author’s name, current postal and e-mail address and 

telephone and fax numbers 

__________________________________________________________ 

For Editorial Correspondence 

Dr KMK Masthan 

Professor and Head 

Department of Oral Pathology and Microbiology 

Sree Balaji Dental College and Hospital 

Velachery Main Road, Narayanapuram, Pallikaranai 

Chennai - 600 100, E-mail: masthankmk@yahoo.com, 

ijmdent@gmail.com, www.ijmdent.com 


539

540

Volume 2 - Issue 3 (May-Jul)

Create successful ePaper yourself

Delete template?

Save as template?