Supplementum 1+2/2010 - Společnost pro pojivové tkáně

The stimulus for remodeling can comefrom internal factors (e.g., hormones, cytokines-growthfactors) and external factors(e.g., physical activity and mechanical loading).It is widely accepted that physicalactivity benefits the musculoskeletal systembut the mechanisms affecting bonemass and density that are set off by physicalactivity in general and mechanical loadingin particular are still poorly understood.It appears that mechanical strain inhibitsRANKL production and up-regulates OPGproduction in vitro. Hence, lack of mechanicalstrain during immobilisation (disuse)may favour an enhanced RANKL-to-OPG ratio leading to increase bone loss.Nowadays, it is believed that the staticloading is not osteogenic. Instead, thedynamic loading plays the essential role ofstimulating the bone remodelling process,which is supported by many experimentaland clinical studies. Increasing age,declining levels of sex hormones, or calciumdeficiencies produce an imbalancebetween resorption and formation resultingin bone loss. Physical activity throughits mechanical effects on bone can mitigatethis bone loss. Optimal mechanical stimulidiffer between growing and mature bone,and mature bone is influenced by ageingor other systemic factors such as nutritionand hormones.MethodsWith the development of computer-aidedstrategies and based on theknowledge of bone geometry, applied forces,and elastic properties of the tissue, itmay be possible to calculate the mechanicalstress transfer inside the bone (FiniteElements analysis or FE analysis). The changeof stresses is followed by a change ininternal bone density distribution. Thisallows formulate mathematical models thatcan be used to study functional adaptationquantitatively and furthermore, to createthe bone density distribution patterns.Such mathematical models have been builtin the past. Since they calculate just mechanicaltransmission inside the bone and notconsidering cell-biologic factors of bonephysiology, they just partially correspondto the reality seen in living organisms.Basically, there are essentially two groupsof models for bone remodelling. One assumesthat the mechanical loading is thedominant effect, almost to the exclusion ofother factors, and treatment of biochemicaleffects are included in parameter with littlephysical interpretation. The results or predictionsof these models yield the correctdensity distribution patterns in physiologicalcases. However, they have a limitedability to simulate disease. The secondgroup, the biochemical models, considercontrol mechanisms of bone adaptation ingreat detail, but with limited possibilitiesfor including mechanical effects that areknown to be essential.We realize that biochemical reactionsare initiated and influenced primarily bygenetic effects and then by external biomechanicaleffects (stress changes). Ourthermodynamic model enables to combinebiological and biomechanical factors. Sucha model may also reflect changes in remodellingbehaviour resulting from pathologicalchanges to the bone metabolism or fromhip joint replacement. However, it is a modeland thus it is a great simplification of thecomplex process of bone remodelling. Inthis talk, a more detailed description of biochemicalcontrol mechanisms will be addedto the mentioned model which in turn leads220 15. Kubátův den