| Residual ridge resorption(RRR) has puzzled prosthetic dentitions for a longtime ,which lead to be difficult for the denture's retention and stabilizationbecause of the loss of bone mass. Many studies had researched the pathologiccause of RRR, and tried to find out the way of prevention and treatment. Howeverthe conclusions were conflict due to the limit of the animal model and way ofclinic research, difficult to control the condition of the stress. So the physiologicaland pathological mechanism of the RRR was not clear.The stress condition of thealveolar is changed because of the lack of the teeth. If the chewing force comingfrom the denture is over the normal stress the residual ridge will cause traumaticresorption;if below, it will cause disuse atrophy. However it is not clear about thepathology mechanism of the traumatic resorption. There are four major etiologicfactors that cause RRR: anatomic, prosthetic, metabolic, and functional factors,but the local mechanical stress often generated by removable prostheses is themost important and is the main way to prevent through reducing the stress. Bydeeply researching the physiological and pathological mechanism of RRR, we candesign and build the reasonable, scientific, suitable prostheses, on the other handwe can control the pathological process of the residual ridge from the level of themolecule and gene.The sequelae of tooth extraction have been investigated in animals such asmonkeys, dogs, rats and hamsters. These animal studies have shown that healingof extraction sockets and remodeling changes of the residual ridges are similar tothose in humans, but the healing period was much shorter in small laboratoryanimals than in humans. In rats the histological healing period of tooth extractionsockets was about two weeks. So in this study a rat traumatic resorption of RRRanimal model have developed. The change of the number of TRAP stainingpositive cells and OPNmRNA expression level in the residual ridge hasinvestigated, discussed the relationship between the active of the bone resoptionand effect of OPNmRNA in traumatic resorption of RRR, and shown themechanism of traumatic resorption of RRR.The 50 healthy ten weeks male Wistar rats were allotted at random into twogroups, experiment group and control group. The left and right maxilla firstmolars were extracted ,then took impression in a custom impression tray after 2weeks. The denture bases were made of the self-cured acrylic resin. The height ofthe denture base of the experiment group was about 0.8mm over occlusalplane ,but equal to occlusal plane for the control one. 50 rats were perfused andsacrificed at 3 day, 1 week, 2 week,4 week, 8 week. All the buccolingual sectionsin the first molar region were processed, then proceeded with HE staining ,TRAPstaining and OPNmRNA in-situ-hybridization staining. Observing the histologicalchanges of tissue, and the result was analyzed by the Computer Image AnalyzingSystem and treated by statistics test.The result showed that there was no significant histopathological change, noevidence inflammation, no bone resorption in the mucous of the controlgroup,there was few TRAP staining positive cells in the residul ridge andOPNmRNA expression level was low, lying in the few of osteoblasts a. For theexperiment group, at 3 day, the number of TRAP staining negtive cells and theOPNmRNA expression level was a bit stronger in the osteoblasts, but there was nosignificant different compared with the control group. At 1 week and 2 week , thesignificant histopathological change was noted for the mucous of the alveolar .Theepithelium, the lamina propria mucosa were severely compressed. Numbers ofosteoclasts and Howshiop's lacunae were observed on the bone surface. Thenumber of the TRAP staining positive cells and OPNmRNA expression level inthe osteoclasts was much stronger comparing with the control group. For 4 weekand 8 week, the histopathological of the mucosa had no evidence change and thenumber of osteoclasts on the bone surface was decreased but the number ofosteoblasts was increased. The number of the TRAP staining positive cells and theOPNmRNA expression level was lower, no evident different comparing with thecontrol group.For experiment group, the chewing force through the denture base to thealveolar is more over normal. The epithelial cells which are produced under theincreased masticatory pressure have the potential deficits in the cell kinetics suchas over-expression of death promoters and/or under-expression of death inhibitors,and then the lowered proliferative activity and accelerated cell death may lead tothe epithelial thickness. The over masticatory pressure can lead to a series ofbiology reactions in the alveolar bone. At last osteoblasts' proliferative activity isinhibited and cell death is accelerated, the reverse result to the osteoclasts, whichdestroys the balance between the resorption and the formation of the bone. At 1week and 2 week, the OPNmRNA expression in the osteoblasts and matrix cells isincreased, which leading to the OPN increase in the bone.it can strong the bindbetween the osteoclast and bone ,it can make the osteoclast polyfied ,make theosteoclast cytoskeleton relined,form the ring of actin,form the sealed areabetween the osteoclast and bone.those can lead to bone resoption. Finally thenumber of the osteoclast is increased and the osteoclastic resorption is acceleratedin the alveolar bone. At 4 week and 8 week, the number of osteoclast is decreasedand the OPNmRNA expression in the osteoblasts ,osteoclast of the marrow islower because of the decreased masticatory pressure.In this study ,an animal model about residual ridge traumatic resorptionhas developed. The result of the study has suggested that excessive maticatorypressure can lead to traumatic resorption of the residual ridge. The denture baseand the normal masticatory pressure will not cause the pathological change of thetissue under the denture base. The change of the OPNmRNA expression level is acomplex of biology reaction, that is induced by mechanical forces on alveolarbone. Under the modulation of OPN, osteoclast can polify ,which leads to theresidual ridge traumatic resorption. The reveal of the molecule mechanism ofRRR provides the strong theory proof about the molecule and gene treatment forRRR.
|
PDF Full Text Request