Study Of The Effect Of Increased Masticatory Pressure On The Expression Of RANKL In Rat Residual Ridge

Residual ridge resorption(RRR)has puzzled prosthetic dentitions for a long time ,which lead to be difficult for the denture's retention and stabilization because of the loss of bone mass. Many studies had researched the pathologic causeof RRR, and tried to find out the way of prevention and treatment. However the conclusions were conflict due to the limit of the animal model and way of clinic research, difficult to control the condition of the stress. The stress condition of the alveolar is changed because of the lack of the teeth. If the chewing force coming from the denture is over the normal the residual ridge will cause traumatic resorption; if below, it will cause disuse atrophy. However it is not clear about the pathology mechanism of the traumatic resorption. There are four major etiologic factors that cause RRR: anatomic, prosthetic, metabolic, and functional factors, but the local mechanical stress often generated by removable prostheses is the most important and is the main way to prevent through reducing the stress. By deeply researching the physiological and pathological mechanism of RRR, we can design and build the reasonable, scientific, suitable prostheses, on the other hand we can control the pathological process of the residual ridge from the level of the molecule and gene. The sequelae of tooth extraction have been investigated in animals such as monkeys, dogs, rats and hamsters. These animal studies have shown that healing of extraction sockets and remodeling changes of the residual ridges are similar to those in humans, but the healing period was much shorter in small laboratory animals than in humans. In rats the histological healing period of tooth extraction sockets was only from two to four weeks. So in this study a rat traumatic resorption of RRR animal model have developed. The change of the RANKL expression level in the residual ridge has investigated, discussed the effect of RANKL in traumatic resorption of RRR, and shown the mechanism of traumatic resorption of RRR. The 50 healthy ten weeks male Wistar rats were allotted at random into two groups, experiment group and control group. The left and right maxilla first molars were extracted ,then took impression in a custom impression tray after 4 weeks. The denture bases were made of the self-cured acrylic resin. The height of the denture base of the experiment group was about 0.8mm over occlusal plane ,but equal to occlusal plane for the control one. 50 rats were perfused and sacrificed at 3 day, 1 week, 2 week,4 week, 8 week. All the buccolingual sections in the first molar region were processed, then proceeded with HE staining and RANKL immunohistochemical staining. Observing the histological changes of tissue, and the result was analyzed by the Computer Image Analyzing System and treated by statistics test. The result showed that there was no significant histopathological change, no evidence inflammation, no bone resorption in the mucous of the control group, and RANKL expression level was low, lying in the few of osteoblasts and fibroblasts. For the experiment group, at 3 day, the RANKL expression level was a bit stronger and the osteoblasts ,matrix cells in themarrow had positive granules, but there was no significant different compared with the control group. At 1 week and 2 week , the significant histopathological change was noted for the mucous of the alveolar .The epithelium, the lamina propria mucosa were severely compressed. Numbers of osteoclasts and Howshiop's lacunae were observed on the bone surface. The RANKL expression level in the osteoclasts was much stronger comparing with the control group. For 4 week and 8 week, the histopathological of the mucosa had no evidence change and the number of osteoclasts on the bone surface was decreased but the number of osteoblasts was increased. The RANKL expression level was lower, no evident different comparing with the control group. For experiment group, the chewing force through the denture base to the alveolar is more over normal. The epithelial cells which are produced under the increased masticatory pressure have the potential deficits in the cell kinetics such as over-expression of death promoters and/or under-expression of death inhibitors, and then the lowered proliferative activity and accelerated cell death may lead to the epithelial thickness. The over masticatory pressure can lead to a series of biology reactions in the alveolar bone. At last osteoblasts'proliferative activity is inhibited and cell death is accelerated, the reverse result to the osteoclasts, which destroys the balance between the resorption and the formation of the bone. At 1 week and 2 week, the RANKL expression in the osteoblasts and matrix cells is increased, which binding with RANK in the preosteoclasts accelerates the differentiation of the preosteoclasts...