The Microdamage And Expression Of Scl In Peri-implant Bone Under Impact Load

Implant denture is supported by the implant which is inserted in the alveolar bone. Implant denture can improve masticatory function significantly without uncomfort, and it does not bring about any damage to adjacent teeth. So the implant denture is well known and accepted as restoration by more and more people. The osseointegration between the surfaces of the implant and bone is a fundamental prerequisite for implant to maintain its stability and support the bite force.Dental implant may suffer from impact load in the process of sports and physical training. Impact force refers to the strength that occurs and increases suddenly when the object suffers collision, and then disappears quickly. When the implant suffers impact, the strength would spread in the form of stress wave in alveolar bone which would cause the microdamage of alveolar bone around the dental implant, but the mechanism of trauma is still unclear.There are a lot of cells and molecules participating in the process of bone trauma and its remodeling. Sclerostin has been reported having close relation with mechanical signal pathway of Wnt(bone formation) and RANKL(bone loss). But the effect of sclerostin on the process of microdamage and remodeling of alveolar bone around implant is still unclear. Analysis of the correlation between microdamage of alveolar bone around implant due to impact load and the expression of sclerostin is the key to this problem.In order to achieve these objectives, the animal model with implant under impact force will be established. Micro-CT, histological staining, and RT-q PCR are used to study the characteristic of microdamage and the expression of sclerostin??-catenin and RANKL, in order to reveal the mechanism of damage and repair of alveolar bone around implant due to impact load. The results could be used to evaluate the influence of impact load on the alveolar bone trauma around implant, and help to promote bone remodeling in clinical dental practice. The study includes the following three experiments: 1. The establishment of the impacted implant experimental animal model.The pure titanium implants were inserted into rabbit distal femoral condyle. Three months after implant surgery, the osseointegration was tested through Micro-CT scan. After implant stability was tested, the implants of experimental group were given different impact load using a drop hammer. The implant steadiness change and bone damage were studied by tissue specimens observation and vibration frequency test. The experimental model which suffered impact damage was established eventually.The results show that the cortex around implant had no obvious change after impact injury. But vibration frequency decreased from 8463.4±384.8Hz to 5111.5±100.9Hz(p<0.05), and implant stability declined. The experimental model established by this method can reflect load magnitudes and bone damage around implant. The results constitute basis for subsequent damage feature study. 2. The microdamage of the implant-bone interface and surrounding bone after impact.Animals were sacrificed at different time points to take the implants and their surrounding bone tissues in order to study implant-bone interface and surrounding microstructure changes after impact load. The microdamage was studied through tissue restruction and analyse by Micro-CT and mineralized tissue slicing with VG and HE staining.The results show that impact load could lead to destruction of interface between implant and bone, and fracture and disorder of trabecular around implant. BV/TV reduced from 65.5±0.7% to 42.0±2.8%(p<0.05), Tb.Th decreased from 0.28±0.01?m to 0.20±0.01?m(p<0.05) and Tb.Sp increased from 0.15±0.01?m to 0.26±0.01?m(p<0.05). The greater magnitudes of impact load were exerted, the more obvious bone injury and microstructure changes were. In the 14 days after impact, bone tissue mostly presented bone resorption, and bone microstructure returned to normal morphology gradually and osseointegration reformed in the day 28 after impact. 3. The change of relative molecular expression in the process of bone injury and reconstruction around implant after impact load.According to tissue slice results, bone tissue was taken in the area where obivious bone damge surrounding implant was found. In order to study the effect of sclerostin on bone impact injury and remodeling, the expression of sclerostin, ?-catenin and RANKL were tested respectively using immunofluorescence staining and RT-q PCR method.The results show an increased sclerostin expression after impact load, and it reached maximum at day 14 and then decreased gradually. Sclerostin expression returned to normal level till day 28. The tendency of RANKL expression was in accord with sclerostin. A negative correlation was found between ?-catenin and sclerostin expression. The results show that sclerostin regulates bone formation and resorption through affecting Wnt/?-catenin and RANKL/RANK pathway in the process of impacted bone damage and remodeling. Conclusion: 1. Impact load can cause implant-bone boundary destruction and surrounding bone tissue damage. The implant stability decreases after impact load, and no obvious change of cortex around implant neck is found. But partial areas of the interface present separation and break, and bone microstructure changes such as trabecular fracture. The results have a guiding significance for damage assessment and subsequent treatment of patients whose implants suffer impact injury. 2. The bone microstructure changes around implant can cause change of sclerostin expression after impact damage. The process of bone injury and reconstruction is related to Wnt/?-catenin pathway and RANKL/RANK pathway which are regulated by sclerostin. Sclerostin can be a biomechanical target molecule for analyzing the relationship between sclerostin and Wnt/?-catenin and RANKL/RANK pathway through degrading sclerostin expression in subsequent expriments, in order to reveal molecular mechanism of bone impact injury and remodeling.