| Osteoarthritis (OA) is a degenerative disease, which is characteristic in chondrocytes degeneration. Chondrocyte damage contributes much to the articular dysfunction in OA. Many researches have certificated that chondrocyte lost mostly by apoptosis. Temporomandibular joint anterior disk displacement (ADD) was one kind of temporomandibular joint disorders (TMD). ADD appeared very often in clinic. Some studies have suggested temporomandibular joint showed chongdrocytes apoptosis early after disk displacement. But the mechanism of chondrocyte apoptosis and its role after ADD was not understood.Apoptosis was a complex procedure, including many factors and enzymes. Studies had improved that chondrocyte apoptosis had two independent kinds, namely, Fas/FasL interaction induced apoptosis and NOinduced apoptosis.Fas was one of the most important factors that induced apoptosis. Fas located on cell surface. When interacted with FasL, Fas would form trimmers, then the part inside of cell would combined with FADD, which was inevitable in Fas induced apoptosis. FADD could act as a bridge, which combined Fas on one terminal, and combined Caspase-8 on another terminal, so, the signal induced by Fas/FasL interaction was transferred to caspase-8.Caspases consisted of a family that at least included 13 enzymes. The family had very important function in apoptosis. After activated by FADD, caspase-8 would activate caspase-3, then caspase-3 activates other caspases, at last they induced terminal elements changing like apoptosis. Caspase-8 was promoter in this signaling transfer pathway.Apoptosis was regulated by many factors, including many genes and enzymes. In those regulating genes, bcl-2 gene family was most important. The family consisted of many elements, and they could be divided into two sub-families according to their function, namely, pro-apoptosis and anti-apoptosis families. Bcl-2 and bax were most important respectively in the two subfamilies, and their expression would impact much on cells survival. Studies have certificated that Bcl-2 protein located on internal mitochondria surface, but Bax located out of mitochondria. When cells received death signaling, they would change Bcl-2 and Bax expression, especially, the expression of Bcl-2, thus, apoptosis would be regulated.In this experiment, using western immnoblotting we studied Fas, Caspase — 8, Bcl —2, Bax expression in control rabbits , sham-operating rabbits ,wealso studied their expression in temporomandibular joint following anterior disk displacement to investment signaling transfer pathway of chondrocyte apoptosis and its regulating factors. At last, we studied bcl-2 and bax mRNA expression of mouse , rat and rabbit by RT-PCR.So far, there were arguments about whether temporomandibular joint disk displacement was pathologic. Some studies have showed that after ADD there was adaptive remodeling in arthticular. After remodeling, condyle and disk could resume their function. In this experiment, we also studied articular histological changes, and we studied apoptosis by TUNEL to investment the role of apoptosis in condyle adaptive remodeling.Materials and MethodsTotal 47 Japanese rabbits(one year old, weighting 2.0-2.5 kg) were used in the experiments. They firstly were divided into two groups: one group had 17 rabbits and another had 30 rabbits.Fas induced apoptosis is one of the two most important pathways in chondrocyte apoptosis, and chondrocytes apoptosis increased following temporomandibular joint anterior disk displacement (ADD). To study the signaling transfer pathway of chondrocytes and to evaluate the role of bcl-2 and bax gene in temporomandibular joint chondrocyte apoptosis after ADD, we investigated the expression paterns of Fas , caspase-8, Bcl-2, Bax in TMJ condylar chondrocytes following ADD. The TMJ ADD model of rabbits was created by surgical operation. Total of 17 Japanese rabbits were used. Among these rabbits, 2 were used as controls, and 6 of them were sham-operated onright TMJ without displacing disk anterior. 9 rabbits were operated... |
