A histopathologic study of the controlling role of T cells on experimental periodontitis in rats.

Background/purpose: The onset and progression of periodontitis involve bacterial infection and the immune response. T cells function in the immune response and reportedly induce bone resorption in inflammatory bone loss. However, the exact role of T cells in periodontal destruction remains unclear.

Histopathological comparison of the onset of peri-implantitis and periodontitis in rats.

Background And Objective: There are a few experimental models that clearly describe the pathological differences in tissue destruction between periodontitis and peri-implantitis. We recently reported that the formation of immune complexes accelerates site-specific loss of attachment and alveolar bone resorption when an antigen is topically applied in the gingival sulcus of an immunized rat. We applied this model to the peri-implant tissues and compared peri-implant destruction to periodontitis without using a ligature.

RANKL pretreatment plays an important role in the differentiation of pit-forming osteoclasts induced by TNF-α on murine bone marrow macrophages.

Background: Osteoclasts differentiated from bone marrow macrophages (BMMs) induced by TNF-α alone do not have resorbing activity. When BMMs are stimulated with receptor activator of NF-κB ligand (RANKL) before TNF-α stimulation, pit-forming osteoclasts are differentiated. However, the details of the effect of RANKL pretreatment on the pit-forming osteoclast differentiation by TNF-α have not been established.