Recently, involvement of the immune system, which has an influence on the bone metabolism under pathological conditions, in inflammatory bone destruction in rheumatoid arthritis and periodontal disease has attracted attention. Periodontal disease is thought to result from acquired immune responses triggered by the innate immunity against bacterial infection, which lead to alveolar bone destruction because of the switch from acute inflammation to chronic inflammation.
The immune system shares the microenvironment of the bone marrow and several proinflammatory factors with bone and mutually influences each other. In orthodontic tooth movement, various immunoresponsive inflammatory cytokines are expressed, participating in alveolar bone resorption, which is indispensable for orthodontic tooth movement. Osteocytes which are buried in the bone, form remarkable cellular networks in response to mechanical stress enabling communication not only among each other, but also with osteoclasts and osteoblasts on the bone surface; osteocytes play a headquarters-like role in osteoclastogenesis and bone resorption in orthodontic tooth movement. On the pressure side of the alveolar bone during orthodontic tooth movement, osteocytes produce osteopontin (Opn) and a connective tissue growth factor (CTGF/CCN2), also called the osteoimmune factor, which are involved in osteoclastogenesis and induce active bone resorption.
This review summarizes our knowledge about the molecular mechanisms of orthodontic tooth movement stimulated by mechanical stress, and describes the new role of osteocyte in the regulation of the marrow environment supporting immune cells.