RANKL From Osteocytes Contributes to Periodontal Bone Loss
نویسندگان
چکیده
Periodontal bone loss results from bacterial infection and the associated host response. The ligand for the receptor activator of NF-κB (RANKL) induces the differentiation of osteoclasts, resulting in periodontal bone loss. The role of osteocytes in periodontal bone loss was investigated in this study. Transgenic mice expressing RANKL under the control of dentin matrix protein 1 (DMP1) were infected with Porphyromonas gingivalisFusobacterium nucleatum bacteria (Pg-Fn) to induce periodontitis, and type 1 diabetes was induced in groups of mice. Control (DMP1Cre−.RANKLf/f) mice with periodontal infection showed increases in bone loss, osteoclast counts, eroded bone surfaces, and RANKL expression compared to experimental (DMP1-Cre+.RANKLf/f) mice. RANKL deletion from osteocytes resulted in less periodontal bone loss. Diabetes enhanced periodontal bone loss in the control mice. The diabetic control (DMP1Cre−.RANKLf/f) mice had more bone loss than the non-diabetic control (DMP1Cre−.RANKLf/f) mice. In the experimental (DMP1-Cre+.RANKLf/f) mice, diabetes had no influence. This study demonstrated, for the first time, the essential role of osteocytes in periodontal bone loss.
منابع مشابه
Osteoblast Lineage Cells Play an Essential Role in Periodontal Bone Loss Through Activation of Nuclear Factor-Kappa B
Bacterial pathogens stimulate periodontitis, the most common osteolytic disease in humans and the most common cause of tooth loss in adults. Previous studies identified leukocytes and their products as key factors in this process. We demonstrate for the first time that osteoblast lineage cells play a critical role in periodontal disease. Oral infection stimulated nuclear localization of NF-κB i...
متن کاملCortical bone loss caused by glucocorticoid excess requires RANKL production by osteocytes and is associated with reduced OPG expression in mice.
Glucocorticoid excess is a major cause of low bone mass and fractures. Glucocorticoid administration decreases cortical thickness and increases cortical porosity in mice, and these changes are associated with increased osteoclast number at the endocortical surface. Receptor activator of NF-κB ligand (RANKL) produced by osteocytes is required for osteoclast formation in cancellous bone as well a...
متن کاملMitochondrial superoxide in osteocytes perturbs canalicular networks in the setting of age-related osteoporosis
Osteocytes are major bone cells that play a crucial role in maintaining the quality of and healing damage to bone tissue. The number of living osteocytes and canalicular networks declines in an age-dependent manner. However, the pathological effects of mitochondrial redox imbalances on osteocytes and bone metabolism have not been fully elucidated. We generated mice lacking mitochondrial superox...
متن کاملRole of periodontal pathogenic bacteria in RANKL-mediated bone destruction in periodontal disease
Accumulated lines of evidence suggest that hyperimmune responses to periodontal bacteria result in the destruction of periodontal connective tissue and alveolar bone. The etiological roles of periodontal bacteria in the onset and progression of periodontal disease (PD) are well documented. However, the mechanism underlying the engagement of periodontal bacteria in RANKL-mediated alveolar bone r...
متن کاملEffect RANKL Produced by Periodontal Ligament Cells on Orthodontic Tooth Movement
The bone remodeling process involved in orthodontic tooth movement consists of bone resorption on the compression side and bone formation on the tension side of the teeth. Osteoclasts play an important role in bone remodeling and are necessary for orthodontic tooth movement. Receptor activator of nuclear factor-κB ligand (RANKL) is essential for osteoclast formation and differentiation. Several...
متن کامل