The roles of osteocytes in alveolar bone destruction in periodontitis

Abstract

Periodontitis, a bacterium-induced inflammatory disease that is characterized by alveolar bone loss, is highly prevalent worldwide. Elucidating the underlying mechanisms of alveolar bone loss in periodontitis is crucial for understanding its pathogenesis. Classically, bone cells, such as osteoclasts, osteoblasts and bone marrow stromal cells, are thought to dominate the development of bone destruction in periodontitis. Recently, osteocytes, the cells embedded in the mineral matrix, have gained attention. This review demonstrates the key contributing role of osteocytes in periodontitis, especially in alveolar bone loss. Osteocytes not only initiate physiological bone remodeling but also assist in inflammation-related changes in bone remodeling. The latest evidence suggests that osteocytes are involved in regulating bone anabolism and catabolism in the progression of periodontitis. The altered secretion of receptor activator of NF-κB ligand (RANKL), sclerostin and Dickkopf-related protein 1 (DKK1) by osteocytes affects the balance of bone resorption and formation and promotes bone loss. In addition, the accumulation of prematurely senescent and apoptotic osteocytes observed in alveolar bone may exacerbate local destruction. Based on their communication with the bloodstream, it is noteworthy that osteocytes may participate in the interaction between local periodontitis lesions and systemic diseases. Overall, further investigations of osteocytes may provide vital insights that improve our understanding of the pathophysiology of periodontitis.

Aggravating Effects of Psychological Stress on Ligature-Induced Periodontitis via the Involvement of Local Oxidative Damage and NF-κB Activation

“…One might therefore speculate that further activation of NF- κ B signalling occurs in the periodontitis gingiva of stressed rats, in which severe inflammatory reactions and oxidative damage are observed. Alveolar bone homeostasis depends on the functional balance between osteoblasts and osteoclasts [ 46 ]. With the development of periodontitis, alveolar bone exhibits bone resorption as a result of abnormal bone remodelling.…”

Inflammasomes in Alveolar Bone Loss

“…Furthermore, Wnt/β-catenin signaling, which participates in osteoblast proliferation, differentiation, and apoptosis, may regulate NLRP3 inflammasome activity in osteoblasts; indeed, the Wnt/β-catenin pathway inhibitor Dickkopf-related protein 1 (DKK1) reversed the decreased expression of NLRP3 and active IL-1β in osteoblasts ( 148 ). Hence, increased DKK1 levels generated by osteocytes in osteolytic diseases, such as periodontitis, may also contribute to the increased activity of the NLRP3 inflammasome in these scenarios, although stronger, direct evidence is still needed ( 1 ). In addition, pyroptosis triggered by inflammasome activation can also determine the death of osteoblasts, thereby decreasing the rate of osteogenesis ( 149 ).…”

“…The alveolar bone, an important part of the maxillofacial skeleton, is a connective tissue that supports teeth, is subjected to mechanical stress, and undergoes continuous bone remodeling ( 1 ). Similar to other bone tissues, osteoclasts and osteoblasts are the main components responsible for the highly dynamic equilibrium between bone resorption and formation in the alveolar bone.…”

Effects of Colocasia antiquorum var. Esculenta Extract In Vitro and In Vivo against Periodontal Disease

“…As periodontitis progresses, the height of the alveolar bone gradually decreases, eventually resulting in tooth loss if not treated [ 25 ]. In this study, the amount of alveolar bone loss in the PC group was not significantly different from the NC group.…”