The roles of osteocytes in alveolar bone destruction in periodontitis

Xiaofei Huang,Xiaoshuang Li,Xiaofeng Lu,Feng Mei,Yanling Xie,Mengru Xie,Lili Chen

doi:10.1186/s12967-020-02664-7

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.

Highlights

Periodontitis is a complicated, multifaceted process that results in the disorganization of the underlying ligament and alveolar bone
A high prevalence of apoptosis in osteocytes induced by bone uploading was found to increase the expression of the osteocytic factor receptor activator of Nuclear factor-kappa B (NF-κB) ligand (RANKL), which exacerbated bone resorption in response to skeletal unloading [22]
Osteocytes upregulate the expression of Receptor activator of NF-κB ligand (RANKL) in periodontitis Periodontitis tissue is flooded with many pathological factors, including biologically active substances within bacterial plaques and inflammatory mediators released by immune cells

Summary

Introduction

Periodontitis is a complicated, multifaceted process that results in the disorganization of the underlying ligament and alveolar bone. Studies on the mechanisms of periodontitis have always focused on alveolar bone loss, especially the function of osteoclasts and osteoblasts in this process. A high prevalence of apoptosis in osteocytes induced by bone uploading was found to increase the expression of the osteocytic factor receptor activator of NF-κB ligand (RANKL), which exacerbated bone resorption in response to skeletal unloading [22].

Results

Conclusion