Current perspectives of residual ridge resorption: Pathological activation of oral barrier osteoclasts

Abstract

Tooth extraction is a last resort treatment for resolving pathological complications of dentition induced by infection and injury. Although the extraction wound generally heals uneventfully, resulting in the formation of an edentulous residual ridge, some patients experience long-term and severe residual ridge reduction. The objective of this review was to provide a contemporary understanding of the molecular and cellular mechanisms that may potentially cause edentulous jawbone resorption. Study selection: Clinical, in vivo, and in vitro studies related to the characterization of and cellular and molecular mechanisms leading to residual ridge resorption. Results:The alveolar processes of the maxillary and mandibular bones uniquely juxtapose the gingival tissue. The gingival oral mucosa is an active barrier tissue that maintains homeostasis of the internal organs through its unique barrier immunity. Tooth extraction not only generates a bony socket but also injures oral barrier tissue. In response to wounding, the alveolar bone socket initiates regeneration and remodeling through coupled bone formation and osteoclastic resorption. Osteoclasts are also found on the external surface of the alveolar bone, interfacing the oral barrier tissue. Osteoclasts in the oral barrier region are not coupled with osteoblastic bone formation and often remain active long after the completion of wound healing, leading to a net decrease in the alveolar bone structure. Conclusion:The novel concept of oral barrier osteoclasts may provide important clues for future clinical strategies to maintain residual ridges for successful prosthodontic and restorative therapies.

Cyclic pressure-induced cytokines from gingival fibroblasts stimulate osteoclast activity: Clinical implications for alveolar bone loss in denture wearers

“…In a mouse model, physiological mechanical damage from mastication induced IL-6 production from gingiva, thereby resulting in accumulation of gingiva-resident T helper 17 (Th17) cells at the oral mucosal barrier [42]. The cyclic pressure-induced secretion of cytokines from hGFs observed in this study could thus be partly explained as an intrinsic mechanism in the gingiva to condition local osteoimmunity [43]. It will be of interest and important to analyze the effects of cyclic pressure-induced hGF factors, including anti-inflammatory cytokines, on osteoclasts together with osteoblasts and other immune cells, such as Th17 cells.…”

Mechanism of bisphosphonate-related osteonecrosis of the jaw (BRONJ) revealed by targeted removal of legacy bisphosphonate from jawbone using competing inert hydroxymethylene diphosphonate

“…It has been well established that tooth extraction induces not only bone regeneration and remodeling by osteoclasts in the bony socket but also a unique set of osteoclasts on the surface of alveolar bone ( Kondo et al, 2022 ). Histologically, osteoclasts are distinct as multinuclear large cells adhered to the bone lacunae.…”

“…N-BP adsorbed on bone mineral stays relatively firmly until bone resorption by osteoclasts, and active bone resorption may release N-BP from bone surface to the local environment. Tooth extraction induces not only bone remodeling in the bony socket but also unusual osteoclastogenesis on the external surface of alveolar bone ( Kondo et al, 2022 ). The present study demonstrated the oral barrier inflammation of ZOL-pretreated mice, which was densely localized adjacent to the alveolar bone surface ( Figure 5 ).…”

Effects of Super-Activated Platelet Lysate on Early Healing of Tooth Extraction Sockets in Rats

“…Osteoclasts that interface the oral barrier tissues remain active in the alveolar crest during wound healing in the tooth extraction socket, 38 , 39 and various cytokines and chemokines are involved in the immune response after tooth extraction. 40 Therefore, chemokine expressions in the healing gingival tissue at the crest of the alveolar ridge should be investigated.…”