Purpose: 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.
Conclusions: 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.
Keywords: Oral barrier tissue; Osteoclast; Residual ridge resorption; Tooth extraction.