牙周炎為牙齒周圍發炎引起的附連組織喪失以及齒槽骨的破壞;相同地,植體周圍炎亦為細菌感染所引起植體周圍軟組織和骨組織產生的炎症和破壞。因此,骨合成和吸收的調節會影響未來疾病的發展和進程。骨硬化蛋白(sclerostin)主要是由骨細胞(osteocyte)所分泌,其會作用於成骨細胞(osteoblast),抑制骨形成;除此之外,亦會促進蝕骨細胞(osteoclast)的活性和分化,增加骨吸收。本篇回顧將探討骨硬化蛋白的由來與結構、生物學特性、其與牙周炎及植體周圍炎之間的關係和新興治療性藥物:骨硬化蛋白抗體(Scl-Ab)目前研究的結果,希望本篇文獻回顧能夠提供閱者有關骨硬化蛋白於牙周炎和植體周圍炎的評估及骨硬化蛋白抗體運用於牙周骨缺損處再生和植體骨整合有新的視角和想法。
Periodontitis results from persistent inflammation that is not adequately controlled and surrounds the tooth, which causes the loss of both periodontal attachment and alveolar bone. Similarly, peri-implantitis arises due to bacterial infection and tissue inflammation, leading to soft and bone tissue destruction around the implant. Therefore, the regulation of bone formation and resorption can significantly impact the development and progression of these diseases. Sclerostin, primarily secreted by osteocytes, acts on osteoblasts to suppress bone formation. Furthermore, it can enhance the activity and differentiation of osteoclasts, leading to an increase in bone resorption. This literature review aims to delve into the origin, structure, and biological characteristics of sclerostin, its relationship with periodontitis and peri-implantitis, and the findings of recent studies on a novel therapeutic drug: sclerostin antibody (Scl-Ab). Our intention is for this review to provide readers with innovative insights and novel ideas related to the assessment, diagnosis, and utilization of sclerostin in the context of periodontitis and peri-implantitis, along with the application of Scl-Ab to facilitate the regeneration of bony defects in periodontal tissue and implant osseointegration.