Yu Bo, Wang Cun-Yu
Division of Regenerative and Constitutive Sciences, School of Dentistry, University of California at Los Angeles, Los Angeles, California, USA.
Division of Oral Biology and Medicine, School of Dentistry, University of California at Los Angeles, Los Angeles, California, USA.
Periodontol 2000. 2022 Jun;89(1):99-113. doi: 10.1111/prd.12422. Epub 2022 Mar 4.
Periodontitis and osteoporosis are prevalent inflammation-associated skeletal disorders that pose significant public health challenges to our aging population. Both periodontitis and osteoporosis are bone disorders closely associated with inflammation and aging. There has been consistent intrigue on whether a systemic skeletal disease such as osteoporosis will amplify the alveolar bone loss in periodontitis. A survey of the literature published in the past 25 years indicates that systemic low bone mineral density (BMD) is associated with alveolar bone loss, while recent evidence also suggests a correlation between clinical attachment loss and other parameters of periodontitis. Inflammation and its influence on bone remodeling play critical roles in the pathogenesis of both osteoporosis and periodontitis and could serve as the central mechanistic link between these disorders. Enhanced cytokine production and elevated inflammatory response exacerbate osteoclastic bone resorption while inhibiting osteoblastic bone formation, resulting in a net bone loss. With aging, accumulation of oxidative stress and cellular senescence drive the progression of osteoporosis and exacerbation of periodontitis. Vitamin D deficiency and smoking are shared risk factors and may mediate the connection between osteoporosis and periodontitis, through increasing oxidative stress and impairing host response to inflammation. With the connection between systemic and localized bone loss in mind, routine dental exams and intraoral radiographs may serve as a low-cost screening tool for low systemic BMD and increased fracture risk. Conversely, patients with fracture risk beyond the intervention threshold are at greater risk for developing severe periodontitis and undergo tooth loss. Various Food and Drug Administration-approved therapies for osteoporosis have shown promising results for treating periodontitis. Understanding the molecular mechanisms underlying their connection sheds light on potential therapeutic strategies that may facilitate co-management of systemic and localized bone loss.
牙周炎和骨质疏松症是常见的与炎症相关的骨骼疾病,给老龄化人口带来了重大的公共卫生挑战。牙周炎和骨质疏松症都是与炎症和衰老密切相关的骨骼疾病。人们一直对诸如骨质疏松症这样的全身性骨骼疾病是否会加剧牙周炎中的牙槽骨丧失存在浓厚兴趣。对过去25年发表的文献进行的一项调查表明,全身性低骨矿物质密度(BMD)与牙槽骨丧失有关,而最近的证据也表明临床附着丧失与牙周炎的其他参数之间存在相关性。炎症及其对骨重塑的影响在骨质疏松症和牙周炎的发病机制中起着关键作用,并且可能是这些疾病之间的核心机制联系。细胞因子产生增加和炎症反应增强会加剧破骨细胞的骨吸收,同时抑制成骨细胞的骨形成,导致净骨丢失。随着年龄的增长,氧化应激和细胞衰老的积累推动了骨质疏松症的进展和牙周炎的加重。维生素D缺乏和吸烟是共同的危险因素,可能通过增加氧化应激和损害宿主对炎症的反应来介导骨质疏松症和牙周炎之间的联系。考虑到全身性和局部性骨丢失之间的联系,常规牙科检查和口腔内X光片可作为一种低成本的筛查工具,用于检测全身性低BMD和骨折风险增加。相反,骨折风险超过干预阈值的患者发生严重牙周炎和牙齿脱落的风险更高。美国食品药品监督管理局批准的各种骨质疏松症治疗方法在治疗牙周炎方面已显示出有希望的结果。了解它们之间联系的分子机制有助于揭示潜在的治疗策略,这些策略可能有助于对全身性和局部性骨丢失进行联合管理。