慢性肾脏病患者牙槽骨变化及牙槽手术风险的研究进展

doi:10.3969/j.issn.1674-8115.2026.07.017

上海交通大学学报（医学版） ›› 2026, Vol. 46 ›› Issue (7): 981-989.doi: 10.3969/j.issn.1674-8115.2026.07.017

• 综述 • 上一篇

慢性肾脏病患者牙槽骨变化及牙槽手术风险的研究进展

鲁婷玮¹, 袁灏¹, 刘英莉²(), 江凌勇¹()

^1.上海交通大学医学院附属第九人民医院口腔颅颌面科，上海交通大学口腔医学院，国家口腔医学中心，口腔疾病国家临床医学研究中心，上海市口腔医学重点实验室，上海市口腔医学研究所，上海 200011
^2.上海交通大学医学院附属第九人民医院肾内科，上海 200011

收稿日期:2025-12-26 接受日期:2026-02-24 出版日期:2026-07-28 发布日期:2026-07-28
通讯作者: 江凌勇，教授，主任医师，博士；电子信箱：E-mail：jianglingyong@sjtu.edu.cn。
刘英莉，教授，主任医师，博士；电子信箱：18616375719@163.com。
作者简介:第一联系人：为共同第一作者（co-first authors)。
基金资助:
国家重点研发计划(2024YFC2510700);国家自然科学基金(82430032);上海市科技创新行动计划国际科技合作项目/政府间国际科技合作项目(23410713600);上海交通大学医学院“双百人”项目(20221809)

Advances in alveolar bone changes and risks of alveolar surgery in patients with chronic kidney disease

Lu Tingwei¹, Yuan Hao¹, Liu Yingli²(), Jiang Lingyong¹()

^1.Department of Oral and Maxillofacial Surgery, Shanghai Ninth People′s Hospital, Shanghai Jiao Tong University School of Medicine; College of Stomatology, Shanghai Jiao Tong University; National Center for Stomatology; National Clinical Research Center for Oral Diseases; Shanghai Key Laboratory of Stomatology; Shanghai Research Institute of Stomatology, Shanghai 200011, China
^2.Department of Nephrology, Shanghai Ninth People′s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200011, China

Received:2025-12-26 Accepted:2026-02-24 Online:2026-07-28 Published:2026-07-28
Contact: Jiang Lingyong, E-mail: jianglingyong@sjtu.edu.cn.
Liu Yingli, E-mail: 18616375719@163.com。
Supported by:
National Key Research and Development Program of China(2024YFC2510700);National Natural Science Foundation of China(82430032);Shanghai Science and Technology Innovation Action Plan-International Science and Technology Cooperation Program(23410713600);“Two-hundred Talents” Program of Shanghai Jiao Tong University School of Medicine(20221809)

摘要/Abstract

摘要：

慢性肾脏病（chronic kidney disease，CKD）是全球重大公共卫生问题，严重影响患者的健康及生活质量。慢性肾脏病矿物质与骨代谢紊乱（chronic kidney disease-mineral and bone disorder，CKD-MBD）作为CKD常见并发症，不仅可导致全身性骨代谢异常，亦可引发牙槽骨骨量下降等局部改变。其病理机制涉及钙磷代谢失衡、尿毒症毒素损伤、炎症与氧化应激、营养代谢紊乱，以及激素与生长因子失调等多个方面。肾功能下降可引发高磷血症、低钙血症及继发性甲状旁腺功能亢进症，进而打破成骨与骨吸收间的动态平衡。尿毒症毒素及炎症因子蓄积会诱发氧化应激，从而抑制成骨细胞分化并促进破骨细胞活化。此外，维生素D缺乏与蛋白质能量消耗等营养代谢紊乱，以及激素与生长因子水平异常，也会破坏牙槽骨稳态，进一步加重骨组织病变。CKD患者在接受拔牙、种植等牙槽手术时，面临出血、感染及愈合不良等风险，需实施针对性的围手术期管理，包括与肾内科协作综合评估肾功能与凝血功能、合理安排手术时机、采用微创技术并强化感染预防。该文综述了CKD相关牙槽骨改变特征、机制及临床风险，为相关机制探索及口腔诊疗提供参考。

关键词: 慢性肾脏病, 矿物质与骨代谢紊乱, 口腔, 牙槽骨, 牙槽手术

Abstract:

Chronic kidney disease (CKD) is a major global public health issue that significantly impacts patients′ health and quality of life. Chronic kidney disease-mineral and bone disorder (CKD-MBD), a common complication of CKD, not only leads to systemic bone metabolic abnormalities but also causes local changes such as a decrease in alveolar bone mass. Its pathological mechanisms involve multiple aspects, including calcium-phosphorus metabolism imbalance, uremic toxin damage, inflammation and oxidative stress, nutritional and metabolic disorders, as well as hormonal and growth factor dysregulation. Renal dysfunction leads to hyperphosphatemia, hypocalcemia, and secondary hyperparathyroidism, disrupting the dynamic balance between bone formation and resorption. The accumulation of uremic toxins and inflammatory cytokines induces oxidative stress, thereby suppressing osteoblast differentiation while promoting osteoclast activation. Moreover, metabolic disturbances, including vitamin D deficiency and protein-energy wasting, along with hormonal and growth factor dysregulation, impair alveolar bone homeostasis and exacerbate bone disorders. When patients with CKD undergo alveolar surgeries, such as tooth extraction and dental implant placement, they face risks of bleeding, infection, and poor wound healing. Therefore, targeted perioperative management is necessary, including multidisciplinary collaboration with nephrologists to comprehensively assess renal and coagulation functions, appropriate surgical timing, the use of minimally invasive techniques, and enhanced infection prevention. This article reviews the characteristics, mechanisms, and clinical risks of CKD-related alveolar bone changes, providing reference for related mechanism exploration and oral diagnosis and treatment.

Key words: chronic kidney disease, chronic kidney disease-mineral and bone disorder, oral cavity, alveolar bone, alveolar surgery

中图分类号:

R782.13

鲁婷玮, 袁灏, 刘英莉, 江凌勇. 慢性肾脏病患者牙槽骨变化及牙槽手术风险的研究进展[J]. 上海交通大学学报（医学版）, 2026, 46(7): 981-989.

Lu Tingwei, Yuan Hao, Liu Yingli, Jiang Lingyong. Advances in alveolar bone changes and risks of alveolar surgery in patients with chronic kidney disease[J]. Journal of Shanghai Jiao Tong University (Medical Science), 2026, 46(7): 981-989.

图/表 2

参考文献 61

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Potential mechanism	Key factor	Pathway and effect	Reference
Calcium-phosphate metabolism imbalance	PTH, FGF-23, Klotho, 1, 25(OH)₂D, calcium, phosphate	Declining renal function triggers hyperphosphatemia and hypocalcemia, inducing secondary hyperparathyroidism	[17-21]
		Dysregulation of the FGF-23/Klotho pathway exacerbates mineral metabolism imbalance
		Vitamin D deficiency impairs calcium absorption and disrupts PTH regulation
		IS accumulation induces oxidative stress, disrupting the balance between osteoblasts and osteoclasts
Uremic toxin-induced damage	IS, AhR, Wnt/β-catenin, SOST, DKK1	IS activates the AhR pathway, thereby impairing bone formation and mineralization	[22-33]
		IS-induced PTH resistance contributes to impaired bone formation
		IS induces osteocyte dysfunction, leading to bone loss
		Inflammation promotes osteoclast activation and osteoblast inhibition through the RANKL/OPG and NF-κB pathways
Inflammation and oxidative stress	IL-6, TNF-α, IL-17, NF-κB, RAGE	Oxidative stress induces ROS-mediated osteoblast damage and aggravates PTH resistance	[28-39]
		AGEs promote apoptosis and oxidative stress, thereby aggravating bone fragility
		Severely impaired calcium absorption and utilization
Nutritional and metabolic disorder	Calcium, phosphate, vitamin D, FGF-23, PTH	High phosphorus intake disrupts bone remodeling	[34-44]
		Protein intake exerts complex effects on bone metabolism
		Vitamin D deficiency and muscle loss synergistically suppress bone formation
		Estrogen loss accelerates bone loss and fragility
Hormonal and growth factor disorder	Estrogen, activin A, SMAD2, TGF-β, TβRI	Activation of the TGF-β pathway promotes fibrosis and disrupts bone homeostasis	[40-44]
		Activin A promotes osteoclastogenesis and inhibits bone formation
		Inflammatory and hormonal signals interact to exacerbate bone damage

Potential mechanism	Key factor	Pathway and effect	Reference
Calcium-phosphate metabolism imbalance	PTH, FGF-23, Klotho, 1, 25(OH)₂D, calcium, phosphate	Declining renal function triggers hyperphosphatemia and hypocalcemia, inducing secondary hyperparathyroidism	[17-21]
		Dysregulation of the FGF-23/Klotho pathway exacerbates mineral metabolism imbalance
		Vitamin D deficiency impairs calcium absorption and disrupts PTH regulation
		IS accumulation induces oxidative stress, disrupting the balance between osteoblasts and osteoclasts
Uremic toxin-induced damage	IS, AhR, Wnt/β-catenin, SOST, DKK1	IS activates the AhR pathway, thereby impairing bone formation and mineralization	[22-33]
		IS-induced PTH resistance contributes to impaired bone formation
		IS induces osteocyte dysfunction, leading to bone loss
		Inflammation promotes osteoclast activation and osteoblast inhibition through the RANKL/OPG and NF-κB pathways
Inflammation and oxidative stress	IL-6, TNF-α, IL-17, NF-κB, RAGE	Oxidative stress induces ROS-mediated osteoblast damage and aggravates PTH resistance	[28-39]
		AGEs promote apoptosis and oxidative stress, thereby aggravating bone fragility
		Severely impaired calcium absorption and utilization
Nutritional and metabolic disorder	Calcium, phosphate, vitamin D, FGF-23, PTH	High phosphorus intake disrupts bone remodeling	[34-44]
		Protein intake exerts complex effects on bone metabolism
		Vitamin D deficiency and muscle loss synergistically suppress bone formation
		Estrogen loss accelerates bone loss and fragility
Hormonal and growth factor disorder	Estrogen, activin A, SMAD2, TGF-β, TβRI	Activation of the TGF-β pathway promotes fibrosis and disrupts bone homeostasis	[40-44]
		Activin A promotes osteoclastogenesis and inhibits bone formation
		Inflammatory and hormonal signals interact to exacerbate bone damage

慢性肾脏病患者牙槽骨变化及牙槽手术风险的研究进展

Advances in alveolar bone changes and risks of alveolar surgery in patients with chronic kidney disease

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