随着社会人口老龄化程度的日益严峻,骨质疏松症患者数量逐渐攀升,目前已成为严峻的公共健康问题.绝经后骨质疏松症(postmenopausal osteoporosis,PMOP)属于原发性骨质疏松症之一,由于女性绝经后雌激素缺乏,加快骨质流失,主要表现为疼痛、易发生骨折,给日常生活带来极大不便.骨免疫学着重于骨骼系统与免疫系统之间的联系,被激活的淋巴细胞释放各种细胞因子参与骨重塑的过程.中医药临床应用广泛,对PMOP治疗效果明显.本文基于骨免疫学,介绍中医药对骨代谢的影响,探讨中医药治疗PMOP的作用机制.

骨再生不仅受骨骼肌肉系统调节，还受免疫系统、血液系统等的影响。其中，免疫系统与骨骼系统共同受多种细胞因子的调节，这些因子作为骨免疫微环境的主要组成，在骨再生的过程中发挥重要作用。其中，巨噬细胞极化相关因子已越来越被人关注。巨噬细胞的极化受骨免疫微环境调控，并根据其方向的不同产生不同的细胞因子以调控骨再生，巨噬细胞还可与骨髓来源间充质干细胞(BMSCs)相互串扰以促进成骨。最近的研究也显示了通过改变骨免疫微环境以调节巨噬细胞的极化方向并促进骨再生的可能性。本文重点讨论了骨免疫微环境调节的不同巨噬细胞调节骨再生的作用及机制。

在正畸牙移动过程中，破骨细胞和成骨细胞等细胞的功能行使受免疫系统多种细胞或分子的影响，因此越来越多的学者开始探索免疫系统在正畸骨改建中的作用。本文基于不同免疫细胞或细胞因子的生物学作用，简要阐述免疫调控在正畸牙移动中的相关作用，并展望其未来趋势，以期对口腔正畸牙移动中的生物学机制有更全面的认识和了解。

Cellular immune responses as well as generalized and periarticular bone loss are the key pathogenic features of rheumatoid arthritis (RA). Under the pathological conditions of RA, dysregulated inflammation and immune processes tightly interact with skeletal system, resulting in pathological bone damage via inhibition of bone formation or induction of bone resorption. Single-cell omics technologies are revolutionary tools in the field of modern biological research. They enable the display of the state and function of cells in various environments from a single-cell resolution, thus making it conducive to identify the dysregulated molecular mechanisms of bone destruction in RA as well as the discovery of potential therapeutic targets and biomarkers. Here, we summarize the latest findings of single-cell omics technologies in osteoimmunology research in RA. These results suggest that single-cell omics have made significant contributions to transcriptomics and dynamics of specific cells involved in bone remodeling, providing a new direction for our understanding of cellular heterogeneity in the study of osteoimmunology in RA.

骨质疏松症是一种常见的代谢性骨病，其病理机制是正常骨重塑过程被破坏，骨吸收大于骨形成。成骨细胞和破骨细胞对维持骨稳态起着关键作用。近年来，越来越多的研究发现免疫细胞通过释放各种趋化因子和细胞因子参与成骨细胞和破骨细胞活性的调节，并据此提出免疫性骨质疏松的概念。本文旨在综述骨质疏松中免疫系统作用的研究进展，展望骨免疫学的未来发展前景，以便更好地从免疫学角度去研究和防治骨质疏松。

骨重建和骨再生对于保持骨骼完整性和维持矿物质稳态至关重要.T淋巴细胞为适应性免疫的关键成员,通过产生一系列细胞因子和生长因子,在骨重建和骨再生过程中起着举足轻重的作用.在生理状态下,T淋巴细胞通过与间充质干细胞、成骨细胞、破骨细胞的交互作用参与骨稳态的维持;在病理状态下,T淋巴细胞通过与雌激素、糖皮质激素、甲状旁腺激素的协作参与不同类型骨质疏松的病理过程;在损伤后修复的骨折愈合过程中,T淋巴细胞在炎症血肿期、骨痂形成期和骨重建期发挥了不同的作用.因此,靶向T淋巴细胞成为调节骨稳态的潜在策略.本文综述了T细胞免疫参与骨重建和骨再生的研究进展及相关机制,以期为靶向T淋巴细胞调控骨重建和骨再生提供科学依据.

强直性脊柱炎(Ankylosing spondylitis,AS)是以炎性背痛为主要临床特点的慢性炎症性自身免疫性疾病,其病理特征主要包括炎症、骨破坏和病理性新骨形成.AS病因错综复杂,主要与遗传、感染、环境及肠道菌群等因素相关,其病机暂未明确.近年来,骨免疫学作为研究炎症性关节炎的新主题,其在AS发病机制及发生发展中扮演着重要角色,主要体现在炎症反应和骨代谢失衡等方面.中医药具有多途径、多组分、多靶点、多层次的特点,可以通过调节骨骼系统的骨细胞及免疫系统的相关因子,改善AS炎症反应及骨代谢失衡,以达到防治AS的目的.基于此,该文总结了骨免疫学在AS发病机制中的作用,并综述了中医药通过干预骨免疫治疗AS的研究现状,以期为AS的治疗提供参考.

Periodontitis is a common chronic inflammatory disease that causes the periodontal bone destruction and may ultimately result in tooth loss.With the progression of periodontitis,the osteoimmunology microenvironment in periodontitis is damaged and leads to the formation of pathological alveolar bone resorption.CD301b+macrophages are specific to the osteoimmunology microenvironment,and are emerging as vital booster for conducting bone regeneration.However,the key upstream targets of CD301b+macrophages and their potential mechanism in periodontitis remain elusive.In this study,we concentrated on the role of Tim4,a latent upstream regulator of CD301b+macrophages.We first demonstrated that the transcription level of Timd4(gene name of Tim4)in CD301b+macrophages was significantly upregulated compared to CD301b-macrophages via high-throughput RNA sequencing.Moreover,several Tim4-related functions such as apoptotic cell clearance,phagocytosis and engulfment were positively regulated by CD301b+macrophages.The single-cell RNA sequencing analysis subsequently discovered that Cd301b and Timd4 were specifically co-expressed in macrophages.The following flow cytometric analysis indicated that Tim4 positive expression rates in total macrophages shared highly synchronized dynamic changes with the proportions of CD301b+macrophages as periodontitis progressed.Furthermore,the deficiency of Tim4 in mice decreased CD301b+macrophages and eventually magnified alveolar bone resorption in periodontitis.Additionally,Tim4 controlled the p38 MAPK signaling pathway to ultimately mediate CD301b+macrophages phenotype.In a word,Tim4 might regulate CD301b+macrophages through p38 MAPK signaling pathway in periodontitis,which provided new insights into periodontitis immunoregulation as well as help to develop innovative therapeutic targets and treatment strategies for periodontitis.

目的 基于免疫系统对骨代谢的影响,从"肾藏精"理论出发,分析通过肾调控免疫系统改善骨代谢以防治骨质疏松症的可行性,以期为骨质疏松症的深入研究及防治提供更多的思路.方法 通过检索中国知网、Pubmed等数据库中有关免疫系统与骨代谢的文献,探讨免疫系统与骨代谢的联系;通过查阅中医古籍中"肾藏精"相关的论述,探讨肾与免疫系统的联系.结果 免疫细胞源于骨髓,且免疫细胞、免疫分子均可影响骨代谢.肾因其"主藏精"的功能,可通过"阴阳之宅"、主骨化血、化髓上通于脑等方式与免疫系统密切相关.结论 基于免疫系统对骨代谢的影响和"肾藏精"理论,通过肾调控免疫系统改善骨代谢从而防治骨质疏松症在理论上具有可行性,值得进一步深入研究.

Inflammation induced-bone loss is an universal phenomenon in chronic inflammatory diseases and age-related diseases.However,its mechanism is still not clear.Following the development of osteoimmunology,the effects of inflammatory cytokines in bone immune-microenvironment on osteoclasts and osteoblasts through osteoprotegerin/receptor activator of nuclear factor kappa-B(NF-κB)ligand/receptor activator of NF-κB(OPG/RANKL/RANK)pathway have been researched widely.Meanwhile,immunotherapy aiming at chronic inflammation hasbeen already applied in treating immunoporosis.This article will review the essential signaling mechanism of pro-inflammatory cytokines,including the suppression of osteoblastogenesis and promotion of osteoclastogenesis,as well as the current therapies based on cytokines and lymphocytes for inflammatory bone loss.