Osteoporosis (OP) is a systemic disease characterized by decreased bone mass and degeneration of bone microstructure. In recent years, more and more researches have focused on the close relationship between gut microbiota (GM) and the occurrence and progression of OP, and the regulation of probiotics and prebiotics on bone metabolism has gradually become a research hotspot. Based on the influence of brain-gut-bone axis on bone metabolism, this review expounds the potential mechanisms of probiotics and prebiotics on OP from next perspectives: regulation of intestinal metabolites, regulation of intestinal epithelial barrier function, involvement of neuromodulation, involvement of immune regulation and involvement of endocrine regulation, so as to provide a novel and promising idea for the prevention and treatment of OP in the future.

Osteoporosis (OP) is a systemic bone disease characterized by the decreased bone mass and destruction of bone microstructure, which tends to result in the enhanced bone fragility and related fractures, as well as high disability rate and mortality. Exercise is one of the most common, reliable and cost-effective interventions for the prevention and treatment of OP currently, and numerous studies have revealed the close association between gut microbiota (GM) and bone metabolism recently. Moreover, exercise can alter the structure, composition and abundance of GM, and further influence the body health via GM and its metabolites, and the changes of GM also depend on the choice of exercise modes. Herein, combined with relevant studies and based on the inseparable relationship between exercise intervention-GM-OP, this review is aimed to discuss the moderating effects and potential mechanisms of exercise intervention on GM and bone metabolism, as well as the interaction between them.

Patients with diabetes mellitus (DM) often suffered with many musculoskeletal disorders, such as tendon rupture and tendinopathy. However, the understanding of the pathogenesis of these alternations is limited. This study was designed to investigate the role of tendon-derived stem cells (TDSCs) in histopathological alterations of DM tendons. Forty-two SD rats were randomly and equally divided into a diabetes group (DG) and control group (CG). DM was induced by streptozotocin (65 mg/kg). The patellar tendons were isolated at weeks 1, 2, and 4 for histological analysis. TDSCs were isolated at week 2 for osteo-chondrogenic differentiation analysis. Mann-Whitney U test was used with SPSS. p < 0.050 was statistically significant. Micro-tears of collagen fibers and altered appearance of tendon cells were observed in DG tendons. DG tendons exhibited significantly higher expression of OPN, OCN, SOX9, and Col II and decreased expression of Col I and tenomodulin (TNMD) at week 2. Diabetic TDSCs (dTDSCs) demonstrated significantly decreased proliferation ability and increased osteogenic and chondrogenic differentiation ability. Osteo-chondrogenic markers BMP2, ALP, OPN, OCN, Col II, and SOX9 were also significantly increased while tenogenic markers Col I and TNMD were decreased in dTDSCs. These results suggested the erroneous differentiation of dTDSCs might account for the structural and non-tenogenic alternations in DM tendons, which provided new cues for the pathogenesis of tendon disorders in DM.

Aged tendon-derived stem/progenitor cells (TSPCs) lead to age-related tendon disorders and impair tendon healing. However, the underlying molecular mechanisms of TSPC aging remain largely unknown. Here, we investigated the role of connective tissue growth factor (CTGF) in TSPC aging. CTGF protein and mRNA levels were markedly decreased in the aged TSPCs. Moreover, recombinant CTGF attenuates TSPC aging and restores the age-associated reduction of self-renewal and differentiation of TSPCs. In addition, cell cycle distribution of aged TSPCs was arrested in the G1/S phase while recombinant CTGF treatment promoted G1/S transition. Recombinant CTGF also rescued decreased levels of cyclin D1 and CDK4 and reduced p27^kip1 expression in aged TSPCs. Our results demonstrated that CTGF plays a vital role in TSPC aging and might be a potential target for molecular therapy of age-related tendon disorders.