Gut Microbiome and Bone: to Build, Destroy, or Both?

Yan, Jing; Charles, Julia F.

doi:10.1007/s11914-017-0382-z

Cited by 80 publications

(72 citation statements)

References 54 publications

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“…More and more studies have shown that the intestinal flora may regulate the immune system and endocrine system through the gut-brain axis to participate in the body's bone metabolism. The imbalance of gut microbiome can cause the imbalance of osteogenesis and osteoclast reaction and cause osteopenia, while the specific mechanism has not been determined (Ohlsson and Sjögren, 2015;Yan and Charles, 2017;Ibáñez et al, 2019). As far as we know, there are few studies on the relationship between intestinal flora and osteoporosis, we characterized the disease-related microbiota by 16s rDNA Amplicon Sequencing, proving that there are possible biomarkers (including microbial composition and function) in gut microbiome group in patients with PO.…”

Section: Discussionmentioning

confidence: 88%

“…Studies have shown that abnormal gut microbiome is associated with more and more health status (Sekirov et al, 2010;Kundu et al, 2017;Song et al, 2018). Related basic and clinical studies have shown that gut microbiome may be involved in bone metabolism through gut-brain axis regulation of immune system, endocrine system, and so on (Ohlsson and Sjögren, 2015;Yan and Charles, 2017;Ibáñez et al, 2019). A large number of studies have shown that there is an interaction between solid hormones and gut microbiome (Baker et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

“…Although the previous small sample size study showed differences in the composition and quantity of gut microbiota between PO patients and HC patients (Wang et al, 2017), sufficient sample size studies have not been conducted to assess the association between osteoporosis and microbiota. The mechanism by which intestinal flora regulates bone metabolism needs further study (Yan and Charles, 2017).…”

Section: Introductionmentioning

confidence: 99%

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Gut Microbiome Reveals Specific Dysbiosis in Primary Osteoporosis

Xie

Sun

et al. 2020

Front. Cell. Infect. Microbiol.

104

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Object: Primary osteoporosis (PO) is the most common bone disease, which is characterized by decreased bone mass, damage of bone tissue microstructure, increased bone fragility, and is prone to fracture. Gut microbiome may be involved in bone metabolism of PO through gut-brain axis regulation of immune system and endocrine system, however, the specific mechanism is still unclear. The purpose of this study was to characterize the gut microbiome of patients with PO and its possible role in the occurrence and development of the disease. Methods: Fecal samples were collected from 48 PO patients and 48 healthy controls (HC). The composition of gut microbiome community was analyzed by 16s rDNA amplification sequencing, and the difference of gut microbiome composition between PO patients and HC individuals was compared. PICRUSt was also used to predict the biological function of gut microbiome in patients with PO, and to explore its possible role in the occurrence and development of this disease. The classification model is constructed by random forest algorithm so as to screen the key biomarkers. Result: The diversity of gut microorganisms in PO patients was significantly higher than that in HC group (p < 0.05) and there was significant difference in microbial composition in PO group. The abundance of Dialister (0.036 vs. 0.004, p < 0.001) and Faecalibacterium (0.331 vs. 0.132, p < 0.001) were significantly enriched which were the key flora related to PO. Although no significant correlation between bone mineral density and the richness of microbial communities are found, PICRUST results show that there are a wide range of potential pathways between gut microbiome and PO patients, including genetic information processing, metabolism, environmental information processing, cellular processes, human diseases, and organic systems. Notably, the discriminant model based on dominant microflora can effectively distinguish PO from HC (AUC = 93.56). Conclusions: The findings show that PO is related to the change of gut microbiome, especially the enriched Dialister and Faecalibacterium genera, which give new clues to understand the disease and provide markers for the diagnosis and new strategies for intervention treatment of the disease.

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Section: Discussionmentioning

confidence: 88%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Gut Microbiome Reveals Specific Dysbiosis in Primary Osteoporosis

Xie

Sun

et al. 2020

Front. Cell. Infect. Microbiol.

104

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“…This increase in bone density was attributed to a decrease in osteoclast, as well as, inflammatory cytokines in the bone and bone marrow in the germ free mice vs conventionally raised mice [132]. However, the effects of microbiome on bone density, as determined by studies using germ free mice, are not consistent across mouse strains and/or sex [136][8][130][132]. In addition, the impact of the microbiota changes on the epithelial barrier were not been fully examined.…”

Section: Barrier Pathophysiology In Diseasementioning

confidence: 99%

Epithelial Barrier Function in Gut-Bone Signaling

Rios‐Arce

Collins

Schepper

et al. 2017

Advances in Experimental Medicine and Biology

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The intestinal epithelial barrier plays an essential role in maintaining host homeostasis. The barrier regulates nutrient absorption as well as prevents the invasion of pathogenic bacteria in the host. It is composed of epithelial cells, tight junctions, and a mucus layer. Several factors, such as cytokines, diet, and diseases can affect this barrier. These factors have been shown to increase intestinal permeability, inflammation, and translocation of pathogenic bacteria. In addition, dysregulation of the epithelial barrier can result in inflammatory diseases such as inflammatory bowel disease. Our lab and others have also shown that barrier disruption can have systemic effects including bone loss. In this chapter, we will discuss the current literature to understand the link between intestinal barrier and bone. We will discuss how inflammation, aging, dysbiosis and metabolic diseases can affect intestinal barrier-bone link. In addition, we will highlight the current suggested mechanism between intestinal barrier and bone.

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“…There are mixed findings regarding the bone phenotype of germ-free mice. Germ free mice may have increased bone mass/density or reduced bone mass/density compared to conventionally raised animals [29, 30, 11, 31]. A major challenge in interpreting differences among studies of germ free mice is that the studies are not consistent in terms of mouse strain, sex or age.…”

Section: Bonementioning

confidence: 99%

The Microbiome and Bone and Joint Disease

Hernandez

2017

Curr Rheumatol Rep

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Purpose of Review Changes in the constituents and activity of the microbiome have been associated with a number of conditions linked to bone and joint disease. This review concentrates on ways in which the microbiome is known to influence osteoarthritis and osteoporosis. Recent Findings Animal studies have demonstrated that changes in the microbiome can mediate the effects of obesity on cartilage degeneration. Additionally, the microbiome influences the amount of bone (bone quantity), as well as bone tissue material properties (bone quality). Early clinical findings support the effects of the microbiome on osteoporosis and osteoarthritis. Summary Although animal studies implicate the microbiome in the development of bone and joint disease, available results are limited and can be conflicting. Further investigation of the mechanisms leading from changes in the microbiome to alterations in bones and joints are necessary.

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Gut Microbiome and Bone: to Build, Destroy, or Both?

Cited by 80 publications

References 54 publications

Gut Microbiome Reveals Specific Dysbiosis in Primary Osteoporosis

Gut Microbiome Reveals Specific Dysbiosis in Primary Osteoporosis

Epithelial Barrier Function in Gut-Bone Signaling

The Microbiome and Bone and Joint Disease

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