Diffuse Idiopathic Skeletal Hyperostosis (DISH): Potential Links Between Gut Microbiota and Spinal Degenerative...

Diffuse Idiopathic Skeletal Hyperostosis (DISH) is a systemic, non-inflammatory skeletal disorder characterized by progressive calcification and ossification of spinal ligaments and entheses. Its strong associations with aging, obesity, type 2 diabetes, and metabolic syndrome raise the possibility that metabolic and inflammatory pathways may contribute to disease development. The gut microbiota participates in nutrient metabolism, short-chain fatty acid production, bile-acid transformation, intestinal-barrier maintenance, and immune regulation; these functions provide a plausible framework for examining whether intestinal dysbiosis may influence spinal and musculoskeletal tissues. This narrative review therefore evaluates the potential relationship between gut microbiota, DISH, and related spinal degenerative diseases. It considers the nutritional, metabolic, immunological, and host-interaction functions of the gut microbiota before examining proposed gut-spine, gut-bone, gut-joint, gut-disc, gut-ligament, and gut-muscle pathways. Particular attention is given to the apparent paradox that most microbiome-bone evidence concerns osteoporosis and bone loss, whereas DISH is characterized by excessive ectopic bone formation. Differences in short-chain fatty acid concentration, receptor expression, local versus systemic signaling, and osteoblast-osteoclast microenvironments may produce divergent skeletal effects, but these mechanisms have not been tested directly in DISH. Recent studies support associations between selected microbial taxa and intervertebral disc degeneration or spinal stenosis; however, direct clinical evidence linking gut microbiota to DISH remains limited. Consequently, dietary modification, probiotics, prebiotics, and fecal microbiota transplantation should be regarded as research considerations rather than established treatments for DISH. Well-characterized case-control and longitudinal studies integrating microbiome profiling, metabolomics, inflammatory markers, and serial imaging are required to determine whether reproducible microbial or metabolite signatures precede DISH onset or progression. The pathways discussed in this review are therefore presented as biologically plausible, testable hypotheses and not as established causal relationships.