Abstract
Some say that all diseases begin in the gut. Interestingly, this concept is actually quite old, since it is attributed to the Ancient Greek physician Hippocrates, who proposed the hypothesis nearly 2500 years ago. The continuous breakthroughs in modern medicine have transformed our classic understanding of the gastrointestinal tract (GIT) and human health. Although the gut microbiota (GMB) has proven to be a core component of human health under standard metabolic conditions, there is now also a strong link connecting the composition and function of the GMB to the development of numerous diseases, especially the ones of musculoskeletal nature. The symbiotic microbes that reside in the gastrointestinal tract are very sensitive to biochemical stimuli and may respond in many different ways depending on the nature of these biological signals. Certain variables such as nutrition and physical modulation can either enhance or disrupt the equilibrium between the various species of gut microbes. In fact, fat-rich diets can cause dysbiosis, which decreases the number of protective bacteria and compromises the integrity of the epithelial barrier in the GIT. Overgrowth of pathogenic microbes then release higher quantities of toxic metabolites into the circulatory system, especially the pro-inflammatory cytokines detected in osteoarthritis (OA), thereby promoting inflammation and the initiation of many disease processes throughout the body. Although many studies link OA with GMB perturbations, further research is still needed.
Highlights
Osteoarthritis (OA) has long been considered a degenerative disease that affects the hyaline cartilage alone
Cytokines related to OA pathogenesis include tumor necrosis factor (TNF)-α, matrix metalloproteinases (MMPs), interleukin (IL)-1, IL-6, IL-2, IL-7, IL-15 and IL-21, and other chemokines which contribute to catabolic activity and detrimental effects [11,12]
Upon activation of the intestinal epithelial cells with toll-like receptors (TLRs), B-cell activating factor (BAFF) and a proliferation inducing ligand (APRIL) are secreted which promotes the differentiation of immunoglobulin A (IgA) producing plasma cells, whereas in dysbiotic status of gut microbiome with the loss of barrier integrity and breach in the intestinal epithelial cell barrier, translocation of bacterial components, pathogen-associated molecular patterns (PAMPs), intestinal immune system is triggered through TLR activation
Summary
Osteoarthritis (OA) has long been considered a degenerative disease that affects the hyaline cartilage alone. Cytokines related to OA pathogenesis include tumor necrosis factor (TNF)-α, matrix metalloproteinases (MMPs), interleukin (IL)-1, IL-6, IL-2, IL-7, IL-15 and IL-21, and other chemokines which contribute to catabolic activity and detrimental effects [11,12] These findings prove to be of particular significance since OA itself is influenced by the complex interplay between local, systemic and external factors, which dictate disease progression and the manner in which patients respond to the treatment [13]. Sci. 2022, 23, 1494 revealing a pathogenic OA-associated microbial shift [20,21,22] This reinforces the concept that under biological stress the microbes in the GIT (gastrointestinal tract) can be pushed out of equilibrium, promoting pathological alterations that culminate in the manifestation of various disorders, especially OA. The question remains: could osteoarthritis really begin in the gut? In this review we aim to illustrate a possible link
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