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Osteoarthritis (OA) is the most common chronic degenerative joint disease, characterized by cartilage damage, synovial inflammation, subchondral bone sclerosis, marginal bone loss, and osteophyte development. Clinical manifestations include inflammatory joint pain, swelling, osteophytes, and limitation of motion. The pathogenesis of osteoarthritis has not yet been fully uncovered. With ongoing research, however, it has been gradually determined that OA is not caused solely by mechanical injury or aging, but rather involves chronic low-grade inflammation, metabolic imbalances, dysfunctional adaptive immunity, and alterations in central pain processing centers. The main risk factors for OA include obesity, age, gender, genetics, and sports injuries. In recent years, extensive research on gut microbiota has revealed that gut dysbiosis is associated with some common risk factors for OA, and that it may intervene in its pathogenesis through both direct and indirect mechanisms. Therefore, gut flora imbalance as a pathogenic factor in OA has become a hotspot topic of research, with potential therapeutic connotations. In this paper, we review the role of the gut microbiota in the pathogenesis of OA, describe its relationship with common OA risk factors, and address candidate gut microbiota markers for OA diagnosis. In addition, with focus on OA therapies, we discuss the effects of direct and indirect interventions targeting the gut microbiota, as well as the impact of gut bacteria on the efficacy of OA drugs.

Tumoral dynamics and antitumor immunotherapies are likely to be influenced by the modalities of interaction between tumor cells and immune system effectors, and by the inter-effectors interactions. Within the framework of the theory of competing populations, we study here the influence of the proliferation response of effectors to tumor burden, and of cooperation and/or competition between immune system effectors, by means of three inter-related bi-dimensional meta-models. After studying their null-clines, we study the location and the local stability of the equilibria. Then, we investigate the existence and, in some cases, the uniqueness of stable limit cycles. The condition for the global asymptotically stable eradication under constant or slightly variable periodic immunotherapy is given. Finally, implications of strong saturation in the effectors ability to kill tumor cells are discussed.

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