Gut-bone Cross Talks and Implications in Celiac Disease

Abstract

Metabolic bone disease is a frequent extra-intestinal co-morbidity in newly diagnosed, mostly adult patients who have 70% low bone mineral density. Musculoskeletal signs and symptoms, osteopenia, osteoporosis and fractures are the most frequent manifestations. The etiology is multifactorial, however, micronutrient malabsorption, mainly of calcium and vitamin D, secondary hyperparathyroidism and inflammation are the main driving forces. The diagnosis is based on signs and symptoms, biochemical and endocrinologic laboratory evaluation and imaging by dual x-ray absorptiometry. Treatment of low bone mineral density in CD comprises: a gluten free diet, coverage of nutritional deficiencies (including calcium and vitamin D), changes in life style and if necessary, pharmacologic and hormonal replacement therapy. The cost effectiveness of those therapy methods were barely assessed. Understanding the pathophysiology of bone loss in celiac disease might bring new therapeutical strategies for the patient's benefit.

Unraveling the intricate dance of the Mediterranean diet and gut microbiota in autoimmune resilience

“…Butyrate has beneficial effects on intestinal barrier integrity, as it enhances the expression of tight junction proteins. Moreover, it helps prevent deleterious intestinal permeability and bacterial translocation, thereby exerting a protective influence on the initiation of pro- inflammatory responses ( 106 , 108 , 109 ). To relevance in collagen-induced arthritis, an animal model of RA, butyrate is able to suppress RA features and this is achieved via a butyrate- mediated increase of IL-10 producing Tregs and a decrease of Th17 ( 110 ).…”

Gluten, Transglutaminase, Celiac Disease and IgA Nephropathy

“…Due to recent expanding knowledge on the two entities, on the central role played by nutrients, microbiome, IgA metabolism and functions and the mucosal and systemic immune systems [1][2][3][4]17,[28][29][30], cross-talks between the two diseases, were discovered [16,18,[29][30][31][32][33]. Table 1 summarizes the epidemiological, clinical and pathophysiological aspects of CD and IgAN.…”

“…The gut-kidney axis is a part of a much wider network, centered in the gut and irradiating to remote organs, conveying the messages of loss of tolerance and autoimmunogenesis [1][2][3][4]. This axis appears crucial in IgA nephropathy (IgAN) physiopathology [5].…”

GUT-the Trojan Horse in Remote Organs’ Autoimmunity

“…Their food related problems might reflect an adverse additive effect of multiple modest hypersensitivity reactions mediated, for instance, by food originated immune complexes promoting autoimmune reactions in the joints [54].…”