Brian D. Nielsen

Studies have attempted to demonstrate the benefits of silicon on bone health using a wide range of Si amounts—provided in the diet or through supplementation—and several different animal species. Previous studies in humans have also demonstrated a positive correlation between Si intake and bone health measures. The aim of the current review is to determine the effective levels of Si intake or supplementation that influence bone health to better inform future study designs and guidelines. Articles were identified using one of two search terms: “silicon AND bone” or “sodium zeolite A AND bone”. Articles were included if the article was a controlled research study on the effect of Si on bone health and/or mineral metabolism and was in English. Articles were excluded if the article included human subjects, was in vitro, or studied silica grafts for bone injuries. Silicon type, group name, Si intake from diet, Si supplementation amount, animal, and age at the start were extracted when available. Dietary Si intake, Si supplementation amount, and the amount of Si standardized on a kg BW basis were calculated and presented as overall mean ± standard deviations, medians, minimums, and maximums. Studies that left out animal weights, amount of food or water consumed, or nutrient profiles of the basal diet were excluded from these calculations. Standardized Si intakes ranged from 0.003 to 863 mg/kg BW, at times vastly exceeding current human Si intake recommendations (25 mg/d). The lack of data provided by the literature made definitively determining an effective threshold of supplementation for skeletal health difficult. However, it appears that Si consistently positively influences bone and mineral metabolism by around 139 mg Si/kg BW/d, which is likely unfeasible to attain in humans and large animal species. Future studies should examine this proposed threshold more directly and standardize supplemental or dietary Si intakes to kg BW for better study replication and translation.

Objective To determine the effects of clodronate disodium (CLO) on control and recombinant equine interleukin‐1β (IL‐1β)‐treated equine joint tissues. Study design In vitro experimental study. Sample population Cartilage explants, chondrocytes, and synoviocytes ( n = 3 horses). Methods Monolayer cultures of chondrocytes and synoviocytes from three horses were subjected to: control media (CON), 5 ng/ml CLO (C/low), 50 ng/ml CLO (C/med), 100 ng/ml CLO (C/high), with and without IL‐1β, and 10 ng/ml IL‐1β (IL) alone for 72 hours. Cartilage explants from three horses were subjected to CON, IL, C/low, and C/med with and without IL‐1β for 72 hours. Culture media was analyzed for prostaglandin‐E 2 (PGE 2 ), interleukin‐6 (IL‐6), and nitric oxide (NO). Explant media was analyzed for glycosaminoglycan (GAG) content and NO. At 72 hours, explant and monolayer culture viability were assessed, and explant GAG content was measured. Results IL‐1β treatment resulted in higher media concentrations of GAG, NO, PGE 2 , and IL‐6 compared to the CON treatment ( p < .05), demonstrating a catabolic effect of IL‐1β on explants and monolayer cultures. CLO treatments did not increase media concentrations of GAG, NO, PGE 2 , or IL‐6 compared to CON, indicating no cytotoxic effect. Nevertheless, CLO treatments administered to IL‐1β‐treated monolayer cultures and explants did not significantly reduce the inflammatory response regardless of concentration. Conclusion CLO did not demonstrate cytotoxic nor cytoprotective effects in normal and IL‐1β‐stimulated chondrocytes, synoviocytes or explants in culture. Clinical significance This study does not support the use of CLO as an anti‐inflammatory treatment. Further research is necessary to confirm any anti‐inflammatory effects of CLO on joint tissues.