Abstract

ObjectiveThe purpose of this investigation was to elucidate the relationship between the zinc and iron intake and the advancement of subchondral sclerosis among patients with osteoarthritis (OA). The goal was to establish personalized, nutritionally-informed strategies designed to retard the progression of subchondral sclerosis and conserve joint structure. MethodsFor the purposes of this research, we derived data from the Bone Ancillary Study (BAS), a constituent study of the Osteoarthritis Initiative (OAI). The intake of zinc and iron was evaluated via a food frequency questionnaire. Magnetic Resonance Imaging trabecular morphometry was employed to ascertain the microarchitecture of the subchondral bone. For the analysis of collected data, we employed logistic regression along with generalized additive models (GAMs). ResultsThe participant cohort was comprised of 474 OA patients (216 females, 258 males, mean [SD] age 64.1[9.2]). Notably, an increment in zinc consumption was linked with a significantly reduced likelihood of deterioration in Tb.N (OR = 0.967, 95 % CI, 0.939–0.996, P-value = 0.026), Tb.Th (OR = 0.958, 95 % CI, 0.929–0.989, P-value = 0.008), and Tb.Sp (OR = 0.967, 95 % CI, 0.939–0.996, P-value = 0.013). An elevation in iron intake seemed to enhance the risk of subchondral sclerosis, as indicated by the GAM. Subgroup analysis revealed an interaction between the effectiveness of zinc intake and factors such as gender, age, radiographic severity, and macronutrient consumption. An increased intake of calcium amplified the beneficial impact of zinc on subchondral sclerosis. ConclusionsOur findings indicate a positive association between elevated zinc intake and a slowdown in the progression of subchondral sclerosis in OA patients, notably among females, middle-aged individuals, and those with higher calcium and magnesium intake. Conversely, a higher iron intake might intensify subchondral sclerosis. These results suggest that personalized, diet-based interventions focusing on zinc consumption, in tandem with adequate calcium intake, could potentially decelerate the progression of subchondral sclerosis in individuals afflicted with OA.

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