Abstract
Osteoarthritis (OA), the most common chronic rheumatic disease, is mainly characterized by a progressive degradation of the hyaline articular cartilage, which is essential for correct joint function, lubrication, and resistance. Articular cartilage disturbances lead to joint failure, pain, and disability. Hyaline cartilage is also present in the growth plate and plays a key role in longitudinal bone growth. Alterations of this cartilage by diverse pathologies have been related to longitudinal bone growth inhibition (LBGI), which leads to growth retardation. Diet can play a crucial role in processes involved in the OA and LBGI’s onset and evolution. Specifically, there is ample evidence pointing to the negative impacts of caffeine consumption on hyaline cartilage. However, its effects on these tissues have not been reviewed. Accordingly, in this review, we summarize all current knowledge in the PubMed database about caffeine catabolic effects on articular and growth plate cartilage. Specifically, we focus on the correlation between OA and LBGI with caffeine prenatal or direct exposure. Overall, there is ample evidence indicating that caffeine intake negatively affects the physiology of both articular and growth plate cartilage, increasing consumers predisposition to suffer OA and LBGI. As a result, caffeine consumption should be avoided for these pathologies.
Highlights
Osteoarthritis (OA) is the most common worldwide chronic rheumatic disease and the main culprit of disability among the middle-aged and elderly [1,2,3,4,5,6,7,8]
Considering that the extracellular matrix (ECM) of the cartilage contributes to preserving chondrocyte viability, it is noteworthy that the in vitro caffeine stimulation of rat growth plate chondrocytes (GPChs) decreased the expression of cartilage-specific matrix genes, such as ACAN, COL2A1, and collagen type X (COLX), as well as key transcription factors involved in chondrocyte differentiation, such as Runx2 and Sox-9 [27] (Figure 2)
Animal PCE models showed that caffeine intake, comparable to the same intake observed in some pregnant women, induces an OA-like phenotype in the articular cartilage, which is preserved into adulthood
Summary
Osteoarthritis (OA) is the most common worldwide chronic rheumatic disease and the main culprit of disability among the middle-aged and elderly [1,2,3,4,5,6,7,8] It is characterized by progressive articular cartilage degradation. The etiology of OA is not fully understood, it is well-known that OA chondrocyte phenotypic changes that affect ECM composition promote cartilage degradation [8,9] One of these changes involve the acquisition of a hypertrophic-like phenotype [8,9], which resembles the differentiation process of growth plate chondrocytes (GPChs) [8]. Multiple modifiable risk factors are closely related to dietary habits, which suggests that diet could play a key role in OA pathogeny
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