Osteoarthritis (OA) is a complex degenerative disease that affects the entire joint and causes pathological changes in a number of joint structures, including cartilage, subchondral bone, synovium, ligaments, menisci, and surrounding muscles (1, 2). OA is a complex disease driven by multiple factors, of which aging and joint damage are recognized as major risk factors (3). At the same time, chronic diseases such as obesity, diabetes, and cardiovascular disease play an important role in the development and progression of OA by promoting systemic inflammation and metabolic disorders (1). OA causes chronic pain and limited mobility in patients, significantly impacting daily life and mental health (4, 5). From a societal perspective, the loss of labor and decreased productivity due to OA significantly impact the economy (6, 7). The prevalence of OA is anticipated to rise globally as a result of the growing number of elderly individuals, which will present a significant challenge to public health systems (8). In OA, the infrapatellar fat pad (IPFP), as an important adipose tissue in the joint, plays a dual role in the onset and development of OA with its inflammatory response and fibrosis, and its altered biomechanical properties are closely related to joint injury and cartilage degeneration (9, 10). Given the unique role of the infrapatellar fat pad in OA, evaluating the relationship between obesity and the prevalence of OA is critical for the prevention and effective management of OA.

Over the past few years, there has been an increasing interest in the relationship between obesity and OA (11–13). Obesity increases the mechanical load on the joints, especially the knee, leading to increased cartilage wear and tear (14). Furthermore, the systemic low-grade inflammation that accompanies obesity is a key factor in OA, and pro-inflammatory factors secreted by adipose tissue, such as IL-6 and TNF-α, exacerbate cartilage damage and joint inflammation (15). Obesity also leads to macrophage infiltration in adipose tissue, further exacerbating local inflammation and driving the pathological process of OA (16). Body mass index (BMI) is frequently used to screen for weight issues and to identify obese individuals (17). However, BMI has limitations because it ignores the heterogeneity of fat distribution and cannot differentiate between muscle and fat mass (18). The body roundness index (BRI) was first proposed by Thomas et al. in 2013, aiming to assess an individual’s body fat distribution, especially abdominal fat, through simple height and waist circumference measurements (19). Unlike the traditional BMI, the BRI not only takes into account body weight but also more accurately reflects the shape and fat distribution of the body and is particularly sensitive in assessing the risk associated with abdominal obesity (20). The BRI has been widely used in a variety of studies to predict the risk of a number of chronic diseases, including cardiovascular disease, metabolic syndrome, depression, and cancer (21–23). Specifically, a cross-sectional study found a significant positive correlation between the prevalence of depression and BRI levels (23). Another study further showed a significant positive correlation between BRI levels and the prevalence of colorectal cancer, emphasizing the importance of controlling BRI levels for the prevention of colorectal cancer (21). In addition, the BRI levels have been rising in U.S. adults over the past 20 years, and studies have shown a U-shaped relationship between the BRI and the risk of all-cause mortality, suggesting that either too high or too low BRI levels may increase the risk of death (20). However, the precise correlation between the BRI and OA remains unclear. Therefore, this study utilized NHANES survey data from 2011 to 2018 to explore the association between the BRI and OA. This study aimed to establish an empirical foundation for future public health interventions and to provide new evidence that substantiates the application of the BRI in OA.

The present study was a cross-sectional analysis using the NHANES database designed to assess the association between the BRI and OA prevalence among U.S. adults. The results showed a significant positive association between high BRI levels and OA prevalence, which was consistently confirmed across subgroups. In addition, the efficacy of the BRI in predicting OA was found to be superior to that of traditional BMI in this study, which suggests that the BRI can be used as an effective tool for assessing the prevalence of OA, which is an important reference value for early clinical prevention and intervention.

Recently, the association between obesity and OA has garnered widespread attention, as the prevalence of both conditions has significantly increased globally (8, 27). In addition to increasing the likelihood of cardiovascular disease, diabetes, and specific malignancies, obesity also has a detrimental impact on bone and joint health (28–30). The progression of OA is significantly influenced by adiposity, as demonstrated by a multitude of studies (12, 31, 32). A Mendelian randomized study showed a positive genetic correlation between BMI and OA (33). Another study showed that increased BMI is an important risk factor for OA and increases the prevalence of OA (34). These findings are consistent with the results of the present study and further emphasize the key role of obesity in OA. The results of the present study showed that the BRI has higher sensitivity and specificity than the BMI in predicting OA, and in particular, the BRI is more sensitive to the assessment of abdominal adiposity, which is an important contributor to inflammation and metabolic abnormalities that may accelerate the onset and progression of OA (35, 36). This study also verified that the BRI has greater sensitivity and specificity than the BMI in predicting OA. Subgroup analyses indicated that the association between the BRI and OA remained significant across various age and sex groups, suggesting that the BRI may serve as a universal indicator for assessing OA. These results offer new insights into the early prevention and intervention of OA and present a more comprehensive approach to managing obesity-related diseases.

The pathophysiological mechanisms linking the BRI and OA involve multiple complex and interrelated factors. First, increased mechanical load is a significant factor through which obesity leads to OA. Increased body weight in obese individuals results in greater mechanical pressure on weight-bearing joints, especially the knees and hips, accelerating joint cartilage wear and degeneration (37, 38). In addition, mechanical load not only directly damages the cartilage matrix but also alters the inflammatory state of chondrocytes (39). Obesity-induced systemic inflammation is a critical component in the pathogenesis of OA (11). In obese individuals, adipocytes release significant quantities of pro-inflammatory cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α), which intensify joint inflammation and cartilage damage (40). Obesity is often accompanied by metabolic syndrome, including hyperglycemia, hypertension, and hyperlipidemia, which also adversely affect joint health (13, 41, 42). For instance, hyperglycemia promotes the formation of advanced glycation end products, which harm chondrocytes and the extracellular matrix (43). In summary, the relationship between the BRI and OA results from multifactorial and multi-pathway interactions, and further research into these mechanisms may aid in developing more effective prevention and treatment strategies.

This study has several significant strengths. First, the study used nationally representative NHANES data, which ensured the broad applicability and reliability of the results through weighted analyses. The study also incorporated multiple covariates, effectively controlling for potential confounders. However, there are some limitations to this study. Due to the cross-sectional design, it was not possible to determine the causal relationship between the BRI and OA. In addition, the diagnosis of OA relies on patient self-report, which may introduce information bias. The lack of specific imaging or clinical diagnostic data may not accurately reflect the true prevalence of OA. The present study also lacked data on the site of OA prevalence (e.g., knee, hip, and hand joints) and its severity, limiting in-depth exploration of the association between the BRI and different types and severities of OA. In addition, questionnaires that assess the level of pain and its impact on daily life in patients with OA were not included in this study, making it difficult to fully assess the impact of OA on patients’ quality of life. Future studies should consider incorporating assessment tools for pain and activities of daily living to explore the relationship more fully between the BRI and OA. To further confirm the results of this study, larger longitudinal studies should be conducted in the future, and the accuracy of the data should be improved by introducing imaging or clinical examinations.

The BRI and OA are significantly associated in adults in the United States. The risk of developing OA may be increased by elevated BRI levels. Monitoring BRI levels is essential to prevent or reduce the prevalence and advancement of OA.