Osteoarthritis (OA) is a chronic, degenerative joint disorder characterised by progressive cartilage degradation and low-grade synovial inflammation (1). Knee osteoarthritis (KOA) is the most prevalent phenotypic subtype of OA (2), and its global prevalence is projected to increase in prevalence by 74.9% by 2050 (3). KOA causes persistent pain and functional impairment in patients, significantly compromising patients’ quality of life and imposing a substantial socioeconomic burden (4). Despite the large number of individuals affected by KOA, current treatment methods primarily focus on alleviating symptoms, with analgesics and anti-inflammatories being the mainstay of therapy. Joint arthroplasty is typically reserved for end-stage disease (5). Such end-stage interventions are inherently incapable of reversing disease progression and therefore represent a pressing public health challenge requiring urgent attention (6).

Against the backdrop of a global ageing population, China—with its large population undergoing rapid demographic change—provides a unique perspective on quantifying the burden of KOA (7). By 2050, the proportion of older adults in China is expected to more than double, leading to a corresponding increase in age-related conditions such as KOA and putting unprecedented strain on its healthcare system (8). Concurrently, rapid economic expansion, accelerating globalisation and relentless urbanisation have caused a significant increase in the prevalence of overweight and obesity among Chinese adults (9). When indexed using body mass index (BMI), adiposity constitutes a readily modifiable risk factor. Cross-sectional analyses by Lv et al. (10) revealed a monotonic gradient between successively higher BMI strata and the prevalence of radiographic KOA. Shao et al. (11) quantified this association, reporting odds ratio of 1.91 for overweight individuals and 4.63 for obese individuals relative to normal-weight individuals. Similar findings reported by Ji et al. (12) yielded corresponding multivariable-adjusted relative risk estimates of 1.51 and 2.24, respectively. Despite the consistency of these findings, existing investigations have predominantly operationalised BMI as a categorical exposure variable, partitioning the continuous adiposity distribution according to conventional epidemiological cut-points. This analytical discretisation inherently constrains insight into potential nonlinearity and obscures fine-grained dose–response relationships. Meanwhile, although a growing body of literature has sought to contextualise the burden of KOA attributable to elevated BMI in China (7, 13, 14), quantitative elucidation of the precise functional form linking BMI to KOA risk remains limited. This evidence gap restricts the formulation of optimally targeted, metric-specific public health interventions.

Therefore, to generate actionable evidence for guiding public health strategy development and alleviating the growing burden of KOA in ageing societies, this study used Global Burden of Disease (GBD) 2021 data to describe the burden of KOA attributed to high BMI among Chinese adults. We observed that the burden of disability-adjusted life years (DALYs) increased markedly among individuals aged 45 years and older. To further elucidate the relationship between BMI and KOA in this population, we analyzed data from the China Health and Retirement Longitudinal Study (CHARLS) among adults aged 45 years and over to quantify the impact of BMI on KOA prevalence. Our findings indicate that once BMI exceeds 26.89 kg/m², each additional unit increase is associated with a 10% increase in KOA prevalence. However, because this study relies on cross-sectional CHARLS data collected in 2011, the findings may not fully reflect the contemporary relationship between BMI and KOA among middle-aged and older adults in China. Accordingly, extrapolation of these results should be interpreted with caution.

From 1990 to 2021, the burden of KOA in China has steadily increased, evolving into a major and increasingly complex public health challenge. Among modifiable risk factors, elevated BMI is of particular concern, as it represents a key driver of the KOA burden. High BMI increases mechanical stress on weight-bearing joints and promotes systemic inflammation, both of which accelerate disease progression (24). Given the substantial rise in obesity prevalence in China, future projections of the KOA burden are likely to be significantly underestimated unless this risk factor is explicitly considered (25). Furthermore, public awareness of early prevention and treatment remains persistently low, with many individuals only seeking medical attention when symptoms become apparent, thereby intensifying the long-term societal and clinical burden. Consequently, a rigorous appraisal of contemporary KOA epidemiology, coupled with the formulation of evidence-based weight management strategies, is imperative for preventing disease onset and attenuating progression.

This study provides an updated overview of the burden of KOA in China. In 2021, the ASIR, ASPR and ASDR were 406.42, 5,016.52 and 162.44 per 100,000 population, respectively. In 2021, 0.31% of total KOA DALYs were attributable to high BMI exposure, which is a 78.50% increase since 1990. DALYs attributed to BMI reached 1.11 million, marking a 369.28% increase since 1990. After age standardization, the ASDR increased by 91.68%. These findings are consistent with previous reports (7, 26) and confirm that the burden of KOA related to BMI has increased continuously between 1990 and 2021. Rapid economic development, coupled with shifts in dietary habits and reductions in physical activity, has driven population-level increases in BMI (27). As population ageing intensifies and the chronic disease burden escalates in China, KOA, a prototypical age-related disorder, has an incidence that rises steeply with age. This directly translates into a significant disease burden within this demographic (28). Stratified analysis across age groups revealed that the crude DALYs rate attributable to high BMI increased in every stratum between 1990 and 2021, albeit with fluctuations. Notably, the acceleration was most pronounced among adults aged 45 years and older, with a progressively steeper gradient at older ages, corroborating the observations of Li and Zhou (26). This is likely due to accelerated chondrocyte mitochondrial dysfunction with ageing, leading to metabolic imbalance within the joint matrix. Concurrently, the increased prevalence of metabolic syndrome among middle-aged and older populations amplifies the effects of joint damage through chronic inflammatory pathways. These epidemiological transitions highlight the need to prioritise adults aged ≥45 years in prevention and control programmes, requiring the development of robust and effective public health strategies to address this evolving challenge.

Furthermore, women consistently exhibited a higher burden of KOA and a steeper temporal increase in incidence, prevalence, and DALYs than men. This sex disparity is multifactorial. Anatomically, the female pelvis is wider and the Q-angle is larger, which amplifies mechanical loading across the tibiofemoral compartment and increases the risk of cartilage damage (29). Endocrine factors further magnify the risk. Dramatic hormonal fluctuations during the perimenopausal period, especially the abrupt decline in oestrogen after menopause, attenuate the chondroprotective effects of oestrogen and disrupt cartilage matrix turnover, accelerating joint degeneration and increasing susceptibility to KOA (30). Cyclical variations in sex steroid concentrations during the menstrual cycle and pregnancy also modulate ligamentous laxity and joint biomechanics, potentially compromising joint stability (31). Finally, age-related declines in bone mineral density and cartilage thickness are more pronounced in women, and the smaller, more fragile bony architecture of the female skeleton makes it more vulnerable to degenerative changes in weight-bearing joints, such as the knee (32). Collectively, these biological and biomechanical factors help explain the greater susceptibility of women to KOA.

Using CHARLS data, this study included 12,769 participants aged 45 years or older, among whom 1,254 (9.82%) were diagnosed with KOA—a prevalence consistent with previous estimates (33). We observed that KOA patients tended to have lower educational attainment, potentially because individuals with lower education levels are more likely to be employed in physically demanding occupations. Higher mechanical loads in such roles may increase susceptibility to joint cartilage damage, thereby elevating disease risk. A notably lower proportion of KOA sufferers were married, potentially because unmarried, divorced, or widowed individuals lack spousal companionship and care, leading to greater adverse health impacts. Smoking and alcohol consumption rates among KOA patients were comparatively low, possibly because patients voluntarily quit smoking and drinking after diagnosis—either following medical advice or due to self-perceived health risks—creating an illusion of “low exposure” in current surveys. Compared with individuals without KOA, those with KOA exhibited a significantly higher prevalence of hypertension, diabetes mellitus, renal disease, gastrointestinal disorders and dyslipidaemia. Both hypertension and KOA may share chronic systemic inflammation as a common risk factor, which could explain the elevated prevalence of hypertension in individuals with KOA (34). Hyperglycaemia accelerates joint inflammation and cartilage degradation via oxidative stress, activation of pro-inflammatory mediators and the accumulation of advanced glycation end-products (35). The chronic, low-grade inflammatory state that is characteristic of KOA, together with long-term use of non-steroidal anti-inflammatory drugs (NSAIDs), increases the incidence of renal and gastrointestinal disorders (36). With respect to lipid metabolism, high-density lipoprotein has been shown to suppress nuclear factor-κB activation and downregulate the expression of pro-inflammatory cytokines, such as interleukin-6 and tumour necrosis factor-α. This has the potential to attenuate synovial inflammation and cartilage catabolism. In contrast, low-density lipoprotein may accumulate in synovial fluid and cartilage, amplifying oxidative stress and inflammatory signalling and ultimately promoting cartilage breakdown and exacerbating joint symptoms (37). These findings highlight the importance of integrated, multimorbidity-oriented management of KOA patients to optimise therapeutic efficacy and improve long-term prognosis.

Consistent with prior studies (38, 39), overweight and obesity were significantly more prevalent among individuals with KOA. Meanwhile, the correlation analysis between KOA and BMI revealed that KOA prevalence increased with rising BMI, a trend that persisted even after adjusting for demographic and morbidity-related covariates. Piecewise regression modelling revealed a non-linear relationship between BMI and KOA, with a statistically derived inflection point at 26.89 kg/m². Below this threshold, the prevalence of KOA remained essentially constant, whereas above it, each additional unit of BMI was associated with a 10% increase in the likelihood of developing the disease. Large-scale genetic correlation analyses corroborate this quantitative association: a one-standard-deviation increase in BMI was found to confer an odds ratio of 1.10 for KOA (40). Similarly, Lv et al. (41) observed a BMI odds ratio of 1.02 per unit, while a pooled meta-analysis estimated an excess risk of 35% for every 5-unit increment in BMI (42). Taken together, these findings confirm that a high BMI increases the risk of KOA. Excess weight increases mechanical loading across the knee joint, accelerating cartilage wear and degradation (43). Meanwhile, the strength of key muscle groups such as the quadriceps femoris decreases, leading to impaired joint alignment and stability (44). In addition to local mechanical stress, adipose tissue secretes pro-inflammatory cytokines, including interleukin-6, tumour necrosis factor-α and leptin, that upregulate matrix metalloproteinase activity, thereby exacerbating cartilage breakdown and synovial inflammation (45). In addition, an imbalance between leptin and adiponectin in obesity fosters a catabolic environment that favours cartilage destruction over repair and disrupts subchondral bone remodelling, thereby facilitating the initiation and progression of KOA (46). Precision public health initiatives should therefore implement personalised weight management protocols based on current BMI values to effectively reduce the population-level disease burden.

The World Health Organization advocates three complementary obesity management strategies: weight reduction, weight maintenance, and prevention of further weight gain, all aimed at sustaining a healthy body weight (13). There is robust evidence that structured weight management interventions for overweight or obese individuals can significantly reduce the incidence of KOA, highlighting their pivotal role in the primary prevention of this disease and reducing its impact on the population (47). In regions with a high concentration of individuals with an elevated BMI, comprehensive, multicomponent interventions are recommended. These should promote healthy diets with calorie restriction and portion control. It is also important to ensure adequate protein and micronutrient intake to support muscle and bone health. People should be encouraged to participate in joint-friendly activities such as swimming and cycling to support joint health and alleviate KOA-related pain. Early intervention is especially important for high-risk groups. Those with a BMI of 26.89 kg/m² or higher should receive targeted, intensive management. This approach can lower their risk and help reduce the burden of KOA.

This study integrates GBD and CHARLS data to examine the relationship between BMI and KOA in Chinese adults aged 45 years and older; however, several limitations merit consideration. Firstly, the diversity of data sources may lead to variations in KOA diagnostic criteria and data collection methods, which could compromise the reliability of the findings. Secondly, the definition of KOA in the CHARLS cohort relies on self-reported data, which may introduce information bias due to inaccurate recall or socially desirable responses. Furthermore, the cross-sectional design of this study restricts our ability to infer a causal relationship between BMI and KOA risk. Even after adjusting for multiple covariates, unmeasured confounding factors could still influence the interpretation of the results. Meanwhile, given the limitations of cross-sectional design, we cannot rule out the reverse causality where KOA-induced pain and reduced activity may lead to increased BMI. Fourthly, BMI does not differentiate between fat and lean mass, nor does it capture variations in fat distribution. Therefore, using it as the sole indicator of body composition may not fully characterise an individual’s weight status or its influence on KOA risk. Finally, as this study is based on cross-sectional data from 2011, its findings may not accurately reflect the current relationship between BMI and KOA among middle-aged and older populations in China. These limitations suggest caution when extrapolating study findings and indicate directions for future research. For instance, longitudinal study designs could be employed, with repeated measurements of BMI and KOA incidence to clarify causal directionality, while utilising more comprehensive body composition and health indicators to provide a more detailed assessment.

BMI has emerged as a key modifiable risk factor for KOA-related DALYs. Convergent analyses of GBD 2021 and CHARLS data demonstrate a persistent and accelerating increase in the KOA burden attributable to high BMI across China, with a notable rise among adults aged ≥45 years. Specifically, a BMI threshold of ≥26.89 kg/m² marks the point at which KOA risk escalates sharply in this population. This threshold should therefore be central to a multidimensional and integrated prevention framework that prioritises weight management, early intervention, and community-based health education. In addition, coordinated management of coexisting chronic conditions and the establishment of a precision prevention strategy stratified by age and sex are essential to curbing the continued expansion of the KOA burden in China.