Dynapenic abdominal obesity and symptomatic knee osteoarthritis: results from a large cross-sectional study of middle-aged and older adults in China
Highlight box
Key findings
• Dynapenia combined with abdominal obesity was associated with the highest likelihood of symptomatic knee osteoarthritis (KOA), whereas abdominal obesity alone showed no independent association after full adjustment, suggesting a prominent role of muscle strength.
• Higher grip strength was consistently associated with a lower prevalence of symptomatic KOA across sexes.
What is known and what is new?
• Muscle weakness and obesity are established risk factors for KOA, but their combined phenotypes have been less well characterized in large population-based studies.
• This study shows that dynapenic abdominal obesity is more strongly associated with symptomatic KOA than abdominal obesity alone, and that the association of dynapenia with KOA persists after accounting for metabolic factors.
What is the implication, and what should change now?
• Assessment of muscle strength may provide additional information beyond traditional anthropometric measures when evaluating KOA risk.
• Interventions aimed at preserving or improving muscle strength may be relevant components of KOA prevention strategies, particularly in midlife populations.
Introduction
Knee osteoarthritis (KOA) is one of the most prevalent chronic musculoskeletal disorders and a leading cause of disability worldwide, posing a growing public health challenge in both developed and developing countries (1,2). The prevalence of symptomatic KOA and radiographic KOA among individuals aged 60 years and older ranges from 10.0% to 16.0% and from 35.0% to 50.0%, respectively (3,4). Globally, approximately 250 million individuals are affected by KOA, with a steadily increasing burden driven by population aging and rising obesity rates (5). In the United States, the prevalence of KOA has doubled among men and tripled among women over the past two decades, affecting an estimated 15.1 million individuals with symptomatic disease (6). Beyond high-income countries, the burden of KOA is also substantial in developing regions. A cross-sectional study conducted in Argentina, Brazil, and Mexico involving 1,210 patients reported a mean age of 61.8 years, with women accounting for 80.8% of cases, highlighting the widespread impact of KOA across diverse socioeconomic and healthcare settings (7). Similarly, China has experienced a marked increase in KOA burden, with an estimated 37.35 million individuals aged 60 years or older affected by symptomatic KOA (8). Correspondingly, the age-standardized disability-adjusted life-year (DALY) rate attributable to KOA in China increased from 151.24 per 100,000 in 1990 to 162.44 per 100,000 in 2021 (9). As the most common form of osteoarthritis, KOA accounts for approximately 87% of years lived with disability related to osteoarthritis worldwide, imposing substantial socioeconomic and healthcare burdens (10).
KOA is increasingly recognized as a whole-joint disease rather than a condition limited to articular cartilage degeneration. In addition to structural joint changes, significant alterations in periarticular muscles are commonly observed, including increased intramuscular fat infiltration in the quadriceps and hamstrings compared with healthy individuals (11). Excessive fat accumulation within skeletal muscle reduces muscle pennation angle and contractile efficiency, leading to impaired strength and poorer performance in functional activities such as walking and stair climbing (12). Although previous studies have predominantly focused on muscle mass and adiposity, emerging evidence indicates that muscle strength may be a more sensitive and clinically relevant predictor of functional decline and adverse outcomes in KOA than muscle mass alone (13). However, commonly used indicators often fail to simultaneously capture muscle strength and adiposity, limiting comprehensive evaluation of their combined effects on KOA risk.
Dynapenia refers to the age-related loss of muscle strength that occurs independently of muscle mass decline. When dynapenia coexists with excess abdominal fat accumulation, the condition is termed dynapenic abdominal obesity (DAO) (14). DAO has attracted increasing attention as a distinct phenotype associated with adverse health outcomes in older adults, including disability, hospitalization, and mortality (15-18). Importantly, dynapenia and abdominal obesity may interact through shared pathophysiological mechanisms such as chronic low-grade inflammation, oxidative stress, and insulin resistance, forming a self-reinforcing cycle that accelerates functional deterioration (19,20). These biological pathways are also central to the development and progression of KOA, suggesting a potential link between DAO and symptomatic KOA (21).
Despite growing interest in the individual roles of muscle weakness and obesity in KOA, the combined impact of dynapenia and abdominal obesity on symptomatic KOA has not been fully elucidated, particularly in large population-based studies from developing countries (22). Therefore, the aim of this study was to investigate the association between DAO and symptomatic KOA among middle-aged and older adults using data from the China Health and Retirement Longitudinal Study (CHARLS). We present this article in accordance with the STROBE reporting checklist (available at https://aoj.amegroups.com/article/view/10.21037/aoj-2025-1-79/rc).
Methods
Study design
This study employed a cross-sectional design using baseline data from the CHARLS 2011 to investigate the association between DAO and symptomatic KOA among middle-aged and older Chinese adults (23). The cross-sectional approach allowed for population-level assessment of health outcomes in relation to muscle strength and adiposity, while adjusting for potential confounders.
Study setting
CHARLS is a nationally representative survey of Chinese adults aged 45 years and older, designed to collect detailed information on socio-demographic characteristics, economic status, and health conditions. The baseline survey, conducted between 2011 and 2012, included 450 communities or villages across 150 districts/counties in 28 provinces (23). A multistage probability-proportional-to-size sampling strategy was used to ensure representativeness, with households randomly selected and all eligible individuals within selected households invited to participate. Data collection included face-to-face interviews with structured questionnaires, physical measurements, and blood sample collection, conducted by trained interviewers following standardized protocols.
Study participants
Participants were eligible if they were aged 45 years or older and had complete information on symptomatic KOA, handgrip strength, waist circumference, and relevant covariates, including demographic, lifestyle, metabolic, and inflammatory variables. Individuals were excluded if they were younger than 45 years, pregnant, or had missing or implausible values for key measurements. After applying these predefined inclusion and exclusion criteria, a total of 7,418 participants were included in the final analytic sample (Figure 1). The CHARLS baseline survey achieved a household response rate of 80.5% (23). This large, population-based sample provides sufficient statistical power to examine the associations between DAO and symptomatic KOA, while survey sampling weights were applied to preserve national representativeness.
Assessment of symptomatic KOA
Symptomatic KOA was defined as the coexistence of physician-diagnosed osteoarthritis and current knee pain, consistent with definitions used in prior CHARLS-based epidemiological studies (24-26). Osteoarthritis status was ascertained through the standardized CHARLS questionnaire, in which participants were asked whether they had ever been diagnosed with osteoarthritis by a medical professional. Those who responded affirmatively were further queried regarding the presence of frequent bodily pain and the specific pain location. Participants reporting knee pain in conjunction with a physician diagnosis of osteoarthritis were classified as having symptomatic KOA (23).
This definition has been widely used in population-based studies leveraging CHARLS data and provides a standardized approach for identifying symptomatic KOA in large, nationally representative samples. The combination of physician diagnosis and current knee pain enhances specificity compared with symptom-only definitions, while reflecting the practical constraints of survey-based epidemiological research.
Assessment of dynapenia and abdominal obesity
Handgrip strength, measured using a dynamometer, served as the indicator of dynapenia (27). Two measurements were taken in the dominant hand, and the maximum value was used for analysis. Dynapenia was defined according to Asian-specific criteria, with handgrip strength less than 28 kg for men and less than 18 kg for women (28). Abdominal obesity was assessed by measuring waist circumference at the midpoint between the iliac crest and the last rib, taking the average of two measurements. Abdominal obesity was defined as a waist circumference of 90 cm or greater for men and 85 cm or greater for women (29). Participants were categorized into four groups based on these criteria: non-dynapenic/non-abdominal obesity (ND/NAO), non-dynapenic/abdominal obesity (ND/AO), dynapenic/non-abdominal obesity (D/NAO), and dynapenic abdominal obesity (DAO).
Covariates
Demographic covariates included age, sex, ethnicity, education level, marital status, retirement status, and place of residence. Lifestyle factors comprised smoking status and alcohol consumption. Body mass index (BMI) was calculated as weight in kilograms divided by the square of height in meters and categorized according to the World Health Organization (WHO) criteria as normal weight (<25 kg/m2), overweight (25–29.9 kg/m2), and obesity (≥30 kg/m2) (30). BMI was included as an adjusting covariate in all multivariable models, while abdominal obesity and body composition were primarily characterized using waist-based indicators. This approach is consistent with prior CHARLS-based studies and allows for comparability with international research (24,26).
Health conditions were ascertained based on physician diagnosis or self-report and included hypertension, diabetes mellitus, cardiovascular disease, and stroke. To further address potential inflammatory and metabolic confounding pathways, biomarkers including C-reactive protein (CRP), triglycerides, and fasting plasma glucose were incorporated into the analyses. These biomarkers were measured using standardized enzymatic colorimetric assays. All covariates were obtained through structured face-to-face interviews conducted by trained interviewers as part of the CHARLS protocol, ensuring standardized data collection and quality control.
Sample size calculation
The required sample size was estimated using the standard formula for prevalence estimation in cross-sectional studies (n = Z2 × P × (1 − P)/d2) (31). Assuming a symptomatic KOA prevalence of approximately 10%, a 95% confidence level, and a margin of error of 1%, the minimum sample size was approximately 3,458 participants. Considering the complex multistage sampling design of CHARLS and planned subgroup analyses, a design effect of 2.0 was applied, yielding a target sample size of approximately 6,916 participants. The final analytic sample of 7,418 participants therefore provided adequate statistical power for the analyses.
Statistical analysis
Participants were classified into four groups according to dynapenia and abdominal obesity status: ND/NAO, ND/AO, D/NAO, and DAO. Grip strength was further categorized into weighted tertiles (Q1–Q3), with Q1 representing the lowest and Q3 the highest levels, to examine dose-response relationships. Weighted continuous variables are presented as mean ± standard error and compared using survey-weighted analysis of variance, while categorical variables are expressed as counts and weighted percentages and compared using χ2 tests. Survey-weighted logistic regression models were used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for the association between DAO and symptomatic KOA. Crude models were unadjusted; Model 1 adjusted for age, sex, and ethnicity; and Model 2 further adjusted for education, lifestyle factors, BMI, comorbidities, and biomarkers. Trend tests (P for trend) were performed by modeling grip strength tertiles as an ordinal variable. Restricted cubic spline models were applied to assess potential non-linear associations between grip strength and KOA, with P for non-linearity derived from likelihood ratio tests comparing linear and spline models. Subgroup analyses were conducted to evaluate effect modification, and P for interaction was obtained from multiplicative interaction terms. Mediation analyses were conducted within a counterfactual-based framework to examine whether triglycerides, fasting plasma glucose, and CRP mediated the association between DAO and symptomatic KOA (Table S1). Total, direct, and indirect effect ORs represent the overall, mediator-independent, and mediator-related effects of DAO on KOA, respectively, with mediation proportions calculated accordingly. All analyses incorporated survey sampling weights and were conducted using R version 4.3.1. A two-tailed P-value < 0.05 was considered statistically significant.
Ethical considerations
The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The original CHARLS study was approved by the Biomedical Ethics Review Committee of Peking University (IRB00001052-11015). All participants provided written informed consent at the time of data collection. This study involved secondary analysis of de-identified publicly available data and was therefore exempt from additional ethical review.
Results
Baseline characters
A total of 7,418 participants were included (mean age 58.64 years, 54.2% female). The prevalence of symptomatic KOA differed significantly across phenotypes (P<0.001), with DAO showing the highest prevalence at 16.67%, nearly twice that of ND/NAO (8.80%), followed by D/NAO (13.66%) and ND/AO (10.33%). Compared to other groups, participants with DAO were older (mean age 65.51 years), predominantly female (65.33%), and had higher prevalence of hypertension (34.67%), diabetes (8.67%), and cardiovascular disease (16.67%). The DAO group also exhibited the largest waist circumference, lowest grip strength, and highest proportion of overweight/obesity (all P<0.001, Table 1).
Table 1
| Variables | Total (N=7418) | ND/NAO (N=4453) | D/NAO (N=454) | ND/AO (N=2361) | DAO (N=150) | P value |
|---|---|---|---|---|---|---|
| Gender | <0.001 | |||||
| Female | 4,022 (54.22) | 2,131 (47.86) | 157 (34.58) | 1,636 (69.29) | 98 (65.33) | |
| Male | 3,396 (45.78) | 2,322 (52.14) | 297 (65.42) | 725 (30.71) | 52 (34.67) | |
| Ethnicity | 0.22 | |||||
| Han Chinese | 6,917 (93.25) | 4,134 (92.84) | 432 (95.15) | 2,211 (93.65) | 140 (93.33) | |
| Non-Han Chinese | 501 (6.75) | 319 (7.16) | 22 (4.85) | 150 (6.35) | 10 (6.67) | |
| Age (years) | 58.64±8.73 | 58.13±8.46 | 65.13±9.01 | 57.93±8.47 | 65.51±8.91 | <0.001 |
| Age group | <0.001 | |||||
| <60 years | 4,252 (57.32) | 2,665 (59.85) | 131 (28.85) | 1,419 (60.10) | 37 (24.67) | |
| ≥60 years | 3,166 (42.68) | 1,788 (40.15) | 323 (71.15) | 942 (39.90) | 113 (75.33) | |
| Education level | <0.001 | |||||
| Below primary school | 3,686 (49.69) | 2,128 (47.79) | 277 (61.01) | 1,175 (49.77) | 106 (70.67) | |
| High school and above | 707 (9.53) | 444 (9.97) | 20 (4.41) | 234 (9.91) | 9 (6.00) | |
| Primary and middle school | 3,025 (40.78) | 1,881 (42.24) | 157 (34.58) | 952 (40.32) | 35 (23.33) | |
| Retirement | 0.003 | |||||
| No | 6,719 (90.58) | 4,061 (91.20) | 422 (92.95) | 2,107 (89.24) | 129 (86.00) | |
| Yes | 699 (9.42) | 392 (8.80) | 32 (7.05) | 254 (10.76) | 21 (14.00) | |
| Marriage | <0.001 | |||||
| With partner | 6,625 (89.31) | 3,999 (89.80) | 376 (82.82) | 2,136 (90.47) | 114 (76.00) | |
| Without partner | 793 (10.69) | 454 (10.20) | 78 (17.18) | 225 (9.53) | 36 (24.00) | |
| Residence | <0.001 | |||||
| Rural | 4,944 (66.65) | 3,083 (69.23) | 326 (71.81) | 1,446 (61.25) | 89 (59.33) | |
| Urban | 2,474 (33.35) | 1,370 (30.77) | 128 (28.19) | 915 (38.75) | 61 (40.67) | |
| Symptomatic KOA | <0.001 | |||||
| No | 6,695 (90.25) | 4,061 (91.20) | 392 (86.34) | 2,117 (89.67) | 125 (83.33) | |
| Yes | 723 (9.75) | 392 (8.80) | 62 (13.66) | 244 (10.33) | 25 (16.67) | |
| Hypertension | <0.001 | |||||
| No | 5,528 (74.52) | 3,495 (78.49) | 339 (74.67) | 1,596 (67.60) | 98 (65.33) | |
| Yes | 1,890 (25.48) | 958 (21.51) | 115 (25.33) | 765 (32.40) | 52 (34.67) | |
| Diabetes | <0.001 | |||||
| No | 6,995 (94.30) | 4,249 (95.42) | 424 (93.39) | 2,185 (92.55) | 137 (91.33) | |
| Yes | 423 (5.70) | 204 (4.58) | 30 (6.61) | 176 (7.45) | 13 (8.67) | |
| Cardiovascular disease | 0.010 | |||||
| No | 6,574 (88.62) | 3,986 (89.51) | 400 (88.11) | 2,063 (87.38) | 125 (83.33) | |
| Yes | 844 (11.38) | 467 (10.49) | 54 (11.89) | 298 (12.62) | 25 (16.67) | |
| Stroke | 0.06 | |||||
| No | 7,254 (97.79) | 4,370 (98.14) | 441 (97.14) | 2,298 (97.33) | 145 (96.67) | |
| Yes | 164 (2.21) | 83 (1.86) | 13 (2.86) | 63 (2.67) | 5 (3.33) | |
| Drinking status | <0.001 | |||||
| No | 4,966 (66.95) | 2,819 (63.31) | 303 (66.74) | 1,730 (73.27) | 114 (76.00) | |
| Yes | 2,452 (33.05) | 1,634 (36.69) | 151 (33.26) | 631 (26.73) | 36 (24.00) | |
| Smoking status | <0.001 | |||||
| No | 5,180 (69.83) | 2,877 (64.61) | 266 (58.59) | 1,919 (81.28) | 118 (78.67) | |
| Yes | 2,238 (30.17) | 1,576 (35.39) | 188 (41.41) | 442 (18.72) | 32 (21.33) | |
| BMI | <0.001 | |||||
| Normal | 3,874 (52.22) | 2,949 (66.23) | 293 (64.54) | 577 (24.44) | 55 (36.67) | |
| Obesity | 895 (12.07) | 465 (10.44) | 43 (9.47) | 365 (15.46) | 22 (14.67) | |
| Overweight | 2,189 (29.51) | 665 (14.93) | 44 (9.69) | 1,408 (59.64) | 72 (48.00) | |
| Underweight | 460 (6.20) | 374 (8.40) | 74 (16.30) | 11 (0.47) | 1 (0.67) | |
| Waist circumference (cm) | 84.44±12.54 | 80.60±13.64 | 79.94±13.03 | 92.08±4.01 | 91.79±3.86 | <0.001 |
| Grip strength (kg) | 31.98±10.63 | 33.87±9.88 | 18.00±7.91 | 32.19±9.59 | 14.72±7.46 | <0.001 |
| CRP (mg/L) | 2.44±6.62 | 2.43±7.24 | 2.76±8.20 | 2.41±5.02 | 2.32±3.48 | 0.76 |
| Triglycerides (mg/dL) | 134.15±112.06 | 123.88±102.83 | 116.97±72.82 | 155.00±126.27 | 162.95±169.47 | <0.001 |
| Glucose (mg/dL) | 109.71±34.99 | 107.12±30.36 | 111.59±40.07 | 113.49±39.87 | 121.49±52.55 | <0.001 |
Data are presented as n (%) or mean ± standard error. BMI, body mass index; CRP, C-reactive protein; DAO, dynapenic abdominal obesity; D/NAO, dynapenic/non-abdominal obesity; KOA, knee osteoarthritis; ND/AO, non-dynapenic/abdominal obesity; ND/NAO, non-dynapenic/non-abdominal obesity.
Association between DAO and symptomatic KOA
Weighted logistic regression analyses revealed consistent associations between phenotypes and symptomatic KOA across progressive models (Table 2). In the crude model, DAO exhibited the strongest association (OR =2.07, 95% CI: 1.33–3.22, P=0.001), substantially higher than D/NAO (OR =1.64, P=0.001) or ND/AO (OR =1.19, P=0.03). After adjusting for sociodemographic factors (Model 1) and additional lifestyle/comorbidity factors (Model 2), DAO consistently demonstrated the highest risk (Model 2: OR =1.74, 95% CI: 1.08–2.78, P=0.02), approximately 14% greater than D/NAO alone (OR =1.53, P=0.007). Notably, ND/AO lost statistical significance after adjustment (Model 2: OR =1.04, P=0.68), while both D/NAO and DAO remained significant across all models, suggesting dynapenia plays a more critical role than abdominal obesity alone in KOA development.
Table 2
| Group | Crude model | Model 1 | Model 2 | |||||
|---|---|---|---|---|---|---|---|---|
| OR (95% CI) | P value | AOR (95% CI) | P value | AOR (95% CI) | P value | |||
| DAO | ||||||||
| ND/NAO | Ref | Ref | Ref | |||||
| D/NAO | 1.64 (1.23, 2.18) | 0.001 | 1.65 (1.23, 2.22) | 0.001 | 1.53 (1.13, 2.07) | 0.007 | ||
| ND/AO | 1.19 (1.01, 1.41) | 0.03 | 1.05 (0.88, 1.25) | 0.58 | 1.04 (0.86, 1.27) | 0.68 | ||
| DAO | 2.07 (1.33, 3.22) | 0.001 | 1.71 (1.08, 2.71) | 0.02 | 1.74 (1.08, 2.78) | 0.02 | ||
Crude model was unadjusted for covariates. Model 1 was adjusted for age, sex, and ethnicity. Model 2 was adjusted for age, sex, ethnicity, education level, smoking status, drinking status, BMI, hypertension, diabetes, cardiovascular disease, stroke, CRP, triglycerides, and fasting plasma glucose. AOR, adjusted odds ratio; BMI, body mass index; CI, confidence interval; CRP, C-reactive protein; DAO, dynapenic abdominal obesity; D/NAO, dynapenic/non-abdominal obesity; KOA, knee osteoarthritis; ND/AO, non-dynapenic/abdominal obesity; ND/NAO, non-dynapenic/non-abdominal obesity; OR, odds ratio.
Association between grip strength and symptomatic KOA
To further investigate the association between muscle strength and KOA, gender-stratified analyses were performed due to sex differences in grip strength (Table 3). Each 1-kg increase in grip strength was associated with a 2.1% reduction in KOA risk for males (Model 2: OR =0.98, 95% CI: 0.97–0.99, P=0.006) and a 3.2% reduction for females (Model 2: OR =0.97, 95% CI: 0.96–0.98, P<0.001). Tertile analyses demonstrated dose-response relationships (all P for trend <0.05), with participants in the highest tertile (Q3) showing significantly lower KOA risk compared to the lowest tertile in both males (OR =0.62, P=0.02) and females (OR =0.56, P<0.001).
Table 3
| Tertiles | Crude model | Model 1 | Model 2 | |||||
|---|---|---|---|---|---|---|---|---|
| OR (95% CI) | P value | AOR (95% CI) | P value | AOR (95% CI) | P value | |||
| Male | ||||||||
| Grip strength | 0.97 (0.96, 0.98) | <0.001 | 0.97 (0.96, 0.99) | <0.001 | 0.98 (0.97, 0.99) | 0.006 | ||
| Q1 | Ref | Ref | Ref | |||||
| Q2 | 0.87 (0.64, 1.17) | 0.35 | 0.89 (0.66, 1.21) | 0.46 | 0.97 (0.71, 1.32) | 0.83 | ||
| Q3 | 0.50 (0.36, 0.71) | <0.001 | 0.53 (0.36, 0.77) | 0.001 | 0.62 (0.42, 0.93) | 0.02 | ||
| P for trend | <0.001 | 0.001 | 0.024 | |||||
| Female | ||||||||
| Grip strength | 0.96(0.95, 0.96) | <0.001 | 0.97 (0.96, 0.98) | <0.001 | 0.97 (0.96, 0.98) | <0.001 | ||
| Q1 | Ref | Ref | Ref | |||||
| Q2 | 0.76 (0.61, 0.95) | 0.01 | 0.79 (0.63, 0.99) | 0.045 | 0.79 (0.62, 0.99) | 0.044 | ||
| Q3 | 0.53 (0.41, 0.67) | <0.001 | 0.57 (0.44, 0.73) | <0.001 | 0.56 (0.43, 0.73) | <0.001 | ||
| P for trend | <0.001 | <0.001 | <0.001 | |||||
Tertiles (Q1, Q2, Q3): grip strength was categorized into weighted tertiles, with Q1 representing the lowest tertile and Q3 the highest tertile, to examine dose-response relationships. P for trend: derived from modeling grip strength tertiles as an ordinal variable to test for linear trends across ordered categories. Crude model was unadjusted for covariates. Model 1 was adjusted for age, sex, and ethnicity. Model 2 was adjusted for age, sex, ethnicity, education level, smoking status, drinking status, BMI, hypertension, diabetes, cardiovascular disease, stroke, CRP, triglycerides, and fasting plasma glucose. AOR, adjusted odds ratio; BMI, body mass index; CI, confidence interval; KOA, knee osteoarthritis; OR, odds ratio.
To explore the dose-response relationship, restricted cubic spline analyses confirmed inverse associations between grip strength and KOA in both genders (Figure 2, all P-overall <0.05). The relationships were predominantly linear (all P-non-linear >0.05), with steeper reductions at lower grip strength levels, particularly in females.
Subgroup analyses between DAO and symptomatic KOA
Subgroup analyses were performed stratified by age (<60 vs. ≥60 years), gender, residence (rural vs. urban), and comorbidities (cardiovascular disease, diabetes, and hypertension). Significant heterogeneity was observed by age (P for interaction =0.002), with DAO showing the strongest association with KOA in individuals aged <60 years (OR =4.92, 95% CI: 2.27–10.65, P<0.001) but not in those aged ≥60 years (OR =1.03, 95% CI: 0.56–1.87, P=0.93). Gender stratification showed that D/NAO was significantly associated with KOA in males (OR =1.56, 95% CI: 1.03–2.38, P=0.03) but not in females (P=0.08), though the interaction was non-significant (P=0.63). Rural residents demonstrated stronger associations for both D/NAO (OR =1.65, P=0.003) and DAO (OR =2.29, P=0.003) compared to urban residents, with a marginally significant interaction (P=0.09). No significant interactions were observed for cardiovascular disease, diabetes, or hypertension (all P for interaction >0.05), though consistent associations were noted in participants without these comorbidities (Table 4).
Table 4
| Variables | Subgroup | Exposure status | Percent (%) | OR (95% CI) | P value | P for interaction |
|---|---|---|---|---|---|---|
| Age | <60 years | ND/NAO | 7.60 | 1.00 (Ref) | Ref | 0.002 |
| D/NAO | 11.50 | 1.44 (0.80, 2.61) | 0.225 | |||
| ND/AO | 9.90 | 1.22 (0.94, 1.58) | 0.136 | |||
| DAO | 29.70 | 4.92 (2.27, 10.65) | <0.001 | |||
| ≥60 years | ND/NAO | 10.60 | 1.00 (Ref) | Ref | ||
| D/NAO | 14.60 | 1.33 (0.93, 1.90) | 0.118 | |||
| ND/AO | 11.00 | 0.93 (0.69, 1.24) | 0.605 | |||
| DAO | 12.40 | 1.03 (0.56, 1.87) | 0.935 | |||
| Gender | Female | ND/NAO | 11.40 | 1.00 (Ref) | Ref | 0.63 |
| D/NAO | 17.80 | 1.50 (0.95, 2.36) | 0.084 | |||
| ND/AO | 12.00 | 1.03 (0.81, 1.30) | 0.826 | |||
| DAO | 18.40 | 1.64 (0.92, 2.91) | 0.091 | |||
| Male | ND/NAO | 6.40 | 1.00 (Ref) | Ref | ||
| D/NAO | 11.40 | 1.56 (1.03, 2.38) | 0.036 | |||
| ND/AO | 6.60 | 1.03 (0.72, 1.46) | 0.884 | |||
| DAO | 13.50 | 1.99 (0.88, 4.53) | 0.1 | |||
| Residence | Rural | ND/NAO | 10.20 | 1.00 (Ref) | Ref | 0.09 |
| D/NAO | 16.90 | 1.65 (1.18, 2.29) | 0.003 | |||
| ND/AO | 11.60 | 1.03 (0.82, 1.30) | 0.778 | |||
| DAO | 22.50 | 2.29 (1.33, 3.92) | 0.003 | |||
| Urban | ND/NAO | 5.60 | 1.00 (Ref) | Ref | ||
| D/NAO | 5.50 | 0.90 (0.39, 2.05) | 0.798 | |||
| ND/AO | 8.30 | 1.23 (0.86, 1.77) | 0.255 | |||
| DAO | 8.20 | 1.11 (0.42, 2.96) | 0.835 | |||
| Cardiovascular disease | No | ND/NAO | 7.90 | 1.00 (Ref) | Ref | 0.24 |
| D/NAO | 13.20 | 1.60 (1.16, 2.21) | 0.004 | |||
| ND/AO | 8.90 | 1.06 (0.85, 1.33) | 0.609 | |||
| DAO | 16.00 | 1.91 (1.14, 3.21) | 0.014 | |||
| Yes | ND/NAO | 16.70 | 1.00 (Ref) | Ref | ||
| D/NAO | 16.70 | 1.21 (0.53, 2.73) | 0.654 | |||
| ND/AO | 20.50 | 1.00 (0.65, 1.53) | 0.991 | |||
| DAO | 20.00 | 1.23 (0.42, 3.58) | 0.703 | |||
| Diabetes | No | ND/NAO | 8.70 | 1.00 (Ref) | Ref | 0.32 |
| D/NAO | 13.90 | 1.60 (1.18, 2.18) | 0.003 | |||
| ND/AO | 9.80 | 0.99 (0.81, 1.22) | 0.926 | |||
| DAO | 16.10 | 1.67 (1.03, 2.73) | 0.039 | |||
| Yes | ND/NAO | 11.80 | 1.00 (Ref) | Ref | ||
| D/NAO | 10.00 | 0.86 (0.20, 3.65) | 0.837 | |||
| ND/AO | 16.50 | 1.51 (0.74, 3.06) | 0.257 | |||
| DAO | 23.10 | 3.03 (0.57, 16.14) | 0.196 | |||
| Hypertension | No | ND/NAO | 8.20 | 1.00 (Ref) | Ref | 0.15 |
| D/NAO | 11.80 | 1.42 (0.99, 2.05) | 0.059 | |||
| ND/AO | 9.10 | 0.93 (0.72, 1.18) | 0.537 | |||
| DAO | 19.40 | 2.18 (1.27, 3.73) | 0.004 | |||
| Yes | ND/NAO | 10.90 | 1.00 (Ref) | Ref | ||
| D/NAO | 19.10 | 1.83 (1.08, 3.10) | 0.026 | |||
| ND/AO | 12.90 | 1.19 (0.86, 1.65) | 0.285 | |||
| DAO | 11.50 | 0.98 (0.40, 2.43) | 0.966 |
CI, confidence interval; D/NAO, dynapenic/non-abdominal obesity; DAO, dynapenic abdominal obesity; KOA, knee osteoarthritis; ND/AO, non-dynapenic/abdominal obesity; ND/NAO, non-dynapenic/non-abdominal obesity; OR, odds ratio.
Receiver operating characteristic (ROC) curve and area under the curve (AUC)
ROC curve analyses were performed to compare the discriminative ability of DAO and BMI for identifying symptomatic KOA (Figure 3). DAO demonstrated moderate discriminative ability with an AUC of 0.673 (95% CI: 0.65–0.69), significantly outperforming BMI (AUC =0.535, 95% CI: 0.52–0.56), which showed only marginal predictive value. These findings suggest that DAO is a superior indicator compared to BMI alone for identifying individuals at risk of symptomatic KOA.
Mediation analyses
Mediation analyses tested whether triglycerides, glucose, and CRP mediated the DAO-KOA association (Table S1). While total effects remained significant (OR =1.61, P=0.045), none of the indirect effects were statistically significant (all P>0.05), with negligible mediation proportions (−3.86% to −0.03%). These findings suggest the DAO-KOA association is not mediated by these inflammatory and metabolic biomarkers.
Discussion
Principal findings
In this nationally representative study of 7,418 middle-aged and older adults, DAO was significantly associated with a higher risk of symptomatic KOA, with dynapenia playing a more prominent role than abdominal obesity alone. Participants with combined dynapenia and abdominal obesity exhibited the highest risk, whereas abdominal obesity without dynapenia was no longer associated with KOA after full adjustment. In addition, higher grip strength was consistently associated with a lower risk of symptomatic KOA, demonstrating a clear dose-response relationship. Importantly, significant age-related heterogeneity was observed, with the strongest DAO-KOA association occurring in individuals younger than 60 years. Collectively, these findings suggest that muscle strength represents a critical and underappreciated determinant of KOA risk beyond adiposity.
Demographic factors and comorbidities
The observed associations were robust after adjustment for a wide range of demographic characteristics and chronic comorbidities, including hypertension, diabetes, cardiovascular disease, and stroke. These findings align with prior evidence that KOA is influenced by a complex interplay of mechanical, metabolic, and systemic factors. While obesity-related metabolic disturbances have long been implicated in KOA pathogenesis, our results indicate that impaired muscle function may exert an independent and potentially dominant influence. This distinction is clinically relevant, as muscle strength is a modifiable factor that can be targeted even in individuals with established metabolic comorbidities.
Age-related effects and clinical implications
One of the most notable findings of this study was the pronounced age-related heterogeneity in the DAO-KOA association. The strongest association was observed among individuals younger than 60 years, whereas no significant association was detected in older adults. This pattern suggests that DAO in midlife may represent a particularly high-risk phenotype, potentially reflecting early metabolic dysfunction, reduced neuromuscular reserve, and maladaptive joint loading before advanced structural degeneration occurs. Previous studies have shown that muscle strength is inversely associated with metabolic disorders such as type 2 diabetes, with stronger effects observed in younger and overweight populations (32). In older adults, the high prevalence of both dynapenia and abdominal obesity, along with multifactorial age-related joint degeneration, may attenuate differential risk estimates. These findings emphasize the importance of early identification and intervention, shifting the focus of KOA prevention toward middle-aged populations rather than exclusively targeting the elderly (33,34).
Potential mechanisms linking dynapenia to KOA
Several biological mechanisms may explain the strong association between dynapenia and symptomatic KOA. From a biomechanical perspective, adequate muscle strength is essential for maintaining joint stability, optimizing lower-limb alignment, and distributing mechanical loads across the knee joint. Reduced muscle strength increases joint contact stress and accelerates cartilage degeneration (35). Neuromuscular mechanisms are also relevant, as joint inflammation can induce arthrogenic muscle inhibition, leading to a vicious cycle of progressive weakness and functional decline (36). Clinically, greater muscle strength has been associated with improved pain control, physical function, and mobility, including performance on functional tests such as the Timed Up and Go (TUG) test, a standardized measure of dynamic balance and mobility (37). Resistance training has been shown to reduce disability risk and improve lower-extremity function in individuals with or at risk of KOA (38,39).
Although abdominal obesity may exacerbate mechanical loading and systemic inflammation, mediation analyses indicated that triglycerides, fasting glucose, and CRP did not significantly mediate the DAO-KOA association. This finding suggests that the protective effects of muscle strength may operate primarily through direct biomechanical and neuromuscular pathways rather than systemic metabolic mechanisms (40,41).
Comparison with previous studies
Previous CHARLS-based studies have examined the associations of sarcopenia or obesity with KOA separately, with mixed conclusions. A longitudinal analysis reported that sarcopenia increased the risk of incident KOA, particularly among women, but focused primarily on muscle mass rather than muscle strength (42). Another cross-sectional study demonstrated positive associations between multiple obesity indices, including BMI, waist-to-height ratio (WHtR), body roundness index (BRI), and body fat percentage (BFP), and KOA, without accounting for muscle function (43). By integrating muscle strength and abdominal adiposity into a single composite phenotype, our study extends this literature and demonstrates that dynapenia is a more informative indicator of KOA risk than adiposity alone.
Strengths and limitations
This study has several strengths, including the use of a large, nationally representative sample, standardized measurements, and comprehensive adjustment for demographic, metabolic, and inflammatory factors. The introduction of DAO as a composite phenotype provides a clinically practical framework that better reflects functional health than traditional anthropometric measures.
Nevertheless, several limitations should be acknowledged. First, grip strength is a global measure of muscle strength and is not specific to the knee extensors; however, it is widely accepted as a reliable surrogate of overall muscle function in epidemiological studies. Second, although dynapenia overlaps conceptually with sarcopenia, the two constructs are distinct, as dynapenia emphasizes muscle function rather than muscle mass. Third, symptomatic KOA was identified using a survey-based definition requiring self-reported physician diagnosis combined with current knee pain, rather than standardized clinical or radiographic criteria such as those proposed by the American College of Rheumatology (ACR). Although this approach has been widely used in population-based studies and improves specificity compared with symptom-only definitions, misclassification due to other causes of knee pain, including inflammatory or periarticular conditions, cannot be fully excluded. Fourth, the absence of direct measurements of muscle mass and intramuscular fat limits mechanistic interpretation; specifically, we could not distinguish whether dynapenia resulted from reduced muscle quantity or impaired muscle quality. This may lead to phenotype misclassification, as individuals with preserved muscle mass but reduced strength due to poor muscle quality could be grouped with those experiencing true muscle atrophy, potentially diluting or masking subgroup-specific associations. Future studies incorporating body composition assessments would enable more precise phenotypic characterization. Finally, the cross-sectional design precludes causal inference.
Public health implications and future directions
Our findings highlight the clinical and public health importance of incorporating muscle strength assessment into KOA risk screening, as grip strength demonstrated superior discriminative ability compared with BMI. Prevention strategies should prioritize resistance training alongside weight management, particularly for middle-aged adults with dynapenia. The marked age-related heterogeneity observed in this study suggests that individuals younger than 60 years with DAO represent a critical high-risk group that may benefit most from early intervention. Future research should focus on longitudinal studies to clarify causal relationships, investigate the role of intramuscular fat infiltration and joint inflammation, and evaluate combined lifestyle interventions through randomized controlled trials. Validation of these findings in diverse populations is also warranted.
Conclusions
This nationally representative study demonstrates that DAO is associated with symptomatic KOA in Chinese adults. Reduced muscle strength, as assessed by grip strength, showed consistent inverse dose-response relationships with KOA risk, suggesting that muscle function may contribute additional information beyond conventional adiposity indicators. Notably, the association appeared more pronounced in individuals younger than 60 years, highlighting the potential value of early identification of high-risk phenotypes. These findings support the incorporation of muscle strength assessment alongside weight management in KOA risk evaluation, while further longitudinal studies are needed to clarify causality and underlying mechanisms.
Acknowledgments
This study used data from the China Health and Retirement Longitudinal Study (CHARLS), which was conducted by the National School of Development at Peking University. We thank the CHARLS research team and all respondents for their contributions to the survey. The content is solely the responsibility of the authors and does not represent the official views of the CHARLS team.
Footnote
Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://aoj.amegroups.com/article/view/10.21037/aoj-2025-1-79/rc
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Funding: This work was supported by
Conflicts of Interest: Both authors have completed the ICMJE uniform disclosure form (available at https://aoj.amegroups.com/article/view/10.21037/aoj-2025-1-79/coif). The authors have no conflicts of interest to declare.
Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The original CHARLS study was approved by the Biomedical Ethics Review Committee of Peking University (IRB00001052-11015). All participants provided written informed consent at the time of data collection.
Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.
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Cite this article as: Chen Y, Jiang J. Dynapenic abdominal obesity and symptomatic knee osteoarthritis: results from a large cross-sectional study of middle-aged and older adults in China. Ann Jt 2026;11:19.

