Racial Disparities in Pain Between Non-Hispanic Whites and Asian Americans with Knee Osteoarthritis: The Role of Pain Catastrophizing

doi:10.21203/rs.3.rs-5228306/v1

Background: Although a few studies have delineated the disparities in knee osteoarthritis (OA) pain between non-Hispanic Whites (NHWs) and Asian Americans, a significant research gap persists in elucidating the mechanisms underlying these differences.

Objective: This pilot study aimed to examine psychological factors, specifically pain catastrophizing and negative affect, as potential explanatory mechanisms for these dissimilarities.

Methods: Forty community-dwelling participants aged 50–70 years with self-reported knee OA pain, including 20 NHWs and 20 Asian Americans, were recruited. Clinical knee OA pain intensity was assessed using the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) and Short -Form-McGill Pain Questionnaire-2 (SF-MPQ-2). Quantitative sensory testing was used to measure experimental sensitivity to heat- and mechanically induced pain. Pain catastrophizing was evaluated using the Coping Strategies Questionnaire-Revised Pain Catastrophizing subscale, while negative affect was assessed using the Positive and Negative Affect Schedule. Bayesian mediation analyses were employed to examine both direct and indirect effects (mediation) between variables.

Results: Asian Americans exhibited higher pain catastrophizing scores than NHWs. Pain catastrophizing, at high levels, contributed to WOMAC- and SF-MPQ-2-measured clinical pain, and it fully mediated the relationship between race and these pain measures. However, race had no indirect effects on experimental pain sensitivity through pain catastrophizing. While Asian Americans yielded higher negative affect scores and greater experimental pain sensitivity than NHWs, race exerted no indirect effects on all pain measures via negative affect.

Conclusions: Pain catastrophizing appears crucial in addressing racial disparities in clinical knee OA pain between NHWs and Asian Americans. The lack of indirect effects of race on experimental pain sensitivity through pain catastrophizing suggests the need to explore other factors, such as genetic and biological influences. Further research using larger sample sizes is essential to validate our findings and clarify the role of negative affect.

Asian American

osteoarthritis

pain

pain catastrophizing

Symptomatic knee osteoarthritis (OA), characterized by pain, disability, and diminished quality of life, is a prevalent joint disorder in middle-aged and older adults [1]. Traditional perspectives have primarily linked knee OA pain to structural joint changes; however, the weak correlation between radiographic findings and clinical symptoms suggests that structural abnormalities alone do not comprehensively account for the pain experienced by sufferers [2-5]. This indicates that additional factors, including psychosocial influences, may significantly impact the severity and perception of OA-related pain [6].

The prevalence of symptomatic knee OA is projected to increase in racially and ethnically marginalized groups [7]. Although significant disparities in clinical and experimental pain sensitivity have been reported across racial/ethnic groups with knee OA, relevant studies have predominantly compared non-Hispanic Whites (NHWs) with African Americans [8]. Asian Americans, a rapidly growing minority, have been underrepresented in pain research despite emerging evidence indicating that they experience greater knee OA-related pain than NHWs [9], challenging cultural stereotypes of stoicism. To date, no studies have delineated the mechanisms underlying the differences between NHWs and Asian Americans.

The biopsychosocial model of pain recognizes the importance of various psychological factors in pain [10]. One such factor, pain catastrophizing—cognitive and affective pain appraisal characterized by the tendency to address and magnify the threat value of painful stimuli and feel helpless owing to pain—is reportedly significantly correlated with increased knee pain severity in both clinical and experimental settings [11-13]. Notably, Asian Americans have been reported to exhibit higher levels of pain catastrophizing, possibly influenced by acculturative stress and cultural practices affecting pain perception and response [14]. The greater use of pain catastrophizing among racial/ethnic minorities can also be attributed to health disparities resulting from structural and systemic barriers to adequate pain treatment and biased healthcare interactions [15,16], possibly promoting negative perceptions regarding pain management and the belief that their pain cannot be controlled and is likely to worsen. Considering the association between higher levels of pain catastrophizing and increased knee OA pain, pain catastrophizing plausibly mediates the racial disparities observed in knee OA pain between NHWs and Asian Americans.

In addition to specific pain-related factors, broader elements, such as depression and negative affect, influence knee pain experiences, and this prevails in situations involving clinical and experimentally induced pain [17-19]. Ahn et al. [20] found higher levels of depression to occur in Asian Americans with self-reported knee OA pain compared with those in age- and sex-matched NHWs, and such variations in depression evidently mediated racial group differences in clinical and experimental pain sensitivity. Negative affect, a general predisposition to experiencing aversive mood states, has been associated with racial discrimination and psychological distress among Asian Americans [21]. Daily microaggressions contribute to higher levels of somatic symptoms and negative affect within this population [22]. To date, the role of negative affect in racial disparities in knee OA pain between NHWs and Asian Americans has not yet been investigated.

Study Aim

This pilot study aimed to investigate psychological factors, specifically pain catastrophizing and negative affect, as potential explanatory mechanisms underlying racial group differences in knee OA pain between NHWs and Asian Americans. Elucidating these mechanisms may inform the development of targeted interventions that improve knee OA pain management in the understudied Asian American population and help address pain disparities across racial groups.

Study Participants

This cross-sectional analysis used baseline data from the randomized controlled trial registered at clinicaltrials.gov (NCT02512393) to examine the efficacy of transcranial direct current stimulation on knee OA pain. Detailed selection criteria and enrollment procedures have been documented previously [23]. In summary, at baseline, 40 participants with knee OA pain (20 NHWs and 20 Asian Americans) were recruited in North Central Florida between September 2015 and August 2016 through local advertisements. Participants were eligible if they were aged 50–70 years, had self-reported unilateral or bilateral knee OA pain as per American College of Rheumatology criteria, could speak and read English, and were willing and able to provide written informed consent before enrollment.

Exclusion criteria ensured participants did not have concurrent medical conditions that could confound OA-related outcomes or coexisting diseases that could impede protocol completion, including (1) prosthetic knee replacement or non-arthroscopic surgery on the affected knee, (2) serious medical illness, such as uncontrolled hypertension, heart failure, or recent history of acute myocardial infarction, (3) peripheral neuropathy, (4) systemic rheumatic disorders, such as rheumatoid arthritis, systemic lupus erythematosus, and fibromyalgia, (5) alcohol or substance abuse, (6) cognitive impairment (i.e., Mini-Mental Status Exam score ≤ 23), (7) history of brain surgery, tumor, seizure, stroke, or intracranial metal implantation, (8) pregnancy or lactation, and (9) hospitalization for psychiatric illness within the past year.

Measurement

The collected basic characteristics included age, gender, body mass index (BMI; kg/m²), Kellgren-Lawrence radiographic grade, employment status, marital status, educational attainment, and household income.

Clinical Knee OA Pain

The Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) pain subscale. Average knee pain for the past 48 hours was measured by the pain subscale of the WOMAC, which consisted of 5 items on a 0-4 Likert scale measuring the pain severity during walking, climbing stairs, sleeping, resting, and standing [24]. The participants’ responses to each pain question were summed up to derive an aggregated score for pain intensity (range 0-20). The subscales in WOMAC demonstrate reliability and validity in evaluating knee OA patients [25,26].

Short-form-McGill Pain Questionnaire-2 (SF-MPQ-2). The SF-MPQ-2 has been validated and widely used to assess the multidimensional qualities of pain [27]. It consists of four subscales, including continuous pain (6 items: throbbing pain, cramping pain, gnawing pain, aching pain, heavy pain, tender), intermittent pain (6 items: shooting pain, stabbing pain, splitting pain, electric-shock pain, piercing), neuropathic pain (6 items: hot-burning pain, cold-freezing pain, pain caused by light touch, itching, tingling or pins and needles, numbness), and affective description of pain (4 items: tiring-exhausting, sickening, fearful, punishing-cruel). Each subscale score was computed as the average of answered items, with higher scores indicating greater pain intensity.

Quantitative Sensory Testing

A multimodal quantitative sensory testing (QST) battery was completed for an assessment of pain sensitivity using precisely controlled protocols that elicit pain with thermal and mechanical stimuli. This includes heat pain (i.e., threshold and tolerance), pressure pain threshold (PPT), punctate mechanical pain (PMP), and conditioned pain modulation (CPM). The sequence of heat and mechanical testing was randomized and counterbalanced, while CPM was always administered last to minimize any potential carryover effects. Standardized recorded instructions were provided to all participants.

Thermal testing procedures. All thermal stimuli were delivered using a computer-controlled TSA-II NeuroSensory Analyzer (Medoc Ltd., Ramat Yishai, Israel) to measure heat pain thresholds and heat pain tolerances on both the index knee and the ipsilateral ventral forearm using an ascending method of limits. At each body site, the thermode position was moved between trials to prevent sensitization and/or habituation of cutaneous receptors. Starting from a baseline of 32°C, the thermode temperature increased at a rate of 0.5°C per second until participants responded by pressing a button on a handheld device. Participants were instructed to press the button when heat first becomes painful to assess the heat pain threshold, and when they could no longer tolerate the heat pain to assess heat pain tolerance. Three trials of heat pain threshold were conducted at the first test site, followed by three trials of heat pain tolerance were conducted. Then, three trials each at the second test site were conducted, with a 5-minute rest period between sites. The average of the three trials was calculated for each individual, providing overall heat pain threshold and tolerance temperatures for analysis.

Mechanical testing procedures. Mechanical pain response was measured via two approaches. First, PPT was assessed by applying blunt mechanical pressure to deep tissues (i.e., muscle and joint) via a handheld digital pressure algometer (Wagner, Greenwich, CT, USA). Increasing pressure was applied at a constant rate of 0.3 kgf/cm² per second to measure the PPT at four sites–– the medial and lateral aspects of the index knee, ipsilateral quadriceps, and trapezius. The order of testing sites was counterbalanced and randomized. For assessing PPT, participants were instructed to inform the experimenter when the sensation “first becomes painful” occurred, and the pressure was recorded. The results of the 3 trials at each body site were averaged for each site, and then these PPTs at four sites were averaged to derive an overall measure of PPT. Second, PMP stimuli evaluated cutaneous mechanical sensitivity on both the index patella and the back of the ipsilateral hand. We used calibrated nylon monofilament that delivered a target force of 300 g to obtain verbal ratings of the pain intensity on a scale of 0 (no pain sensation) to 100 (the most intense pain sensation imaginable) following 10 contacts at the rate of 1 contact per second. An overall score for each site was computed by averaging across two trials.

Conditioned pain modulation (CPM). Ten minutes after assessing the thermal or mechanical pain, the CPM was evaluated. CPM reflects the endogenous pain inhibitory pathway (i.e., descending pain inhibition) also known as the “pain inhibits pain” paradox [28] CPM was assessed by determining the change in PPT on the trapezius, immediately following the immersion of the contralateral hand up to the wrist in the cold water bath (12°C) for 1 minute. The initial pre-immersion PPT measurement was conducted just before placing the hand in the water. Thirty seconds after hand immersion, participants were asked to rate the cold pain intensity (0–100) from the immersed hand followed by the second PPT measurement and were informed to keep their hand in the water bath for as long as tolerable up to 1 minute. After the removal of the hand, the final PPT measurement was taken. This temperature was chosen based on prior experience with middle-aged and older adults with knee OA, where 12°C was found to produce moderate yet tolerable pain for most participants. Water was continually circulated and maintained at a constant temperature by a refrigeration unit (Neslab, Portsmouth, NH, USA). An increase in PPT following cold water immersion demonstrated pain inhibition.

Pain Catastrophizing

The Coping Strategies Questionnaire-Revised (CSQ-R) measures the use of strategies for coping with pain by assessing six domains–– distraction, catastrophizing, ignoring pain sensations, distancing from pain, coping self-statements, and praying. Participants rate how often they use specific strategies on a seven-point Likert scale from 0 (“never”) to 6 (“always”), with higher scores indicating greater usage for each domain. This study used the 6-item catastrophizing subscale, with scores calculated as the mean of the responses. The reliability and validity of the CSQ subscales have previously been shown to be acceptable [29,30].

Negative Affect

The Positive and Negative Affect Schedule (PANAS) includes 20 items that evaluate the frequency of both pleasant and unpleasant emotions individuals experience [31]. The inventory is divided into two subscales, each with 10 items for positive and negative emotions. Negative affect is calculated from the sum of 10 items (afraid, ashamed, distressed, guilty, hostile, irritable, jittery, nervous, scared, and upset), rated on a 5-point scale from 1 (“very slightly or not at all”) to 5 (“extremely”). A lower total negative score (PANAS-) indicates less negative affect (range: 10-50). The PANAS has been validated and demonstrates reliability, with an alpha coefficient range of .84 to .87 for negative affect [31].

Statistical Analyses

Descriptive statistics were used to evaluate participant characteristics. Composite measures for QST were created by calculating z-scores for the heat pain threshold and tolerance at the arm and knee; PPT at the medial and lateral aspects of the index knee, ipsilateral quadriceps, and trapezius; and PMP at the index patella and hand. The z-scores for each pain measure were subsequently averaged across the body sites to yield overall heat pain threshold, heat pain tolerance, PPT, and PMP values for the analyses.

Separate path analytical models were estimated to assess the indirect effects (mediation) of ethnicity (coded 0 for NHWs and 1 for Asian Americans) via pain catastrophizing or negative affect on each clinical and experimental pain measure. The path models facilitated the examination of both direct and indirect effects. Model fit, path coefficient estimates, and 95% highest posterior density (HPD) confidence intervals (CIs; “credibility” in Bayesian terms) for parameter estimates were generated using the Bayesian estimation method in Mplus (version 8.8; Muthén & Muthén, Los Angeles, CA) [32]. Bayesian estimation is advantageous in that it precludes the necessity of the normality assumption in the sampling distribution of estimates and potentially provides more accurate parameters in small-sample cases [33]. Model fit was evaluated using the criteria and methods recommended by Muthén and Asparouhov [34]. Where 95% CIs did not overlap with zero, the effect was considered significant.

Baseline characteristics comparing NHWs and Asian Americans are presented in Supplemental Table 1. Descriptive statistics for variables used in the path models are presented in Table 1. Figure 1 shows mediation path (race → mediator → pain). Fit for each of the models was acceptable, with all 95% CIs for the difference between observed and replicated χ² values encompassing 0, all posterior predictive values > .45, and convergence of posterior parameter trace plots. Tables 2 and 3 provide results of the path analysis, including direct and indirect effects and the 95% HPD CIs for each of the pain measure models.

Table 1. Descriptive statistics for pain-related outcomes, pain catastrophizing, and negative affect among NHWs and Asian Americans (N = 40).

Variable	Mean ± standard deviation
Variable	Non-Hispanic Whites (n = 20)	Asian Americans (n = 20)
WOMAC pain, range: 0-20	4.90 ± 2.55	4.40 ± 2.67
SF-MPQ-2 continuous pain, range: 0-10	1.78 ± 1.94	1.98 ± 1.37
SF-MPQ-2 intermittent pain, range: 0-10	1.28 ± 2.19	1.47 ± 1.83
SF-MPQ-2 neuropathic pain, range: 0-10	0.67 ± 0.93	1.07 ± 1.24
SF-MPQ-2 affective pain, range: 0-10	0.79 ± 1.83	1.46 ± 1.66
Heat pain threshold∗	0.49 ± 0.82	-0.49 ± 0.74
Heat pain tolerance∗	0.51 ± 0.76	-0.51 ± 0.73
Pressure pain threshold∗	0.45 ± 0.86	-0.45 ± 0.61
Punctate mechanical pain∗	-0.62 ± 0.56	0.62 ± 0.76
Conditioned pain modulation	1.29 ± 1.14	1.16 ± 0.71
Pain catastrophizing, range: 0-6	0.31 ± 0.74	1.33 ± 1.25
Negative affect, range: 10-50	14.00 ± 4.29	20.15 ± 9.02

^∗Average z-score.

Abbreviation: SF-MPQ-2, Short-form-McGill Pain Questionnaire-2; WOMAC, Western Ontario and McMaster Universities Osteoarthritis

In each model (Table 2), the direct effect of race on pain catastrophizing (Figure 1; a) indicated that Asian Americans had significantly higher pain catastrophizing scores than NHWs (difference in Ms = 1.03; 95% CI = 0.29, 1.70). Additionally, as shown in Table 3, in each model, the direct effect of race on negative affect indicated that Asian Americans yielded significantly higher negative affect scores than NHWs (difference in Ms = 6.15; 95% CI = 1.11, 10.80).

Table 2. Estimated direct and indirect effects with 95% CI (N = 40; pain catastrophizing as a mediator).

Pain outcomes (R²)	Direct effects		Indirect effect
Pain outcomes (R²)	c’ (95% CI)	b (95% CI)	ab (95% CI)
WOMAC pain (0.179)	-1.53 [-3.39, 0.25]	1.00 [0.21, 1.81]	0.96 [0.03, 2.16]
SF-MPQ-2 continuous pain (0.283)	-0.67 [-1.78, 0.40]	0.85 [0.38, 1.34]	0.84 [0.18, 1.70]
SF-MPQ-2 intermittent pain (0.187)	-0.64 [-2.07, 0.73]	0.81 [0.20, 1.43]	0.78 [0.03, 1.71]
SF-MPQ-2 neuropathic pain (0.215)	-0.06 [-0.83, 0.67]	0.45 [0.12, 0.78]	0.43 [0.03, 0.95]
SF-MPQ-2 affective pain (0.410)	-0.41 [-1.47, 0.60]	1.06 [0.61, 1.52]	1.05 [0.24, 1.99]
Heat pain threshold∗ (0.284)	-1.07 [-1.67, -0.50]	0.08 [-0.17, 0.34]	0.07 [-0.20, 0.39]
Heat pain tolerance∗ (0.304)	-0.94 [-1.52, -0.39]	-0.07 [-0.32, 0.18]	-0.06 [-0.38, 0.19]
Pressure pain threshold∗ (0.259)	-0.96 [-1.54, -0.41]	0.06 [-0.19, 0.31]	0.05 [-0.23, 0.34]
Punctate mechanical pain∗ (0.462)	1.09 [0.58, 1.57]	0.15 [-0.07, 0.37]	0.14 [-0.09, 0.43]
Conditioned pain modulation (0.168)	-0.49 [-1.7, 0.16]	0.36 [0.07, 0.65]	0.34 [0.00, 0.79]

^∗Average z-score.

c’ = direct effect of race on pain measures after controlling for pain catastrophizing; b = direct effect of pain catastrophizing on pain measures after controlling for race; ab = indirect effect of race on pain measures operating through pain catastrophizing. Significant results are indicated in bold.

Abbreviation: CI, credibility interval; SF-MPQ-2, Short-form-McGill Pain Questionnaire-2; WOMAC, Western Ontario and McMaster Universities Osteoarthritis

Direct Effect of Race on Pain Measures After Controlling for Pain Catastrophizing (Table 2)

The direct effect of race on the heat pain threshold (c’ = –1.07), heat pain tolerance (c’ = –0.94), and PPT (c’ = –0.96) indicated that Asian Americans had lower mean scores on these experimental pain measures than NHWs after controlling for pain catastrophizing. The direct effect of race on PMP (c’ = 1.09) indicated that Asian Americans generated higher mean scores on this pain measure than NHWs after controlling for pain catastrophizing. After controlling for pain catastrophizing, Asian American and NHW participants yielded similar mean scores for clinical pain measures.

Direct and Indirect Effect of Pain Catastrophizing on Pain Measures (Table 2)

Pain catastrophizing exhibited positive direct effects, while race exerted positive indirect effects through pain catastrophizing on WOMAC (b = 1.00, ab = 0.96), SF-MPQ-2 continuous (b = 0.85, ab = 0.84), SF-MPQ-2 intermittent (b = 0.81, ab = 0.78), SF-MPQ-2 neuropathic (b = 0.45, ab = 0.43), and SF-MPQ-2 affective (b = 1.06, ab = 1.05) pain. These results indicate that participants with higher pain catastrophizing scores tended to have higher values on these pain measures after controlling for race. Considering that race had no direct effects on these pain scores but exerted indirect effects via pain catastrophizing, the effects of race were likely fully mediated through pain catastrophizing for these measures. After controlling for race, we did not identify any direct effects of pain catastrophizing on the heat pain threshold, heat pain tolerance, PPT, and PMP. Surprisingly, pain catastrophizing exhibited positive direct effects on CPM (b = 0.36).

Table 3. Estimated direct and indirect effects with 95% CI (N = 40; negative affect as a mediator).

Pain outcomes (R²)	Direct effects		Indirect effect
Pain outcomes (R²)	c’ (95% CI)	b (95% CI)	ab (95% CI)
WOMAC pain (0.091)	-1.05 [-2.92, 0.83]	0.09 [-0.03, 0.22]	0.50 [-0.23, 1.59]
SF-MPQ-2 continuous pain (0.094)	-0.17 [-1.36, 1.04]	0.06 [-0.02, 0.14]	0.34 [-0.13, 1.04]
SF-MPQ-2 intermittent pain (0.155)	-0.45 [-1.83, 0.95]	0.11 [0.02, 0.20]	0.59 [-0.04, 1.48]
SF-MPQ-2 neuropathic pain (0.186)	0.04 [-0.70, 0.80]	0.06 [0.01, 0.11]	0.34 [-0.03, 0.80]
SF-MPQ-2 affective pain (0.108)	0.32 [-0.93, 1.59]	0.06 [-0.02, 0.14]	0.32 [-0.17, 1.04]
Heat pain threshold∗ (0.274)	-1.01 [-1.58, -0.43]	0.00 [-0.03, 0.04]	0.02 [-0.25, 0.27]
Heat pain tolerance∗ (0.297)	-1.01 [-1.56, -0.45]	-0.00 [-0.04, 0.04]	-0.00 [-0.25, 0.26]
Pressure pain threshold∗ (0.255)	-0.94 [-1.49, -0.38]	0.01 [-0.03, 0.04]	0.03 [-0.22, 0.29]
Punctate mechanical pain∗ (0.453)	1.13 [0.65, 1.62]	0.02 [-0.01, 0.05]	0.09 [-0.10, 0.36]
Conditioned pain modulation (0.039)	-0.15 [-0.85, 0.56]	0.01 [-0.04, 0.05]	0.02 [-0.31, 0.33]

^∗Average z-score.

c’ = direct effect of race on pain measures after controlling for negative affect; b = direct effect of negative affect on pain measures after controlling for race; ab = indirect effect of race on pain measures operating through negative affect. Significant results are indicated in bold.

Abbreviation: CI, credibility interval; SF-MPQ-2, Short-form-McGill Pain Questionnaire-2; WOMAC, Western Ontario and McMaster Universities Osteoarthritis

Direct Effect of Race on Pain Measures After Controlling for Negative Affect (Table 3)

Based on the direct effect of race on the heat pain threshold (c’ = –1.01), heat pain tolerance (c’ = –1.01), and PPT (c’ = –0.91), Asian Americans yielded higher mean scores on these experimental pain measures than NHWs after controlling for negative affect. The direct effect of race on PMP (c’ = 1.13) indicated that Asian Americans had higher mean scores on this pain measure than NHWs after controlling for negative affect. Race had no direct effect on CPM. After controlling for negative affect, Asian American and NHW participants were found to have similar mean scores for all clinical pain measures.

Direct and Indirect Effect of Negative Affect on Pain Measures (Table 3)

We exclusively detected direct effects of negative affect on SF-MPQ-2 intermittent (b = 0.11) and SF-MPQ-2 neuropathic (b = 0.06) pain after controlling for race. Race exerted no indirect effects on pain measures via negative affect in any of the path models.

This pilot study explored whether variations in pain catastrophizing affect racial group differences in clinical and experimental pain sensitivity between NHWs and Asian Americans with knee OA. Asian Americans had significantly higher pain catastrophizing scores than NHWs. It is plausible that cultural values prevalent in Asian communities may discourage the open expression of chronic pain to avoid burdening others [35,36]. This cultural disposition causes Asian Americans to suffer silently, thus amplifying their mental agony. Furthermore, Asian cultural communication styles often prioritize indirectness and subtlety, which can result in less effective communication with healthcare providers from different cultural backgrounds regarding pain experiences [37]. This communication gap may hinder effective pain management and perpetuate a cycle of unexpressed and poorly managed knee OA pain, thereby contributing to higher levels of pain catastrophizing compared to NHWs.

Additionally, regardless of race, pain catastrophizing was significantly associated with greater clinical pain, resonating with previous studies [11-13]. Our study expands on previous investigations by identifying pain catastrophizing as a significant contributor to racial group differences in clinical pain between NHWs and Asian Americans; specifically, Asian Americans exhibited increasing clinical pain scores with increasing pain catastrophizing. This cycle of increased pain perception and psychological distress highlights the complex interplay between physical pain and mental health [38], emphasizing the need for integrated approaches to pain management that address Asian Americans’ physical and psychological needs.

Asian Americans reported greater experimental pain sensitivity (heat pain, PPT, and PMP) than NHWs, replicating previous findings on middle-aged and older adults with knee OA [9] and similar reports on younger Asian Americans [39]. Furthermore, heightened sensitivity occurred at both the affected knee and unaffected body sites, suggesting increased central sensitization. However, pain catastrophizing could not explain the racial group differences in any measures of experimental pain sensitivity in this study. This contradicts previous studies wherein pain catastrophizing was found to influence racial group differences in QST measures among non-clinical samples [40] and patients with chronic low back pain [41]. Several explanations can be proposed for such findings. First, according to Meints et al. [42], who found that racial group differences in cold pain tolerance (NHWs vs. African Americans) were mediated by the rumination component of pain catastrophizing but not by the magnification or helplessness components, examining the mediatory effects of different pain catastrophizing components may yield varied results. Second, other critical factors, such as biological or genetic mechanisms, possibly influence the observed differences. For instance, Rowell et al. [39] found that differences in endogenous pain regulatory mechanisms, such as mean arterial pressure and heart rate, potentially play a role in the differences in experimental pain sensitivity between young NHWs and Asian Americans. Based on earlier evidence, genetic links to pain phenotypes differ according to racial/ethnic group, potentially generating dissimilarities in pain sensation. For example, pain sensitivity has been associated with variations in the catechol-O-methyltransferase (COMT) [43] and μ-opioid receptor (OPRM1) genes [44]. Moreover, frequency differences in the alleles of pain-related gene polymorphisms may contribute to racial/ethnic disparities in pain responses [45].

Asian Americans yielded significantly greater negative affect scores than NHWs. Although a higher negative affect score significantly correlated with both intermittent and neuropathic pain (measured using the SF-MPQ-2), race had no indirect effects on any pain measures via negative affect. Various negative affect-related constructs are important to pain; nevertheless, they differ in specificity and are conceptually distinct; some constructs are general, such as anxiety, depression, and negative affect, whereas others are more specifically pain-related, such as fear of pain, pain anxiety, and pain catastrophizing [46]. Overall, our preliminary findings suggest that pain-specific variables (i.e., pain catastrophizing) should be prioritized over general negative affect to minimize pain disparities between NHWs and Asian Americans. However, further studies involving larger sample sizes are necessary to confirm our findings. In fact, a study by Ahn et al. [9], which established that higher depression levels in Asian Americans than in NHWs explained racial group differences in clinical and experimental pain sensitivity, included 50 participants per group. Additionally, we could not account for covariates, such as sex, age, and pain-related medication, owing to the small sample sizes in the path models, which might have affected the results.

Limitations

This study has certain limitations. First, the findings may not be generalizable as they are based on a convenience sample from a specific region; moreover, the Asian American participants were limited to English speakers. Second, the cross-sectional design hindered our ability to discern the directionality of the relationships between variables. Indeed, evidence suggests that pain catastrophizing may not be a characterological trait but a complex phenomenon that can both affect and be affected by pain [47]. Kim et al. argue that as clinical pain scores increase, a sense of helplessness or an inability to control chronic knee pain may develop, contributing to higher levels of pain catastrophizing in Asian Americans [35]. These important relationships warrant further investigation in future studies. Finally, we acknowledge that the term “pain catastrophizing” can considered pejorative and stigmatizing, conflicting with patient-centered care approaches [48]. Labeling patients in this manner potentially leads to blame and stereotyping, adversely affecting decision-making and care quality. Recent analyses have proposed that “pain-related worrying” and “pain-related distress” may better capture the essence of what is measured by pain catastrophizing items [49].

Future Research Directions & Clinical Implications

This pilot study’s findings provide a crucial foundation for future research and clinical practice. Considering the limited sample size, we analyzed each mediatory effect separately. Future studies including larger samples may employ more sophisticated models to concurrently examine a broader range of factors, thereby more comprehensively elucidating the mechanisms underlying racial disparities in pain between NHWs and Asian Americans; in addition to pain catastrophizing and negative affect, as previously discussed, future research should investigate biological, genetic, and other psychological variables essential to understanding chronic knee OA pain and evaluate them as explanatory mechanisms to develop more tailored interventions.

Additionally, our findings highlight the need to systematically assess and treat pain catastrophizing in Asian Americans in healthcare settings to ensure effective pain management, which is imperative, considering the cultural emphasis on pain-related stoicism in this minority population. Interventions targeting this maladaptive cognitive style among Asian Americans may help mitigate racial disparities in clinical pain. In particular, the interventions should be culturally sensitive and tailored by further scrutinizing the factors influencing pain catastrophizing in Asian Americans. If acculturative stress influences pain catastrophizing, then therapy for pain catastrophizing (e.g., cognitive behavioral therapy) could be enhanced by focusing on culturally sensitive stress management techniques.

This pilot study examined psychological factors, specifically pain catastrophizing and negative affect, as potential explanatory mechanisms behind racial group differences in clinical and experimental pain sensitivity between NHWs and Asian Americans with knee OA pain. Apparently, pain catastrophizing is essential to addressing racial disparities in clinical knee OA pain; however, further research is warranted to verify our findings and elucidate unresolved mechanisms.

CPM: conditioned pain modulation

CSQ-R: Coping Strategies Questionnaire-Revised

HPD: highest posterior density

NHWs: non-Hispanic Whites

OA: osteoarthritis

PANAS: Positive and Negative Affect Schedule

PPT: pressure pain threshold

QST: quantitative sensory testing

SF-MPQ-2: Short-form-McGill Pain Questionnaire-2

WOMAC: Western Ontario and McMaster Universities Osteoarthritis Index

Acknowledgments

The authors would like to extend their sincere thanks to all participants who took part in the study.

Funding

This study was supported by the NIH/NINR Grant R15NR018050. The original study is registered at www.clinicaltrials.gov (NCT04016272).

Authors' Contributions

Chiyoung Lee: Conceptualization, Investigation, Methodology, Formal analysis, Writing - original draft, Kent Kwoh: Investigation, Resources, Supervision, Writing - review & editing, Juyoung Park: Conceptualization, Investigation, Supervision, Writing - review & editing, Hyochol Ahn: Conceptualization, Funding acquisition, Investigation, Project administration, Resources, Supervision, Writing - review & editing.

Conflicts of Interest

None declared.

Ethics Approval and Consent to Participate

The Institutional Review Board (IRB) of University of Arizona (UA) considers investigators engaged in research if they: (1) interact with participants for research purposes; (2) have access to identifying study information; (3) obtain informed consent from research participants; or (4) the UA directly receives part of federal funds for the study (i.e., UA is the prime awardee). If none of the above are true, then the researchers would not need IRB approval. Thus, this present secondary analysis of de-identified data from an existing randomized controlled trial does not need any IRB approval. Informed and written consent was obtained from all subjects involved in the original study.

Availability of Data and Materials

The datasets generated and/or analyzed during the current study are not publicly available (for the protection of participants’ personal information).

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Supplementary Table 1 is not available with this version.

The authors declare no competing interests.

Racial Disparities in Pain Between Non-Hispanic Whites and Asian Americans with Knee Osteoarthritis: The Role of Pain Catastrophizing

Status:

Version 1

Abstract

Figures

Introduction

Study Aim

Methods

Study Participants

Measurement

Clinical Knee OA Pain

Quantitative Sensory Testing

Pain Catastrophizing

Negative Affect

Statistical Analyses

Results

Direct Effect of Race on Pain Measures After Controlling for Pain Catastrophizing (Table 2)

Direct and Indirect Effect of Pain Catastrophizing on Pain Measures (Table 2)

Direct Effect of Race on Pain Measures After Controlling for Negative Affect (Table 3)

Direct and Indirect Effect of Negative Affect on Pain Measures (Table 3)

Discussion

Limitations

Future Research Directions & Clinical Implications

Conclusion

Abbreviations

Declarations

References

Supplementary Tables

Additional Declarations

Status:

Version 1