The Effect of Stress Urinary Incontinence on Kinesiophobia in Postmenopausal Women with Osteoporosis: A Cross-Sectional Study

Abstract

Background

This study aimed to examine whether stress urinary incontinence (SUI) was associated with kinesiophobia in women with postmenopausal osteoporosis.

Methods

This cross-sectional study included 83 women diagnosed with postmenopausal osteoporosis, including those with SUI (n = 47) and those without (n = 36). Participants’ kinesiophobia level was evaluated using the Tampa Scale of Kinesiophobia (TSK), and their mood was assessed using the Hospital Anxiety and Depression Scale (HADS), which includes two subscales: the HADS-Anxiety (HADS-A) and HADS-Depression (HADS-D). SUI severity was evaluated with the International Consultation on Incontinence Questionnaire-Short Form (ICIQ-SF), and the effect of SUI on quality of life was assessed via the Incontinence Quality of Life Scale (I-QOL). Independent-samples t-tests were used for between-group comparisons, Pearson correlation analyses were used to assess associations between variables, and hierarchical and multiple linear regression analyses were conducted.

Results

The groups are similar in age, bone mineral density, and HADS-A scores. The HADS-D (p = 0.004) and TSK (p = 0.032) scores are higher in the SUI group. A positive correlation is found between the ICIQ-SF and TSK scores (r = 0.59, p < 0.001). According to hierarchical multiple linear regression analysis, adding the SUI as variable to the model further increased the explained variance in the TSK score by 7.3% (p = 0.008). The ICIQ-SF score was associated with the TSK score (B = 0.52, p < 0.001).

Conclusions

These findings support considering SUI as one of several clinically relevant factors in the evaluation of postmenopausal osteoporosis, particularly in relation to kinesiophobia and comprehensive patient assessment.

Introduction

Osteoporosis is a systemic skeletal disease characterized by decreased bone mineral density and impaired bone microarchitecture, which increases the risk of fractures. The incidence of hip fractures, the most serious complication of osteoporosis, increases significantly with age and has become one of the leading causes of mortality and morbidity in older adults. The global prevalence of osteoporosis is 19.7%, and the incidence of hip fracture in individuals aged 55 and older is 681.35 per 100,000 people [1, 2].​ Given the high prevalence of osteoporosis and the serious consequences of hip fractures, clinical management should focus not only on treating established disease but also on reducing factors that accelerate ongoing bone loss. One of the most essential accelerators of bone loss is immobilization. Therefore, physical activity is a fundamental component of osteoporosis management, serving both as a protective and a therapeutic strategy [3​]. However, there is a need to better understand the behavioral and psychosocial barriers that may limit physical activity, as this issue has not been adequately investigated.

Internal and external forces acting during physical activity cause small deformations in bone tissue, thereby creating mechanical stress. This mechanical stress stimulates osteoblastic activity and suppresses osteoclastic activity, thereby facilitating the preservation of bone mass and the formation of new bone tissue. Mechanical loading associated with physical activity has also been reported to improve the quality of trabecular and cortical bone [4, 5]. However, concerns about fracture risk in individuals with osteoporosis may increase the tendency to avoid movement. The fear of fragile bones can lead to a cycle of reduced physical activity and further bone loss [6]. Therefore, identifying fear and avoidance-related barriers to physical activity is clinically important in individuals with osteoporosis.

Kinesiophobia is defined as an excessive and irrational fear of movement due to pain or the risk of re-injury. Within the fear-avoidance framework, pain catastrophizing may lead individuals to avoid activities they anticipate will provoke pain, resulting in reduced physical activity. The resulting prolonged physical inactivity can lead to impaired musculoskeletal function, loss of balance, depression, and social isolation [7, 8]. Factors such as age, history of fractures, and mood significantly influence kinesiophobia [9]. In addition to these factors, stress urinary incontinence (SUI) may represent an important psychosocial stressor that contributes to kinesiophobia. In this context, movement may be avoided not only because of pain-related concerns, but also because of anticipated urinary leakage, embarrassment, or perceived harm. Thus, SUI may contribute to kinesiophobia through behavioral and psychosocial pathways in an osteoporosis population. Despite this plausible fear-avoidance pathway, the relationship between SUI and kinesiophobia in postmenopausal women with osteoporosis has not been adequately investigated.

Urinary incontinence is quite common in women with decreased bone mineral density. Approximately 40% of women with osteoporosis or osteopenia are reported to experience urinary incontinence once a week or more [10]. This high prevalence rate underscores the potential biomechanical and hormonal relationships between osteoporosis and urinary incontinence. Changes such as urethral mucosal atrophy, deterioration of collagen structure, and decreased urethral closure pressure resulting from decreased estrogen levels during postmenopause may predispose women to urinary incontinence [11]. In addition, vertebral compression fractures and postural changes that reduce pelvic floor muscle strength or increase intra-abdominal pressure may also contribute to the development of urinary incontinence [12].

SUI is the most common type of urinary incontinence and affects women of all ages. SUI is particularly common during exercise and is more prevalent in women who participate in high-impact activities [13]. Previously reported that, the presence of urinary incontinence is an important factor that reduces physical activity levels, limits social participation, and increases the risk of falls in women [14]. Therefore, urinary incontinence may indirectly accelerate the progression of osteoporosis.

Although many studies have examined the prevalence of kinesiophobia in individuals with osteoporosis, there is a dearth of research examining the effect of SUI on kinesiophobia in postmenopausal osteoporosis patients [15]. This study aims to fill this gap by investigating the impact of SUI on kinesiophobia in postmenopausal women with osteoporosis. Our study hypothesis suggests that the presence of SUI in individuals with osteoporosis leads to a increase in kinesiophobia levels. Establishing this relationship may contribute to planning multidisciplinary rehabilitation strategies for osteoporosis management and to a more comprehensive approach to pelvic floor dysfunction.

Materials and methods

This cross-sectional study was conducted at the Physical Medicine and Rehabilitation Clinic of Sivas Cumhuriyet University Health Services Application and Research Hospital between April 1, 2022, and March 31, 2023. A total of 83 community-dwelling women participated in the study. The research protocol was approved by the Local Ethics Committee (Decision No: 2022-03/32). The entire research process was conducted in accordance with the ethical principles of the Declaration of Helsinki and the Good Clinical Practice guidelines. All participants were provided with detailed information about the study, and written and verbal informed consent was obtained from all participants prior to enrollment.

Inclusion criteria were: (1) postmenopausal women, (2) osteoporosis defined as a T-score of − 2.5 or lower at either the femoral neck or the lumbar spine (L1–L4) measured by dual-energy X-ray absorptiometry, (3) independence in activities of daily living, and (4) sufficient cognitive ability to complete the questionnaires. Exclusion criteria were: (1) either urge urinary incontinence or mixed urinary incontinence, (2) history of falls or fractures within the past year, (3) acute or chronic musculoskeletal pain, (4) neurological or musculoskeletal diseases that could limit mobility, (5) treatment for urinary incontinence within the past year, and (6) psychiatric disorders.

Participants were divided into two groups according to urinary incontinence status: women with a prior physician-confirmed clinical diagnosis of SUI (n = 47), based on symptom-based clinical criteria consistent with International Continence Society terminology, and women without urinary incontinence (n = 36). No new SUI diagnosis was established as part of this study. SUI status was determined from the participants’ medical history/clinical records at the time of recruitment.

Sociodemographic and clinical data, including age, height, weight, body mass index (BMI), comorbidities, T-score of the femoral neck and the lumbar spine (L1–L4), and current osteoporosis treatment status, were collected for all participants. BMI was calculated by dividing weight in kilograms by height in meters squared (kg/m²).

The assessment process involved several validated scales. Kinesiophobia was measured using the Tampa Scale of Kinesiophobia (TSK), while the Hospital Anxiety and Depression Scale (HADS) evaluated participants’ mood. SUI severity was determined using the International Continence Questionnaire-Short Form (ICIQ-SF), and the impact of SUI on quality of life was assessed with the Incontinence Quality of Life Scale (I-QOL). Questionnaires and assessments were administered during the same study visit in the clinic setting using a standardized assessment procedure. TSK and HADS were administered by one evaluator, whereas ICIQ-SF and I-QOL were scored by a different evaluator. To reduce assessment bias, the evaluator responsible for the TSK and HADS was blinded to participants’ SUI status. Before study initiation, the evaluators were trained in the study protocol and in the administration/scoring of all instruments to ensure consistency. Standardized instructions were provided to all participants, and procedural questions were clarified without influencing responses.

The TSK is a 17-item questionnaire developed for musculoskeletal pain, with established validity and reliability in Turkish version [16]. The scale uses a 4-point Likert scoring system for each question (1 = strongly disagree, 2 = disagree, 3 = agree, 4 = strongly agree). Based on their answers, individuals receive a total score ranging from 17 to 68. A high score on the scale indicates a high level of kinesiophobia.

The Hospital Anxiety and Depression Scale (HADS), comprising the HADS-Anxiety (HADS-A) and HADS-Depression (HADS-D) subscales, was used to assess the patients’ emotional state. There are 14 questions per subscale, each ranging from 0 to 21 points. Higher scores indicate a worse mood. Turkish version of the HADS is valid and reliable [17].

The ICIQ-SF, used to determine the severity of urinary incontinence, assesses the prevalence, frequency, and amount of urinary leakage, the perceived causes of urinary leakage, and its impact on quality of life. Scores on the scale range from 0 to 21. High scores indicate severe incontinence. The validity and reliability of this questionnaire in Turkish version have been confirmed by Çetinel et al. [18].

The I-QOL consists of 22 questions: eight examining behavioral limitations, nine assessing psychosocial impact, and five related to social isolation. Questions are scored on a scale of 1 to 5. Unlike other scales, this one shows that as the score increases, the individual’s quality of life improves. The validity and reliability study for Turkish version of the scale was conducted by Eyigor et al. [19].

Statistical analysis

The sample size was calculated using G*Power 3.1 software (Heinrich-Heine-Universität, Düsseldorf, Germany) based on the pilot study findings. After reaching 10 participants in each group, the analysis found that the TSK score for individuals with osteoporosis and SUI was 45.3 ± 6.0, whereas the score for individuals without incontinence was 41.5 ± 6.2. The effect size coefficient (Cohen’s d) calculated for this difference was 0.63. Based on this value, a G*power analysis was performed using the assumptions of a t-test for two independent groups, α = 0,05, 1 − β = 0,80 (power = 80%), and effect size d = 0.63. The results indicated that 83 participants would be sufficient to achieve the study’s statistical power.

The distribution of continuous variables was assessed using the Shapiro–Wilk test together with visual methods, including histograms and probability plots. For continuous variables, homogeneity of variances across groups was assessed using Levene’s test. No substantial deviation from normality was observed, variances were homogeneous, and the distributions were considered acceptable for the parametric analyses. Descriptive statistics are presented as mean ± standard deviation for continuous variables and as frequencies and percentages for categorical variables. Between-group differences were analysed using the independent-samples t-test for continuous variables and the chi-square test or Fisher’s exact test for categorical variables, as appropriate. In the SUI subgroup, the associations between ICIQ-SF, I-QOL, and TSK were examined using Pearson’s correlation coefficient. In addition, sensitivity analyses were performed using alternative approaches, including Welch’s t-test and the Mann–Whitney U test for between-group comparisons and Spearman correlation analysis for bivariate associations. These sensitivity analyses did not materially alter the direction or statistical interpretation of the findings.

Regression analyses were performed as secondary analyses to further examine the association between SUI and TSK scores after accounting for key measured clinical and psychosocial variables. Two main regression models were specified. First, a hierarchical multiple linear regression analysis was performed in the full sample (observations per predictor: 10.4). Second, a multiple linear regression analysis was conducted in the subgroup of participants with SUI (observations per predictor: 5.9).

A hierarchical multiple linear regression analysis was performed in the full sample using two models to examine the association between SUI and TSK scores. The first model included age, BMI, comorbidity status (present/absent), HADS-A and HADS-D, and femoral neck and lumbar spine T-scores. The second model included SUI (present/absent) variable in addition to these variables. The models’ explanatory power was evaluated using R² and ΔR² values, and their overall fit was assessed using the F test.

In participants with SUI, an additional exploratory multiple linear regression analysis was performed to evaluate the independent association between urinary incontinence severity and TSK scores, given the limited subgroup sample size relative to the number of predictors. In this model, age, BMI, comorbidity, HADS subscales, T-score of the femoral neck and the lumbar spine, and ICIQ-SF score were included as independent variables. The relative effects of the variables were evaluated using standardised beta (β) coefficients. Additionally, to provide a complementary assessment of the robustness of the subgroup findings, a sensitivity analysis was conducted using a more parsimonious regression model including four predictors (age, HADS-D, lumbar spine T-score, and ICIQ-SF), given the relatively limited subgroup sample size and the potential risk of model overfitting with the eight-predictor model.

Regression assumptions were assessed before interpretation of all models. Residual normality was evaluated using graphical and numerical diagnostics, and visual inspection of the histogram and normal P–P plot did not indicate major deviation from normality (full sample: Shapiro–Wilk = 0.982, p = 0.313; subgroup: Shapiro–Wilk = 0.978, p = 0.495). Residual statistics were also examined (full sample: standardized residuals = − 2.749 to 1.851, studentized deleted residuals = − 2.901 to 1.988; subgroup: standardized residuals = − 2.079 to 1.527, studentized deleted residuals = − 2.504 to 1.716). Influential observations were assessed using Cook’s distance, and no highly influential case was identified (full sample: maximum = 0.208; subgroup: maximum = 0.417). The Durbin–Watson statistic suggested no substantial autocorrelation of residuals (full sample: 1.986; subgroup: 2.247). In addition, multicollinearity diagnostics were within acceptable limits in both models (full sample: tolerance 0.688–0.972, VIF 1.029–1.454; subgroup: tolerance 0.544–0.797, VIF 1.254–1.839). Visual inspection of residual plots did not suggest major violations of linearity or homoscedasticity.

All statistical analyses were performed using IBM SPSS Statistics for Windows, version 22.0 (IBM Corp., Armonk, NY, USA). The level of statistical significance was set at 0.05. Effect sizes were reported as Cohen’s d with 95% confidence intervals for continuous between-group comparisons and as Cohen’s f² for the regression analyses.

Results

This study includes a total of 83 participants, 47 with SUI and 36 without SUI. The mean age of the participants was 67.8 (4.7) years in the group with SUI and 66.3 (5.7) years in the group without SUI. All participants were receiving pharmacological treatment for osteoporosis; 91.5% (n = 43) of participants with SUI and 88.9% (n = 32) of participants without SUI were receiving bisphosphonate therapy. No participants were receiving hormone replacement therapy. The sociodemographic and clinical characteristics of the two groups, including age, BMI, comorbidities, and osteoporosis treatment regimen were similar (Table 1).

Table 1.

Demographic and clinical characteristics of the participants according to SUI status

	Patients with SUI (n = 47)	Patients without SUI (n = 36)	p value	Cohen’s d (95% Cl)
Age, years	67.8 ± 4.7	66.3 ± 5.7	0.20	0.29(-0.15 to 0.73)
BMI, kg/m2	26.9 ± 2.8	27.6 ± 4.2	0.33	-0.20 (-0.64 to 0.23)
Comorbidity			0.46
DM	6(12.8)	5(13.9)
HT	15(31.9)	18(50)
Hypothyroidism	1(2.1)	3(8.3)
CAD	1(2.1)	5(13.9)
Asthma	2(4.3)	1(2.8)
DXA T-score
Lumbar Spine T-score	-2.8 ± 0.6	-2.7 ± 0.9	0.49	-0.13 (-0.57 to 0.30)
Femur Neck T-score	-1.2 ± 0.8	-1.3 ± 1.0	0.77	0.11 (-0.32 to 0.55)
Current osteoporosis treatment			0.72
Bisphosphonate + cholecalciferol	43(91.5)	32(88.9)
Alendronate + cholecalciferol	21(44.6)	14(38.8)
Ibandronate + cholecalciferol	17(36.1)	9(25)
Zoledronic acid + cholecalciferol	5(10.6)	8(22.2)
Denosumab + cholecalciferol	4(8.5)	4(11.1)
HADS-A	7.7 ± 4.6	6.1 ± 4.0	0.08	0.37 (-0.07 to 0.81)
HADS-D	9.2 ± 4.6	6.3 ± 3.8	0.004	0.68 (0.23 to 1.13)

Abbreviations: BMI Body mass index, DM Diabetes mellitus, HT Hypertension, CAD Coronary artery disease, DXA Dual-energy X-ray absorptiometry, HADS-A Hospital anxiety and depression scale anxiety score, HADS-D Hospital anxiety and depression scale depression score, SUI Stress urinary incontinence

Participants with SUI had similar HADS-A, lumbar spine T-scores, and femoral neck T-scores to those without SUI, whereas HADS-D scores were higher in those with SUI (p = 0.004, Cohen’s d = 0.68, 95% CI 0.23 to 1.13) (Table 1). The mean TSK score was 44.9 ± 6.3 in participants with SUI and 41.8 ± 6.4 in those without SUI; this between-group difference was statistically significant (p = 0.03, Cohen’s d = 0.49, 95% CI 0.05 to 0.93) (Figure 1).

Fig. 1.

Comparison of the tampa scale of kinesiophobia between participants with (n = 47) and without SUI (n = 36). Bars represent mean values and error bars indicate standard deviations. A significant difference was observed between the groups (p = 0.03). SUI: Stress urinary incontinence

Participants with SUI had a mean ICIQ-SF score of 11.2 (4.4) and an I-QOL score of 86.1 (16.6). A positive statistically significant correlation was observed between the ICIQ-SF score and the TSK score in participants SUI (r = 0.59, p < 0.001) (Figure 2). However, no correlation was found between the I-QOL score and the TSK score in participants SUI (r = 0.17, p = 0.25).

Fig. 2.

Correlation analysis between the tampa scale of kinesiophobia and ICIQ-SF in the participants with SUI (n = 47). Correlation analysis was performed in participants with SUI. Each point represents an individual participant. The solid line represents the linear regresyon line illustrating the association between TSK and ICIQ-SF score. Pearson correlation analysis showed a significant positive correlation between the variables (r = 0.59, p < 0.001)

Whether the presence of SUI contributed to the variance in the TSK score was investigated using hierarchical multiple linear regression (Table 2). The first model, consisting of age, BMI, comorbidity, HADS-D, HADS-A, and femoral neck and lumbar spine T-scores explained 17.2% of the variance in the TSK scale score [F(7,75) = 2.2, p = 0.041, Cohen’s f² = 0.21]. The second model, which was created by adding the SUI variable to the first model, increased the explanatory power of the TSK scale score by an additional 7.3% [ΔF(1,74) = 7.32, p = 0.008, Incremental Cohen’s f² = 0.11].

Table 2.

Results of the hierarchical multiple linear regression analysis for TSK scores in all participants (n=83)

	Unstandardized B	Std. Error	%95 CI		Standardized Beta	t	p
			Lower	Upper
Model 1
Constant	37.167	11.649	13.961	60.374		3.191	0.002
Age, years	-0.118	0.136	-0.390	0.154	-0.094	-0.865	0.39
BMI, kg/m2	0.248	0.205	-0.160	0.656	0.134	1.210	0.23
Comorbidity	0.767	1.003	-1.230	2.764	0.085	0.765	0.44
Lumbar Spine T-score	-0.564	0.842	-2.240	1.113	-0.069	-0.670	0.50
Femoral Neck T-score	0.181	0.986	-1.783	2.144	0.021	0.183	0.85
HADS-D	0.523	0.180	0.164	0.881	0.353	2.903	0.005
HADS-A	0.225	0.173	-0.119	0.569	0.156	1.303	0.19
R = 0.415 R2 = 0.172 Adj. R² = 0.095 Cohen’s f² = 0.21 F(7, 75) = 2.20 p = 0.041
Model 2
Constant	36.014	11.659	12.784	59.245		3.089	0.003
Age, years	-0.114	0.136	-0.385	0.157	-0.091	-0.837	0.40
BMI, kg/m2	0.276	0.206	-0.133	0.686	0.149	1.343	0.18
Comorbidity	0.285	1.080	-1.866	2.436	0.031	0.264	0.79
Lumbar spine T-Score	-0.481	0.842	-2.159	1.197	-0.058	-0.571	0.57
Femoral Neck T-score	0.051	0.989	-1.920	2.021	0.006	0.051	0.95
HADS-D	0.508	0.180	0.149	0.867	0.343	2.821	0.006
HADS-A	0.191	0.175	-0.157	0.539	0.132	1.093	0.27
SUI presence	2.276	1.042	0.108	4.261	0.139	2.185	0.038
R = 0.494 R2 = 0.245 Adj. R² = 0.163 Cohen’s f² = 0.32 F(8, 74) = 3.00 p = 0.006

Abbreviations: BMI Body mass index, HADS-D Hospital anxiety and depression scale depression score, HADS-A Hospital anxiety and depression scale anxiety score, SUI Stress Urinary Incontinence

Bold values indicate statistically significant results (p < 0.05)

The results of the multiple linear regression analysis of TSK scores in participants with SUI are shown in (Table 3). The model accounted for 58.5% of the variance in TSK scores (F(8,38) = 6.70, p < 0.001, Cohen’s f²= 1.41). ICIQ-SF score was independently associated with higher TSK scores (B = 0.748, 95% CI = 0.409 to 1.086, β = 0.521, p < 0.001). In the parsimonious sensitivity model including age, HADS-D, lumbar spine T-score, and ICIQ-SF, ICIQ-SF remained significantly associated with TSK scores (B = 0.771, 95% CI = 0.409 to 1.134, β = 0.538, p < 0.001), while HADS-D was also independently associated with TSK scores (B = 0.460, 95% CI = 0.132 to 0.788, β = 0.334, p = 0.007), although the overall explained variance was lower (R² = 0.466, F(4,42) = 9.153, p < 0.001, Cohen’s f²= 0.873).

Table 3.

Results of Exploratory multiple linear regression analysis of TSK scores in participants with SUI (n = 47)

	Unstandardized B	Std. Error	%95 CI		Standardized Beta	t	p
			Lower	Upper
Constant	9.836	14.104	-18.717	38.388		0.697	0.49
Age, years	0.103	0.171	-0.243	0.449	0.204	0.602	0.55
BMI, kg/m2	0.448	0.283	-0.124	1.021	0.204	1.585	0.12
Comorbidity	0.839	1.003	-1.190	2.869	0.100	0.837	0.40
Lumbar Spine T-Score	-0.504	1.137	-2.805	1.798	-0.055	-0.443	0.66
Femoral Neck T-score	-1.684	1.060	-3.829	0.461	-0.223	-1.589	0.12
HADS-A	-0.006	0.177	-0.363	0.351	-0.004	-0.035	0.97
HADS-D	0.314	0.200	-0.092	0.720	0.228	1.567	0.12
ICIQ-SF	0.748	0.167	0.409	1.086	0.521	4.475	< 0.001
R = 0.764 R² = 0.585 Adj. R² = 0.498 Cohen’s f²= 1.41 F(8,38) = 6.70 p = < 0.001

Abbreviations: BMI Body mass index, HADS-D Hospital anxiety and depression scale depression score, HADS-A Hospital anxiety and depression scale anxiety score, ICIQ-SF International Continence Questionnaire-Short Form, SUI Stress Urinary Incontinence

Bold values indicate statistically significant results (p < 0.05)

Discussion

In this cross-sectional study examining the association between SUI and kinesiophobia in postmenopausal women with osteoporosis, participants with SUI had significantly higher kinesiophobia scores than those without SUI. In addition, greater severity of SUI was associated with higher levels of kinesiophobia. Women with SUI also had higher depressive symptom scores, and higher HADS-D scores were associated with higher TSK scores in the overall sample. Taken together, these findings add to the existing osteoporosis literature by suggesting that SUI may be one of the clinical factors linked to kinesiophobia in this population.

Fear is one of the core protective mechanisms that supports survival and includes both innate and learned emotional responses. Although learned threat responses are largely processed through amygdala-centered neural circuits, the hippocampus and medial prefrontal cortex also play important roles in contextual threat evaluation and safety learning [20]. In musculoskeletal conditions, fear may arise not only from ongoing pain, but also from previous negative experiences, perceived bodily fragility, and beliefs that movement could result in injury or physical harm [21, 22]. Within the fear-avoidance model, individuals who view bodily sensations or movement as temporary and manageable are more likely to develop a more adaptive coping pattern. In contrast, when such sensations are interpreted as indicators of harm, reinjury, or worsening, fear may intensify and avoidance behaviors may follow [21]. In the longer term, this may lead to reduced physical activity, deconditioning, impaired functional capacity, limitations in everyday activities, social withdrawal, increased psychological distress, anxiety and depressive symptoms, and poorer quality of life [23].

In osteoporosis, the fear-avoidance model may be understood in relation to the perception of movement as a possible biomechanical threat [24]. Because bone homeostasis and remodeling are highly dependent on mechanical loading, avoiding movement and weight-bearing activities may represent more than a behavioral response [25]. It may also contribute biologically to the persistence of osteoporotic fragility by reducing the mechanical stimuli necessary for maintaining bone health [25, 26]. At the same time, declines in muscle strength and postural balance may further increase the risk of falls and fractures [27]. From this perspective, the the fear-avoidance model in osteoporosis may be conceptualized as a self-perpetuating cycle in which perceived fragility leads to reduced mechanical loading, which in turn may further reinforce fragility.

The TSK, one of the most commonly used instruments for assessing kinesiophobia, appears to capture not only concerns that activity may increase pain or lead to injury, but also the broader belief that there is an underlying and serious bodily problem [28, 29]. Moreover, qualitative work suggests that high TSK scores are often underpinned by beliefs that painful activity will cause damage, increase suffering, or result in functional loss [30]. Accordingly, the TSK may be interpreted as reflecting cognitive threat appraisals regarding the harmfulness of movement rather than current pain alone. This interpretation is also supported by its use not only in painful musculoskeletal conditions, but also in people with recovered low back pain and asymptomatic controls, in neurological populations such as stroke, multiple sclerosis, and Parkinson’s disease, and in cardiac populations [31–33]. At the same time, although the TSK includes items related to avoidance, its associations with objective movement behaviour appear to be modest overall, with recent meta-analytic evidence showing only a weak association between general fear measures such as the TSK and spinal motor behaviour, while older validation studies reported correlations with physical performance that were largely moderate at most [34, 35]. Thus, in individuals with osteoporosis, the TSK may be interpreted primarily as a measure of perceived bodily fragility and beliefs that movement or loading may be harmful, whereas actual avoidance behaviour is better assessed alongside performance-based or observational measures.

Kinesiophobia is common in osteoporosis, arising not only from the disease itself but also from related complications such as fractures, pain, postural alterations, impaired balance, and falls [36]. Nevertheless, reducing the relationship between osteoporosis and kinesiophobia to bone loss and its biological sequelae alone would be overly simplistic [9, 15, 24]. A more comprehensive interpretation requires a biopsychosocial perspective. In this regard, previous studies have drawn attention to the contribution of mood-related factors. Mısırcı et al. showed that TSK scores were positively correlated with HADS-D in individuals with osteopenia and osteoporosis, while another study, including participants with and without osteoporotic fractures also identified an association between HADS-D and kinesiophobia [37, 38]. Likewise, fear of falling has been reported to be related to kinesiophobia in individuals with osteoporosis [24, 38]. Our findings are broadly consistent with this pattern, as higher HADS-D scores were associated with higher TSK scores in the full-sample models. However, this association was not stable across the exploratory subgroup analyses restricted to participants with SUI, where HADS-D was not significant in the eight-predictor model but became significant in the more parsimonious four-predictor sensitivity model. This inconsistency suggests that the apparent contribution of depressive symptoms in the SUI subgroup may be sensitive to model specification, possibly reflecting shared variance with related psychological constructs and the relatively limited subgroup sample size, rather than a fully stable independent effect. Therefore, while depressive symptoms may be clinically relevant in this context, their apparent contribution in the SUI subgroup should not be overinterpreted as a stable independent association. Collectively, these observations suggest that kinesiophobia in osteoporosis may be shaped not only by biological fragility itself, but also by the interaction of perceived vulnerability, anticipated falls or fractures, and psychological distress.

Our findings also suggest that, beyond psychological factors, SUI may also contribute to the multidimensional relationship between postmenopausal osteoporosis and kinesiophobia. Previous studies have shown that urine leakage, along with related fears such as embarrassment, loss of control, fear of being noticed in social situations, and reduced self-confidence, may serve as important cognitive and behavioural barriers to women’s participation in physical activity and exercise [39–45]. Abakay et al. reported a positive correlation between urinary and fecal incontinence and kinesiophobia in individuals with lower extremity lymphedema following gynecological cancer [44]. In another study, higher levels of kinesiophobia were found in older adults with urinary incontinence. Additionally, a positive correlation has been demonstrated between the severity of incontinence and kinesiophobia [46]. Although the dominant fears in osteoporosis are generally centred on falling, injury, pain, and fracture risk, incontinence-related fear may further reinforce this pattern of avoidance through central threat-processing mechanisms involving limbic and salience networks. From this perspective, kinesiophobia in osteoporosis may, in some individuals, be shaped not only by fracture-related fear but also by leakage-related fear. However, the TSK does not distinguish the source of fear; rather, it reflects the overall level of movement-related fear-avoidance beliefs. Therefore, our findings do not directly indicate which specific fear component is influenced by SUI, but they do suggest that SUI may represent a clinically relevant biopsychosocial contributor to the relationship between osteoporosis and kinesiophobia.

In addition, the association between SUI and kinesiophobia observed in our sample of postmenopausal women with osteoporosis may be interpreted in light of shared biological and biomechanical backgrounds. SUI is a key component of the pelvic floor dysfunction spectrum, and the pelvic floor muscles contribute not only to continence but also to trunk stability and postural adjustments [47]. Accordingly, impaired pelvic floor function may be related not only to urinary symptoms but also to balance strategies and postural control. Previous studies have reported delayed postural activation of the pelvic floor muscles in women with SUI, as well as poorer balance performance and altered pelvic floor/trunk muscle activity compared with continent women [48, 49]. In addition, a recent systematic review concluded that women with urinary incontinence show more impaired standing postural balance control than women without incontinence [50]. Similarly, the decline in estrogen levels after menopause may provide a common biological background affecting both bone tissue and pelvic support structures, as estrogen deficiency is associated with accelerated bone resorption and with atrophic and less elastic pelvic support tissues [51, 52]. In this context, SUI may represent a clinical correlate of pelvic support alterations in postmenopausal women with osteoporosis and may coexist with greater movement-related threat appraisal in the presence of perceived skeletal fragility. However, because of the cross-sectional design of our study, no direct inference can be made regarding the direction of these relationships or the mechanisms underlying them; these interpretations remain speculative.

In addition, although the presence of SUI was associated with an approximately 3-point between-group difference in TSK scores and a statistically significant 7.3% increase in explained variance, both findings point to a modest incremental contribution rather than a pronounced clinical effect. No established minimal clinically important difference has been defined for the TSK in postmenopausal osteoporosis; moreover, the available reference point from another population comes from a lumbar-fusion rehabilitation cohort, in which a within-person change of more than 6 points on the TSK was proposed as clinically meaningful [53]. Accordingly, the observed difference is better interpreted not as evidence of a clear clinical threshold, but as suggesting a small yet consistent contribution of SUI to the level of kinesiophobia. At the same time, the possibility that depressive symptoms may account for part of the association between incontinence severity and kinesiophobia should also be considered. Women with urinary incontinence have been shown to carry a substantial burden of depression and anxiety, moderate-to-severe incontinence has been associated with a higher likelihood of major depression, and longitudinal data further suggest that depression may precede the development of later urinary incontinence symptoms [54–56]. Within this context, more severe SUI may plausibly intensify kinesiophobia not only through symptom expectancy itself, but also through the broader psychological burden that accompanies persistent incontinence. Beyond depressive symptoms, other unmeasured biological, behavioural, and psychosocial factors may also be considered when interpreting the kinesiophobia findings. In particular, physical activity level, fear of falling, and functional status were not assessed in the present study, and these unmeasured factors may have contributed to residual confounding and influenced the observed associations. Also, given the cross-sectional design of our study, no direct inference can be made regarding the direction, potential mediating pathways, or causal nature of these associations.

This study should be interpreted in light of several limitations. First, it was not designed to establish a definitive etiological model or to propose a new conceptual framework, but rather to extend the existing correlational literature on kinesiophobia to the specific context of SUI in postmenopausal women with osteoporosis. For this reason, the multivariable regression analyses are better understood as exploratory models describing observed associations after adjustment for clinically relevant variables, rather than as evidence of fixed causal pathways. The relatively modest amount of explained variance in TSK scores also suggests that kinesiophobia in this population is likely shaped by additional biological, behavioural, and psychosocial factors beyond those captured in our models. Key factors such as physical activity level, fear of falling, and functional status were not assessed in the present study and may have influenced kinesiophobia outcomes. In addition, some other potentially relevant variables, including menopause duration and duration of urinary incontinence, could not be reliably obtained for all participants and were therefore not included in the analyses. Taken together, these unmeasured factors may have contributed to residual confounding. These issues should be addressed in future prospective studies with larger and more diverse samples. In addition, our sample consisted of community-dwelling, functionally independent postmenopausal women with osteoporosis who were physically active in daily life, reported no marked pain at the time of assessment, had no falls or fractures in the previous 12 months, and were not receiving hormone replacement therapy. Although this may have reduced the influence of factors such as functional limitation, medically advised activity restriction, and fear of reinjury or falling, and thus provided a more clinically stable sample, it may also have introduced some degree of selection bias, restricted the variability of kinesiophobia, and limited the generalizability of the findings to a broader osteoporotic population. The single-centre design and the use of self-reported questionnaires should also be acknowledged as limitations, particularly with respect to generalizability and possible recall bias. Finally, although kinesiophobia reflects fear- and belief-related responses to movement, we did not directly assess physical activity, exercise participation, or objective physical performance. As a result, any interpretation of real-world movement avoidance, activity restriction, or functional impact should remain cautious.

Conclusions

This study showed that postmenopausal women with osteoporosis and SUI had higher kinesiophobia than those without SUI. In addition, greater SUI severity was associated with higher levels of kinesiophobia. Given the importance of movement and exercise in osteoporosis management, these findings suggest that SUI may be considered, alongside other biological and psychosocial factors, in the clinical evaluation of barriers to physical activity participation. At the same time, this was a single-centre, cross-sectional study conducted in a specific osteoporosis sample, and both the between-group difference in scores and the contribution of SUI to kinesiophobia were relatively modest. Accordingly, rather than supporting routine screening or proposing a new conceptual framework, our findings support considering SUI as one of several clinically relevant factors that may inform individualized management strategies in postmenopausal osteoporosis. Larger, multicentre, prospective, and interventional studies incorporating objective measures of physical activity and bone-related outcomes are needed to clarify the clinical significance of these findings.

Abbreviations

SUI

Stress Urinary Incontinence

HADS

Hospital Anxiety and Depression Scale

HADS-A

Hospital Anxiety and Depression Scale Anxiety Score

HADS-D

Hospital Anxiety and Depression Scale Depression Score

ICIQ-SF

International Consultation on Incontinence Questionnaire-Short Form

I-QOL

Incontinence Quality of Life Scale

TSK

Tampa Scale of Kinesiophobia

Authors' contributions

PO developed the manuscript design, collected data from postmenopausal participants, performed statistical analysis and drafted the manuscript. MP developed the study design, collected data from postmenopausal participants, performed statistical analysis and revised the manuscript. All authors read and approved the final manuscript.

Funding

This research did not receive external funding.

Data availability

The data that support the findings of this study are available from the corresponding author upon reasonable request.

Declarations

Ethics statement

The research protocol was approved by the Sivas Cumhuriyet University Non-Interventional Clinical Research Ethics Committee (decision no. 2022-03/32, dated 23/03/2022). The entire research process was conducted in accordance with the ethical principles of the Declaration of Helsinki and the Good Clinical Practice guidelines. Informed written and verbal consent was obtained from all the participants.

Consent for publication

Not applicable.

Competing interests

The authors declare no competing interests.