Genetics is a major contributor to OA risk, shaping height, weight, and body mass index (BMI) from childhood through adolescence [37], and this hereditary influence is further supported by family and inheritance studies [38]. A twin study involving 130 monozygotic and 120 dizygotic women aged 48–70 reported a heritability estimate of 0.54 (95% CI: 0.43–0.65), with site-specific estimates ranging from 0.39 to 0.65, and consistently higher intraclass correlations in identical compared with non-identical twins [39]. As a polygenic disease, more than 300 OA genomic loci have been identified by using genetic analyses and genome-wide association studies (GWAS) of affected individuals; results have shown that OA genes are associated with the process of synovial joint development, playing an important role in the onset of OA as well as during the late stages of the disease [38, 40–42]. While mutations in cartilage structural genes like COL2A1 and ACAN can contribute to early-onset OA, they seem less relevant to typical late-onset cases [40, 43]. Most genetic variants found through GWAS affect transcriptional regulation, suggesting that genetics may influence cartilage repair capacity rather than trigger disease onset. Epigenetic mechanisms are also increasingly recognized but require larger studies for clarification [43]. In women, gene expression analyses have identified a set of genes closely tied to molecular heterogeneity in OA, and there is increasing evidence that some genetic markers linked to inflammatory pathways seem to heighten susceptibility to OA. Some variants show clear sex-dependent effects; for example, the FRZB T/G haplotype has been implicated in OA pathogenesis only in women, and COMP haplotypes associated with KOA differ between sexes. Conversely, certain COL2A1 haplotypes may offer some protection in men but not in women [11]. Additionally, other genes involved are part of the Wnt pathway [HMG-Box transcription factor 1 (HBP1); B cell CLL/lymphoma 9 protein (BCL9)] and transforming growth factor (TGF) pathway [TGF beta 1 (TGFβ1)], latent transforming growth factor beta binding protein 1 and 3 (LTBP1, LTBP3), SMAD3 and ROCR long non-coding RNA (lncRNA) that regulates chondrogenesis [38, 44]. Although molecular pathways such as Wnt signaling play a central role in the pathogenesis of OA, current evidence supporting sex-specific differences in these mechanisms remains limited. Therefore, their contribution to the higher burden of disease in women is not yet fully understood. Recent discoveries suggest that OA risk is driven more by altered gene regulation than by structural mutations in cartilage proteins. Epigenetic mechanisms, such as DNA methylation, histone changes, and microRNAs, likely explain why individuals with similar genetic risk can have very different clinical outcomes [45]. Progress in the field requires larger, better-defined cohorts and a clearer separation of OA into biologically distinct endotypes.

A twin study of nearly 60,000 Swedish adults evaluated how strongly genetics contribute to OA compared with other musculoskeletal and rheumatic diseases. The results showed that OA, especially in the hip, has one of the highest heritability estimates among the conditions examined. The researchers also found that OA, at any joint site, commonly co-occurred with shoulder pain and back or neck pain, and a substantial portion of these overlaps could be attributed to shared genetic factors, suggesting underlying biological mechanisms with several pain-related conditions, influenced by heredity [46]. A nationwide Swedish cohort study assessed familial risk of several OA subtypes by linking the Multigeneration Register with national healthcare records. Across more than 6.5 million individuals, all OA forms showed elevated familial hazard ratios, increasing with closer genetic relatedness. The strongest hereditary signals were observed for first carpometacarpal and polyarticular OA, followed by HOA, while knee and other OA types showed weaker but still significant familial effects [47]. Supporting this pattern, Weldingh et al. [48] examined hereditary influences on hip, knee, and hand OA in two population-based Norwegian cohorts, and reported that having a mother with OA increased both risk and severity in daughters, whereas paternal OA showed a weaker association.

Clinical and epidemiological data consistently show that women have a higher prevalence of OA across adulthood, a disparity that becomes more pronounced after menopause as symptom onset and disease progression accelerate [31, 36, 49]. This increased susceptibility is supported by evidence that women exhibit lower cartilage volume and a faster rate of cartilage loss than men; although body size contributes to these differences, sex-specific structural and biochemical characteristics of cartilage, how they change with age, also play a significant role [31]. As a result, women demonstrate higher rates of hip, knee, and hand OA compared with men [36].

A systematic review reported sex-specific risk profiles; in women, high BMI, alcohol use, and atherosclerosis were linked to greater KOA risk, whereas in men, the main factors were high physical activity, soft-drink intake, and abdominal obesity [50]. OA incidence rises around the cessation of menses [16], likely reflecting hormonal changes, body composition, joint anatomy, and muscle strength. Segal et al. [11] noted that 60% of individuals with OA were women, who also showed higher pain perception, radiographic severity, and greater functional limitations, with possible contributions from differences in central pain processing and coping strategies. Other studies similarly reported higher pain scores among women using the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) [51] and visual analogue scale (VAS), with socioeconomic factors further influencing pain perception in older women [52]. These findings might be explained by the influence of psychological aspects related to chronic pain. Catastrophizing, characterized by heightened threat appraisal and persistent pain-related thoughts, has been proposed as a partial explanation for these sex differences and appears more common in women [53–55]. Pain and disability are related to the magnification and rumination of the pain-related information shown in catastrophizing, which tends to happen more often in women [55]. In a cohort of 168 OA patients, women showed greater pain, pain behaviors, and disability [53]. Experimental studies also support increased pain sensitivity and reduced pain inhibition in women [55]. Failla et al. [56] found that women perceived heat-evoked pain at lower temperatures and displayed different age-related patterns in descending pain modulatory system activity compared to men, suggesting neurobiological differences in pain processing across sexes.

The Q angle, the angle formed by the anterior superior iliac spine (ASIS)-patella and patella-tibial tubercle lines, represents the combined vector of quadriceps and patellar tendon forces and serves as a clinical indicator of patellofemoral alignment [57, 58] (See Figure 2). In women, a relatively shorter femur, wider pelvis, and larger Q angle alter lower-limb alignment and increase knee valgus forces, shifting load toward the lateral compartment and elevating the risk of lateral tibiofemoral OA. When combined with greater hip internal rotation, higher knee torque, and increased varus-valgus laxity, these structural and biomechanical features reduce joint stability during landing or rapid directional changes and help explain the markedly higher rate of ligament injuries, particularly anterior cruciate ligament tears [59].

Hormonal fluctuations and pregnancy may further affect ligament laxity and joint mechanics, adding to this vulnerability. Sex-specific differences in bone morphology, such as femoral rotation, condylar curvature, and tibial dimensions, have been documented across Asian populations and appear more pronounced in women. As OA progresses, women also show characteristic changes in joint alignment and morphology that differ from men, potentially contributing to less favorable loading patterns. Consistent with these structural distinctions, women exhibit a larger normalized medial tibiofemoral contact area and reduced joint congruity across OA grades [11, 59].

Women exhibit lower quadriceps strength compared to men, placing them closer to the threshold for insufficient knee stabilization. In women only, quadriceps weakness consistently predicts symptomatic and radiographic KOA, structural progression, functional decline, and future knee arthroplasty, likely reflecting reduced specific strength rather than muscle mass. Strength gains correlate with improved performance in women but not men. Hip abductor weakness similarly increases the risk of worsening knee pain in women alone. Although women demonstrate greater hamstring coactivation during quadriceps activity, this pattern is more strongly associated with cartilage deterioration in men [11]. Studies have shown that higher quadriceps strength was linked to reduced worsening of lateral patellofemoral cartilage damage, bone marrow lesions, and effusion-synovitis in women, and knee pain, suggesting a protective effect on specific joint structures in women with or at risk for KOA [60, 61]. Another study compared quadriceps-only strengthening with a combined exercise program in women aged 50–60 with KOA. After four weeks of training, both interventions significantly improved pain, balance, and the quadriceps-to-hamstring strength ratio (P ≤ 0.05), whereas the control group showed no changes. Both exercise approaches were effective for improving symptoms and function [62]. Overall, resistance training and quadriceps-focused strengthening seem to be an effective strategy for improving pain and quality of life in older women with KOA [63].

Women show a distinct pattern of cervical spine degeneration compared with men, driven in part by anatomical and biomechanical differences, which may contribute to a higher burden of cervical OA in women [64]. More broadly, structural and functional characteristics of joint tissues have been well described [18]. Studies report that women have shorter distances between cervical disc centers, a feature that declines with age and reflects sex-specific degeneration of the vertebrae and discs [65]. Clinically, they are more likely to develop persistent neck pain after trauma, a vulnerability linked to smaller vertebrae, lower muscle support, and more compliant ligaments, all of which reduce stability and increase tissue strain [49, 66]. Computed tomography (CT)-based work further shows that, even when body size is matched, men still have larger vertebral dimensions, offering greater mechanical resistance [64, 67]. These anatomical differences may have important clinical implications, as they influence load distribution and spinal biomechanics, potentially contributing to sex-specific patterns of degeneration. In clinical practice, this may be reflected in differences in pain presentation, functional limitation, and susceptibility to facet joint OA, spinal instability, and chronic low back pain in women.

Variations in collagen, cartilage, and bone properties may predispose women to degenerative conditions and specific joint pathologies across the spine [18, 29, 31, 34, 68]. Some studies report that thoracic degeneration increases with age in both sexes, with a different pattern among sexes. Older women tended to show more eburnation, while older men showed more lipping and porosity, and these contrasts became more pronounced in the elderly group [69]. Estrogen helps maintain intervertebral disc structure by supporting vascular supply, matrix turnover, hydration, and anti-inflammatory signaling while limiting apoptosis [18, 70]. Moreover, large imaging studies also demonstrate more severe disc degeneration after menopause, with the most rapid decline occurring in the first decade following the menopausal transition [71]. When men and women are matched for age and body size, women still exhibit greater disc degeneration, underscoring estrogen’s protective effect [18–20]. Dual-energy X-ray absorptiometry (DEXA)- based analyses similarly show that disc space remains stable until midlife and then decreases substantially, especially in early post menopause [72].

Sex-related differences in lumbar anatomy and degeneration are evident across imaging, biomechanical, and epidemiological studies. CT-based modeling shows that women have a greater lumbar curvature with the upper segment inclined more dorsally and a greater cranial peak height. These features create the appearance of a deeper curve even though the total degree of lordosis is similar to that of men, and may represent adaptations that reduce spinal loading during pregnancy [73]. Biomechanically, smaller vertebral dimensions further disadvantage women. Quantitative CT shows that although cancellous and cortical bone densities are comparable between sexes, women’s vertebral bodies are about 25% smaller in cross-sectional area and volume (P < 0.001). As a result, equivalent loads generate 30–40% higher mechanical stress in female vertebrae, helping explain the greater fracture susceptibility seen later in life [74]. Although this difference has been linked to anatomical and biomechanical factors, the specific contribution of body weight, muscle mass, and fat distribution remains incompletely understood, as sex-stratified data are limited.

Longitudinal evidence from the Framingham Study reinforces these patterns. Disc height narrowing and facet joint OA were already common by midlife and progressed more rapidly in women, particularly in the lumbar spine [20]. Epidemiologic data also point to a higher burden of lumbar OA in women. In a large population-based cohort, symptomatic lumbar OA affected roughly 9% of adults, with higher prevalence in women (P = 0.021) and strong associations with age, obesity, and physical labor among others [75]. Sex-specific bone geometry and joint mechanics likely contribute to the higher prevalence and severity of HOA in women compared to men [76]. Overall, HOA in women tends to occur within a broader polyarticular pattern and is characterized by more pronounced symptomatic and structural burden [77]. Females generally have a wider pelvis, a shorter femoral neck, and a smaller femoral head, along with lower femoral offset and a reduced cervico-diaphyseal (CCD) angle, as well as greater femoral and acetabular anteversion. These features can alter hip congruence and joint mechanics, increasing load on the articular surface [78]. As a result, the effective contact area may be reduced, and with routine daily loading, this configuration can contribute to accelerated cartilage wear and subchondral bone changes [76]. These meaningful differences between sexes might determine how the disease presents and progresses. In a five-year multicenter cohort of 508 adults with painful HOA, women entered the study with more widespread joint involvement, more frequent superomedial femoral head migration, and more severe symptoms than men. Although average joint-space narrowing over the first year was similar across sexes, women were more likely to experience rapid structural deterioration (OR = 2.34). Over the full follow-up period, total hip arthroplasty (THA) was performed more often in women; however, multivariate analyses indicated that surgery was primarily driven by disease severity rather than sex itself [77].

Understanding the morphological differences between sexes is essential for diagnosing and managing disorders linked to anatomical variation, as they influence hip motion before impingement occurs. In a CT-based analysis of 106 healthy hips from older adults, researchers compared acetabular and femoral features and assessed the range of motion (ROM) until bony impingement in four directions. Clear sex differences emerged in both joint orientations, such as acetabular inclination and anteversion, and femoral neck anteversion, and in the contours of the acetabular rim and femoral neck. These anatomical distinctions were accompanied by sex-specific limits in ROM across all tested movements [79]. Muscle mass distribution and lower-limb biomechanics also shape how forces are transmitted through the hip. Gait studies show clear sex differences; men generate higher mass-specific mediolateral ground reaction forces (GRF), whereas women exhibit greater hip abductor moments, a more medially positioned trochanter, and a larger GRF moment arm, indicating that female hip morphology places higher functional demands on the abductors and modifies their mechanical advantage during single-leg stance [80]. As previously mentioned, anatomical differences between men and women play a significant role in the development of biomechanical alterations; however, it is important to note that these factors alone cannot fully explain the development of OA. Other systemic factors associated with the development of the disease must be taken into account, as discussed in the following section.

Endogenous sex hormones influence the pathogenesis, pain perception, and progression of OA [81]. Higher estrogen levels have been linked to reduced pain sensitivity, while hormonal fluctuations during the menstrual cycle and menopause modulate pain responses in women [11, 82]. Although hormonal and reproductive factors appear relevant to OA development, their independent contribution relative to obesity and inflammation remains unclear [81]. Menopause represents a period of significant estrogen decline, associated with loss of bone mineral density and musculoskeletal pain, and women with more intense menopausal symptoms may have increased vulnerability to chronic back pain, arthralgia, and OA [83–87]. A recent systematic analysis showed a 1.3-fold increase in OA incidence, prevalence, and disability-adjusted life-years (DALYs) in postmenopausal women, with higher hand OA incidence at ages 55–64 and HOA at 60–64 [86]. This rise during menopause suggests a link between ovarian function and OA [88].

Sex hormones and their receptors are widely expressed in the central and peripheral nervous system and contribute to pain transmission [55]. During menopausal transition, declining estrogen increases arthralgia and pain sensitivity, whereas testosterone is associated with higher pain thresholds in men [87, 89]. In the Women’s Health Initiative, estrogen therapy reduced total joint replacement by 50% in highly adherent users [90]. Estrogen also promotes cartilage homeostasis by preventing structural damage, enhancing proteoglycan synthesis, and regulating subchondral bone growth and mineralization [91]. Low endogenous estrogen metabolites have also been associated with KOA development. In a cohort of 842 middle-aged women, those with estradiol levels in the lowest tertile (< 47 pg/mL) had increased odds of radiographic KOA (OR = 1.88; 95% CI: 1.07–3.51), as did those with low urinary 2-hydroxyestrone (OR = 2.9; 95% CI: 1.49–5.68) [92]. Hormone replacement therapy (HRT) shows protective effects on cartilage and bone. In a 2-year study of 171 postmenopausal women, both oral and transdermal estradiol, administered as continuous combined therapy (with progestins), reduced the cartilage degradation marker, urinary C-telopeptides of type II collagen (uCTX-II), by 19–30% after one year (P = 0.02 and P = 0.003 vs. placebo), and lowered the bone resorption marker urinary C-telopeptides of type I collagen (uCTX-I) by 70% compared with placebo (P < 0.0001). Oral regimens included 1 mg 17β-estradiol combined with 1–3 mg drospirenone, while transdermal therapy consisted of 45 μg 17β-estradiol combined with 30–40 μg levonorgestrel. These findings support estrogen’s protective effects on cartilage and bone [93].

Progesterone also contributes to cartilage integrity by suppressing matrix-degrading enzymes such as matrix metalloproteinases (MMPs) [87, 94]. In a study of 200 adults, low estradiol, progesterone, and testosterone levels were associated with greater knee effusion-synovitis and other OA-structural abnormalities; among women, progesterone correlated positively with cartilage volume [95]. Despite these findings, the role of HRT in OA remains controversial. Evidence regarding its clinical benefits is not entirely consistent, and most studies have focused on surrogate biomarkers or observational outcomes rather than long-term structural progression. Moreover, HRT is not without risks, including increased incidence of thromboembolic events, breast cancer, and cardiovascular complications in certain populations [90]. Current clinical guidelines do not recommend HRT specifically for the prevention or treatment of OA, and its use should be individualized based on overall risk-benefit assessment. Therefore, while estrogen may exert protective effects on joint tissues, caution is warranted when extrapolating these findings to routine clinical practice.

Age-related testosterone decline contributes to reduced muscle function, bone mass, and increased joint pain [96]. In 272 older adults undergoing unilateral total knee replacement (TKR), higher testosterone levels were associated with lower pain in both sexes and lower disability in women [97]. Similarly, NHANES data (2011–2016) show that low testosterone increases OA risk (OR = 1.22; 95% CI: 1.02–1.46), particularly among obese women with hyperlipidemia [98]. Other studies also link low testosterone to greater arthritis risk [99] and reduced muscle mass and strength, with evidence from interventional studies demonstrating the role of testosterone in muscle adaptation and strength responses [100]. In summary, maintaining adequate levels of estrogen, progesterone, and testosterone may support cartilage integrity, reduce pain, and help limit OA progression.

Obesity is a major modifiable risk factor for OA and appears to have a particularly significant impact in women [13–16, 101]. In many populations, women exhibit higher rates of obesity, influenced by a combination of behavioral, nutritional, and socioeconomic factors, which may contribute to increased disease burden and associated comorbidities. In addition to mechanical loading, systemic and metabolic factors associated with obesity, including low-grade inflammation, may further exacerbate joint degeneration [18–20]. However, it is important to note that several studies evaluating the relationship between obesity and OA include both men and women, and sex-specific analyses remain limited in some cases.

Beyond mechanical overload on weight-bearing joints, adipose deposition, immune dysregulation, dyslipidemia, and insulin resistance contribute to OA in non-weight-bearing joints [102, 103]. Higher BMI consistently increases OA risk. A meta-analysis reported a positive association between BMI and KOA (RR = 1.25; 95% CI: 1.17–1.35), with each 5-unit BMI increment raising risk by 35% and showing stronger effects in women [104]. Obesity markedly increases the likelihood of KOA up to 6.8-fold [101], and this risk increases progressively from 0.1 in subjects with BMI < 20 kg/m² to 13.6 in those with BMI ≥ 36 kg/m² [105]. Associations with knee and hand OA have been confirmed in multiple cohort studies [106, 107] and in a recent meta-analysis identified higher BMI as a major risk factor for incident KOA [108]. Similar trends were observed in an Australian population study [109]. This study demonstrated that the odds of OA, as well as arthritis, were up to 7 times higher for obese individuals compared with those underweight or of normal weight [109].

Weight loss should be the primary goal for overweight or obese patients, as excess body weight strongly increases the risk of knee and hand OA and, to a moderate extent, HOA. Clinical symptoms should always be considered alongside radiographic findings [101–111]. Losing more than 7.5% of body weight reduces the risk of TKR [112], and even a ≥ 5% reduction can improve disability in patients with KOA [113]. Obesity also significantly elevates perioperative risk; in a meta-analysis of over 2 million THA cases, obese individuals had higher rates of complications, infection, dislocation, reoperation, revision, and readmission, with risks further increasing in morbid obesity [114]. Notably, up to 24% of surgeries could be prevented by achieving a normal BMI or losing just 5 kg [105].

The progression of OA in obese patients is multifactorial; mechanical forces, increased joint load, inflammatory cytokines, and the inability to completely repair the tissue are implicated in the degeneration of cartilage [115]. OA in non-bearing joints, such as the hand and wrist, is associated with obesity, suggesting that adipose tissue has a systemic inflammatory effect [103], and some authors even consider that pain intensity might be a reflection of adipose tissue dysfunction [116]. Additionally, overload is associated with matrix degradation and apoptosis of the cartilage, mainly because of activation of inflammatory pathways, as we have described previously [103, 115]. OA-related joint inflammation might be explained by the cartilage fragments of the degraded tissue acting as a foreign body when contacting the synovium, an inflammatory cascade starts when synovial cells react, activating chondrocytes and MMPs synthesis [117]. Patients with OA show differences in the cytokine and chemokine levels in synovial fluid, even in the mild or moderate stages [118]. Furthermore, it has been demonstrated that pain severity is associated with higher high-sensitivity C-reactive protein (CRP) levels in patients with advanced OA [119]. Similar findings showing an association between systemic inflammation and OA have been reported, and interestingly, female sex was associated with greater painful joint count and higher CRP [120].

While several of the mechanisms described in this section are involved in OA pathophysiology in general, evidence specifically addressing sex-related differences remains limited. Where available, female-specific findings are highlighted; however, many studies include both sexes without stratified analyses. Metabolic syndrome is a complex condition characterized by hypertension, dyslipidemia, hyperglycemia, and central obesity, and is closely linked to a chronic low-grade inflammatory state that accelerates OA progression [121–123]. Oxidative stress, advanced glycation end-products, and lipid and glucose dysregulation disrupt cartilage homeostasis, while adipose-derived cytokines such as TNF-α, IL-6, IL-17, and IL-18 promote catabolic enzyme activity, subchondral bone remodeling, and matrix breakdown [122–124]. Epidemiologic data from the UK Biobank show that metabolic syndrome increases the risk of OA by 15%, with an even significantly higher risk among individuals with elevated CRP (HR = 1.35), central obesity (HR = 1.58), hyperglycemia (HR = 1.13), and dyslipidemia in triglycerides (HR = 1.07) [125]. These findings align with other studies reporting metabolic syndrome in 80% of patients with OA vs. 26% in controls, along with higher total cholesterol and LDL levels in the OA group [122]. Vitamin D deficiency, common in metabolic syndrome due to sequestration in adipose tissue, further amplifies inflammatory and degradative pathways, partly through upregulation of MMP-2 and MMP-9 [126–128]. Notably, correcting deficiency may improve symptoms; in a population-based cohort, 25-hydroxyvitamin D (25OHD) levels < 10 ng/mL predicted greater worsening of hip and knee pain, and supplementation attenuated these changes over time [129]. Given its impact on MMP expression, inflammation, and chondrocyte integrity, vitamin D optimization represents a plausible therapeutic target in OA management [130].

PCOS shares several pathophysiological features with metabolic syndrome, including insulin resistance and chronic inflammation, but also presents distinct endocrine characteristics relevant to female-specific OA risk. Characterized by ovarian dysfunction and hyperandrogenism, PCOS is frequently accompanied by obesity and broader metabolic disturbances [131–133]. These patients demonstrate increased cardiometabolic risk, including higher rates of cardiovascular disease, early-onset type 2 diabetes, and systemic inflammation [132–134]. Notably, several rheumatic conditions appear more common in women with PCOS. A retrospective study reported a significantly higher prevalence of OA in PCOS, 5.44% vs. 2.92% in controls (P = 0.0030), with an OR of 1.913 (95% CI: 1.239–2.955) [135]. Similar findings were observed in a large Danish registry, where the PCOS cohort showed increased risks of knee, hip, and hand OA over two decades, along with an earlier onset in both weight-bearing and non-weight-bearing joints [136, 137]. Prospective cohort data further support this association, suggesting that PCOS may act as an independent risk factor for OA; women with KOA and PCOS had more than twice the odds of developing the condition (OR = 2.734) [137]. The biological mechanisms underlying the association between PCOS and OA are likely multifactorial. Hyperandrogenism, a hallmark of PCOS, may influence cartilage metabolism by altering chondrocyte activity and ECM turnover, although its direct effects remain incompletely understood. Insulin resistance, another central feature of PCOS, contributes to systemic metabolic dysfunction [132–134] and has also been implicated in cartilage degradation through increased production of advanced glycation end products and oxidative stress [134, 138]. In parallel, the chronic low-grade inflammatory state observed in PCOS, characterized by elevated cytokines such as TNF-α and interleukins, may promote matrix degradation and synovial inflammation [134, 139, 140]. These metabolic and inflammatory pathways may act synergistically to accelerate joint degeneration, providing a plausible link between PCOS and increased OA risk.

Symptom severity also appears greater, as demonstrated by Kabakchieva et al. [138], who found worse functional limitations and increased femoral cartilage thickness in PCOS patients. Beyond peripheral joints, PCOS has been associated with altered lumbopelvic alignment, including increased pelvic inclination and lumbar lordosis in nulliparous females without obstetric history compared to controls (P < 0.05). Additionally, a strong correlation was found between the luteinizing hormone (LH)/follicle-stimulating hormone (FSH) ratio and lumbar angle and pelvic inclination [134]. Temporomandibular joint disorders (TJD) are also more prevalent, likely reflecting hormonal and inflammatory influences; studies report markedly higher TJD rates in PCOS alongside elevated TNF-α, MMP-1, and MMP-8 levels [139, 140]. Given the presence of estrogen receptors (ERα and ERβ) in cartilage, hormonal dysregulation in PCOS may contribute to OA susceptibility, underscoring the need for more research into joint degeneration in this population [140, 141].