Samuel K. Chu and Joseph Ihm
While researchers have analyzed sex differences in detail in some musculoskeletal conditions, there are limited studies in the literature directly evaluating the sex differences in tendinopathy. Some studies have described epidemiologic differences of various tendinopathies between males and females. There is a larger body of research that has investigated sex differences in the risk factors associated with tendinopathy, including use of oral contraceptives, hormone replacement therapy (HRT) and other pharmaceuticals, body composition, neuromuscular control, strength, and structural properties of tendons. There are additional studies that have evaluated sex differences in response to various treatments of tendinopathy. This chapter reviews the current literature regarding sex differences in the epidemiology of specific tendinopathies, intrinsic and extrinsic risk factors for tendinopathy, and response to treatment of tendinopathy in the sports medicine population.
Studies have shown a higher prevalence in males than females for patellar tendinopathy, sometimes referred to as jumper’s knee. Lian et al. studied male and female elite athletes in nine different sports. They reported that in male and female handball and soccer players, the prevalence of patellar tendinopathy was higher among male athletes (13.5%; 18 of 133) compared to female athletes (5.6%; 6 of 107) (P = .042) (1). Diagnosis of patellar tendinopathy was made by history and physical examination. The training volumes and backgrounds of the male and female handball and soccer players in the study were reported to be similar: 15 to 17 hours/week of total training time and 15 to 18 years of organized training with 5 to 7 years at the elite level (1). Another cross-sectional study of 891 nonelite athletes showed a significantly higher prevalence of patellar tendinopathy in 10.2% of male athletes (51 of 502) and 6.4% of female athletes (25 of 389) (P = .048) (2). The authors of both of these studies hypothesize that the sex differences in prevalence of patellar tendinopathy may be related to lower forces on the patellar tendon in females due to lower quadriceps strength (1,2). Another study of 2,224 volleyball and basketball players (1,006 males, 1,218 females) with a mean age of 25.4 ± 4.7 years found a significantly higher prevalence of patellar tendinopathy in males at 25.3% compared to 13.1% in females (P < .001) (3). The subjects were classified as having patellar tendinopathy if they indicated pain at the inferior pole of the patella or reported prior diagnosis by a physician or physical therapist on a self-reported survey (3). In a study of 134 active, elite basketball players 14 to 18 years of age (70 males, 64 females), the prevalence of current patellar tendinopathy, diagnosed by history and physical examination, was 11% in males and 2% in females (4).
Additional studies have reported that males are at higher risk of developing patellar tendinopathy than females. In one prospective cohort study of 385 elite and nonelite basketball and volleyball players, male sex was found to be a risk factor for developing patellar tendinopathy, with an odds ratio (OR) of 2.0 (95% confidence interval [CI]: 1.1–3.5) (5). Another prospective cohort study of 141 elite volleyball players ages 16 to 18 years (69 males, 72 females) over a 3 year period reported that males had a three to four times higher risk for developing patellar tendinopathy compared with females (6). Out of the 28 athletes that developed patellar tendinopathy, 22 were males and 6 were females, and the mean annual incidence was 21% per year for males compared to 5.08% for females (6). Patellar tendinopathy was diagnosed by history and physical examination, with a minimum of 12 weeks of symptoms reported by the athlete (6). The authors suggested that possible explanations for a sex difference in patellar tendinopathy include larger muscle mass and ability to jump higher in males (6).
A study of 160 asymptomatic elite athletes in basketball (46 males, 53 females), cricket (6 males, 8 females), netball (25 females), and Australian Rules football (22 males) compared sonographic findings of the patellar tendon to 27 nonathletic controls (7). A sonographic abnormality was defined as a hypoechoic region in the patellar tendon and was more prevalent in athletes compared to controls (22% vs. 4%) and in male athletes compared to female athletes (30% vs. 14%) (7). Previous studies have shown an association between sonographic tendon changes in asymptomatic individuals and the subsequent development of symptomatic tendinopathy (8–10). Analysis of the height and weight of the subjects in this study showed that the athletes were taller and heavier than controls (P < .001), and the female athletes and controls were shorter and lighter than their corresponding male athletes and controls (P < .001).
There have been limited studies that have analyzed sex differences in the prevalence and incidence of Achilles tendinopathy. A cross-sectional study of more than 57,000 people showed that mid-portion Achilles tendinopathy equally affects males and females, with an incidence of 1.83 per 1,000 persons for males and 1.87 per 1,000 persons for females (11). In a study of 178 master track and field athletes, sex was not found to influence the development of Achilles tendinopathy (12).
Degenerative tendinopathic changes are the most common histological finding in spontaneous tendon rupture (13–15). With regard to Achilles tendon ruptures, the literature has shown a strong male predominance with male-to-female ratios ranging from 1.67:1 to 6.90:1 (16–22). Vosseller et al. performed a retrospective study of 358 patients with acute Achilles tendon ruptures and reported a male-to-female ratio of 5.39:1, similar to prior studies (23). They also compiled the data from prior studies of Achilles tendon ruptures and reported a total male-to-female ratio of 2.81:1 (23). The authors propose that the Achilles tendon is more likely to be ruptured in males because of a greater force of contraction that may exceed the maximum tendon tensile strength more easily than females (23). Male sex has been found in another study to predict a partial rupture of the Achilles tendon with an odds ratio of 3.6 (95% CI 1.3–9.8) (24). The authors discuss that the male predominance in chronic Achilles tendon disorders may be related to higher participation in sports in males compared to females, but state that there is not enough information to determine if the Achilles tendon degeneration that predisposes people to rupture is directly related to being a male (24).
Rotator Cuff Tendon Disorders
The literature on the epidemiology of rotator cuff tendon disorders is very limited, and studies have analyzed shoulder pain and more generalized rotator cuff syndromes as opposed to specific rotator cuff tendinopathy. White et al. performed a population study of more than 3.7 million patient records from 1987 to 2006 and reported an overall incidence of rotator cuff pathology (as identified by diagnostic codes) of 87 per 100,000 person-years (25). The incidence in females was reported to be significantly higher than males (90 per 100,000 person-years; 95% CI: 88–91 versus 83 per 100,000 person-years; 95% CI: 82–85, P ≤ .001) (25). When comparing the incidence between males and females of different age groups, there was no significant sex difference noted in the peak incidence age group of 55 to 59 years. In the 25- to 34-year-old group, males had a significantly higher incidence of rotator cuff pathology than females (P < .01), while females 40 to 54 years old had a significantly higher incidence than males in that age group (P < .001) (25). The authors did not discuss any potential explanations for the higher incidence of rotator cuff pathology in males in the lower age group.
This overall higher incidence of rotator cuff disorders in females compared to males is consistent with previous, smaller studies (26–28). Bodin et al. studied the risk factors for shoulder pain and rotator cuff syndrome in 3,710 subjects, including 2,161 males with a mean age 38.5 ± 10.4 years, and 1,549 females with a mean age of 38.9 ± 10.3 years (26). Rotator cuff syndrome was diagnosed based on current symptoms of intermittent pain in the shoulder region and at least one positive shoulder test (resisted shoulder abduction, external or internal rotation, resisted elbow flexion, or painful arc test), and the prevalence was reported to be 8.5% in females and 6.6% in males (26). Roquelaure et al. performed a surveillance study of 2,685 males and females in the working population and reported that the prevalence of rotator cuff syndrome was 9.0% in females and 6.8% in males (27). Walker-Bone et al. studied the prevalence of upper limb musculoskeletal disorders in 6,038 people and estimated the prevalence of rotator cuff “tendinitis” (the study authors’ terminology) to be 4.5% in males and 6.1% in females in the general population (28).
Yamamoto et al. performed a population-based study to investigate the prevalence of symptomatic rotator cuff tears. They found that the prevalence of rotator cuff tears in 683 people was 20.7% and reported that rotator cuff tears were more common in males (25%, 114 of 456) than in females (18.6%, 169 of 910) (29). Statistical significance in difference of rotator cuff tear prevalence was not assessed between the males and females in this study.
Overall, the data suggest a higher incidence and prevalence of rotator cuff disorders in females compared to males, although most studies did not evaluate sex differences as a primary outcome variable with regard to rotator cuff tendinopathy. Additional studies looking specifically at sex differences in rotator cuff tendinopathy are needed.
Lateral and Medial Elbow Tendinopathy
No significant sex differences have been reported in the prevalence of lateral and medial elbow tendinopathy. In a population-based study of lateral elbow tendinopathy between 2000 and 2012, there were a total of 5,867 individuals identified with new onset lateral elbow tendinopathy (30). There were 2,769 male and 3,098 female patients, with a slightly lower incidence in male patients (3.3 per 1,000; 95% CI: 3.2–3.5) compared to female patients (3.5 per 1,000; 95% CI: 3.4 –3.7) (30). In another population-based study from Finland, there was no significant difference between males and females for the prevalence of lateral elbow tendinopathy (1.2% for males vs. 1.4% for females) or medial elbow tendinopathy (0.4% for males vs. 0.3% for females) (31). Walker-Bone et al. reported an estimated prevalence of lateral elbow tendinopathy in the general population of 1.3% among males and 1.1% among females (28). Other studies have also demonstrated no sex differences in prevalence of medial and lateral elbow tendinopathy (32,33).
RISK FACTORS ASSOCIATED WITH TENDINOPATHY
There have been studies evaluating sex-specific information for factors associated with tendinopathy, including extrinsic risk factors such as use of oral contraceptives, HRT and other pharmaceuticals, and intrinsic risk factors such as body composition, neuromuscular control and strength, and structural properties of tendon. The following sections discuss the current literature describing the relationship between tendinopathy and these factors with a specific focus on sex differences.
Extrinsic Risk Factors
Oral Contraceptive Pills and Hormone Replacement Therapy (Estrogen and Progesterone)
A significant association has been found between Achilles tendinopathy and oral contraceptive use. In a study by Holmes and Lin involving 44 females with symptomatic Achilles tendinopathy, there was a statistically significant greater prevalence for use of either oral contraceptive pills or HRT in females compared to the national averages (34). Of the 15 females younger than age 35 with Achilles tendinopathy, 53% had history of oral contraceptive use compared to a national average of 26.9% (P < .025) (34), while 68% of females with Achilles tendinopathy over the age of 50 had a history of HRT, which is statistically significant compared to the national average of 38% (P < .01) (34).
Cook et al. studied the effects of HRT and physical activity on Achilles tendons of 85 asymptomatic postmenopausal females, including 53 active females and 32 inactive female controls (35). Ultrasound examination was performed on the Achilles tendons of the participants. Active females on HRT were found to have significantly smaller Achilles tendon diameter (9.6 mm; 95% CI: 8.7–10.5) than active females not on HRT (10.7 mm; 95% CI: 9.9–11.6) (P < .05) as well as fewer sonographic tendon abnormalities, defined as a variation in the fiber structure of the tendon evident in both the longitudinal and the transverse scans (35) Increased diameter of tendons may be indicative of pathologic changes in tendons (35,36). There were no significant differences between the groups in terms of height and weight (35). The authors concluded from these results that HRT may have an impact on tendon structure and can potentially reduce tendon abnormalities in active postmenopausal females (35). While this study presents results that appear to contradict previously presented information on the impact of female hormones on tendons, it was limited by a small number of subjects. Another difference is that the Holmes et al. study evaluated symptomatic Achilles tendinopathy while the Cook et al. study evaluated sonographic tendon changes in asymptomatic females.
Hansen et al. studied the effect of oral contraceptives on collagen synthesis of the patellar tendon in young, healthy females. The tendon collagen fractional synthesis rate (FSR), which has been reported to correspond to the synthesis rate of mature collagen (37), was compared between long-term users of oral contraceptives and controls who had never used oral contraceptives (38). The oral contraceptive group had a 57% lower tendon FSR than the control group, which was statistically significant (P < .05), and the authors concluded that synthetic female hormones inhibit tendon synthesis in young women (38).
Tendon tears have been associated with anabolic steroid use. There have been reported cases in the literature of tendon ruptures in the setting of anabolic steroid use (39–42). In addition, animal studies have reported that anabolic steroids may change tendon collagen properties, leading to decreased tensile strength (43,44). However, a study on ruptured tendons in four patients, two of whom were anabolic steroid users, concluded that anabolic steroids did not induce any ultrastructural collagen changes that would increase the risk of tendon ruptures (45). If anabolic steroids do not affect the structure of tendon, one suggested mechanism for tendon injury in the setting of anabolic steroid use is a rapid increase in mechanical stress on tendons due to increased training intensity and volume, and failure of the connective tissue to withstand the overload (46). Epidemiologic studies have reported significantly higher rates of anabolic steroid use by males compared to females. In one study, the global lifetime prevalence rate of anabolic steroid use was reported as 6.4% for males compared to 1.6% for females (P < .001) (47). Self-reported use of anabolic steroids in adolescents has been shown to range from 5% to 11% in males and between 1.4% and 2.5% in females (48–51). This may explain why males are more likely to have tendon rupture or tendon-related injuries in the setting of anabolic steroid use. It is unknown if endogenous anabolic steroids are associated with an increased risk of tendinopathy.
Fluoroquinolones have been associated with tendon disorders and have been studied primarily in relation to their effects on the Achilles tendon, but fluoroquinolone use has been associated with tendon disorders in other parts of the body (52–57). The average onset of tendinopathy after fluoroquinolone use has been found to be 9 to 17 days, ranging from hours to months (58). Wise et al. performed a large population study of 6.4 million residents in the United Kingdom from 1986 to 2009 and showed that the use of fluoroquinolones had more negative effects on tendons in females than males (58). Fluoroquinolone use was shown to have a significantly larger effect on tendon rupture in females compared to males (OR: 4.0 vs. 1.1, P = .02) as well as a stronger association in females for Achilles tendonitis (OR: 5.0 vs. 3.6) (58). A study by Van Der Linden et al. of 50,000 patients in the United Kingdom identified 1,367 patients with Achilles tendon rupture between 1988 and 1998. The authors showed that the effect of fluoroquinolones on the incidence of Achilles tendon rupture was not modified by sex (55). Compared to the study by Wise et al., this study did not assess for the presence of tendinopathy. In addition, the Wise et al. study looked at a much larger database of patients compared to the sample studied by Van Der Linden et al. (55,58).
Intrinsic Risk Factors
Effects of Endogenous Hormones
Endogenous female hormones such as estrogen have been hypothesized to affect tendon structure and contribute to the development of tendinopathy (34,59,60) However, the impact of endogenous female hormones has been studied primarily in the setting of anterior cruciate ligament injuries, with limited studies specifically looking at their impact on tendons. An animal study by Hart et al. showed the presence of messenger RNA (mRNA) for estrogen and progesterone receptors in rabbit tendons (61). The impact of pregnancy on gene expression was different in the Achilles, patellar, flexor digitorum longus, and extensor digitorum tendons (61). The authors hypothesize that tendons therefore may respond to changes in hormone levels. Miller et al. investigated the rate of patellar tendon collagen synthesis in female subjects, taking into account serum estrogen and progesterone concentrations (62). These authors calculated the tendon collagen fractional synthesis rate and found significantly lower tendon collagen FSR in females compared with males both at rest and after exercise (62). At rest, the tendon collagen FSR for females was 55% of the rate of males (P < .05), while 72 hours after exercise, the tendon collagen FSR for females was 47% of the rate of males (P < .05) (62). The authors concluded that estrogen may play a role in tissue repair, specifically modulating responses of fibroblasts to mechanical loading, and may contribute to a lower rate of repair in females after exercise (62). The lower rate of repair in the tendon may impose a greater risk of injury to females. Additional research is required to determine the relationship between endogenous female hormones and tendons, and whether hormones contribute to sex differences in the development of tendinopathy.
The relationship between body composition and tendinopathy has been investigated. Increased adiposity has been identified as a risk factor for tendinopathy (63). In addition, higher body mass index (BMI) or body weight (64–68), larger waist girth (68), and higher waist-hip ratios (68–70) have also been associated with tendinopathies in various studies. Sex differences have not been studied with regard to these specific anthropometric measures. BMI, waist-hip ratio, and waist circumference have been used to measure general and central obesity and, in turn, to predict the risk of metabolic syndrome (71–76).
Fat distribution has also been studied in relationship to tendinopathy. In the study by Gaida et al. of subjects with asymptomatic Achilles tendon pathology as identified using ultrasound, adipose tissue distribution was measured using dual-energy x-ray absorptiometry (DXA) (70). The 17 males with abnormal Achilles tendons were reported to have higher android/gynoid fat mass ratios (0.616 ± 0.186 vs. 0.519 ± 0.142, P = .014) and higher upper-body/lower-body fat mass ratios (2.346 ± 0.630 versus 2.022 ± 0.467, P = .013) compared to 110 males with normal Achilles tendons (70). Higher android/gynoid fat mass ratios have been associated with metabolic syndrome and increased metabolic risk (77–79). The eight females with asymptomatic Achilles tendon abnormalities on ultrasound were reported to have lower central/peripheral fat mass ratios than the 163 females with normal Achilles tendons (0.711 ± 0.321 versus 0.922 ± 0.194, P = .004) (70). Overall, the study concluded that asymptomatic Achilles tendon pathology is associated with increased peripheral fat distribution in females and increased central fat distribution in males.
There are several hypotheses regarding the relationship between increased adiposity and tendons. There is a proposed direct mechanism where bioactive peptides are released by adipose tissue and directly influence tendon structure (63). Adipose tissue can release free fatty acids and pro-inflammatory cytokines into circulation that may adversely affect tendon function (68). A proposed indirect mechanism involves systemic metabolic changes associated with increased adiposity that could affect tendon structure (63). Another potential explanation is that increased waist girth, which has been demonstrated to correlate with weight, increases mechanical load on tendons, particularly the patellar tendon. Repetitive or excessive loading may lead to failure of tendon remodeling (68).
Mahieu et al. performed a prospective study of 69 male cadets who underwent 6 weeks of military training (80). Ten of the subjects were found to have Achilles tendon overuse injury as diagnosed by history and physical examination. Decreased plantar flexor strength measured prior to the military training was found to be a significant predictor for later development of Achilles tendon overuse injury (80). Plantar flexor strength less than 50 Nm was identified as a risk factor for developing Achilles tendon overuse injury (80). Females have been shown to have decreased absolute muscle strength when compared to males in prior studies (81,82), which may put females at risk for tendon injury in the lower limb. However, females have also been shown to have equal or greater strength relative to lean body mass or cross-sectional area (CSA) compared to males (83). Nevertheless, the Mahieu et al. study reported absolute ankle plantar flexor strength, and the lower absolute strength of females may place them at a higher risk of developing Achilles tendinopathy than males. Additional studies are required to further evaluate the relationship between strength differences and development of tendinopathy.
Neuromuscular Control and Biomechanics
Neuromuscular control has been studied to evaluate sex differences and relationship to tendon loading (84–87). In a comparison of male and female volleyball players, differences were noted in neuromuscular recruitment strategies of lower limb muscles when landing from a jump (84). The male volleyball players had significantly earlier semitendinosus and biceps femoris muscle onset compared to the females during landing. The males also reached peak semitendinosus activity before the time of peak patellar tendon force, while the females reached peak semitendinosus activity after peak patellar tendon force (84). A higher patellar tendon force loading rate was also shown to correlate significantly with lateral rectus femoris, vastus medialis, and biceps femoris muscle recruitment (84). While these neuromuscular recruitment differences between sexes were reported, no significant association was found among these differences and subsequent patellar tendon force magnitude, relative to body weight, at landing (84).
In terms of the influence of biomechanics on tendinopathy, several studies have evaluated the relationship between jumping characteristics and patellar tendinopathy. Visnes et al. performed a prospective cohort study to evaluate the impact of jumping ability at baseline on future development of patellar tendinopathy in 150 elite volleyball players 16 to 18 years old (68 males, 82 females) (88). Patellar tendinopathy was diagnosed by history and physical examination, with a minimum of 12 weeks of symptoms. The subjects performed the counter movement jump (CMJ) test in which they started at a stationary erect position with full extension of the knees, bent down to as low as 90° of knee flexion, and then jumped to the highest level, which is the end measurement. The authors reported that males who developed symptomatic patellar tendinopathy jumped higher in the CMJ test than males who remained asymptomatic and concluded that higher baseline jumping ability is a risk factor for developing jumper’s knee (88). For females, there was no difference in CMJ test at baseline when comparing those that developed patellar tendinopathy to those that did not. No differences were reported between males and females, though assessing sex differences in relation to the development of patellar tendinopathy was not a primary or secondary outcome measure in this study. Cook et al. studied symptomatic and asymptomatic elite junior basketball players and found that females with unilateral or bilateral patellar tendinopathy had a significantly higher vertical jump than those with normal tendons as identified by ultrasound (bilateral 51.0 ± 9.0 cm; unilateral 50.9 ± 6.8 cm; normal 46.1 ± 5.4 cm, P < .05) (89). No significant difference in vertical jump height was found in males with patellar tendinopathy compared to those with normal tendons (bilateral 64.4 ± 6.3 cm; unilateral 63.4 ± 6.0 cm; normal 62.0 ± 6.7 cm) (89). The authors concluded that higher vertical jumps are a risk factor for increased abnormal patellar tendon morphology in females, but not in males (89) and report that this difference between the females and males in their study was an unexpected finding, and expressed the need for further research to explain this difference (89).
Jump frequency and rate has also been studied with respect to risk of developing symptomatic patellar tendinopathy. In elite volleyball players ages 16 to 18 years, 12 of 26 males (46.2%) were diagnosed with patellar tendinopathy compared with 1 of 18 females (5.6%). Patellar tendinopathy was diagnosed by history and physical examination. Individual jump counts were compiled based on a review of recorded training sessions and matches. The males jumped 2.6 times more frequently than females in training and 1.5 times more frequently than females during matches (90). Given this potential sex difference in jump frequency, the authors conclude that jump frequency may be a risk factor for developing patellar tendinopathy.
Structural Properties of Tendon
There have been several studies looking at sex differences in the structure and mechanical properties of tendons. One study that measured patellar tendon elongation during isometric contractions in 10 young males and 10 young females showed differences in structural and mechanical properties between sexes (91). Torque was measured with a dynamometer while structure and mechanical properties were studied using ultrasound and co-contraction was estimated using electromyographic (EMG) activity. The authors report significantly different patellar tendon mechanical properties in males and females, including a 26% greater maximum total tendon stress in males compared to females during isometric knee extension (91). Sex differences have also been shown in the viscoelastic properties of tendons. In a study of Achilles tendon properties, females have been shown to have significantly lower stiffness of tendons than males, indicating more compliant tendons in females (92).
Westh et al. studied the effect of exercise and training on the structural and mechanical properties of the Achilles and patellar tendons. They found greater patellar tendon CSA in male runners than female runners (P < .01). They also reported greater patellar tendon stiffness in male runners (3528 ± 773 N/mm) compared with female runners and female nonrunners (2069 ± 666 N/mm, 2477 ± 381 N/mm, respectively) (P < .01) (60). Male runners were also reported to have greater weight-normalized Achilles tendon CSA compared to female runners (P < .01) (60). Andrew and Jonathan performed a study comparing Achilles tendon loading during running in male and female recreational runners. They concluded that males demonstrated a significantly greater Achilles tendon load than females (P < .05), and that this finding may help explain the increased incidence of Achilles tendon disorders in males (93).
Knobloch et al. studied 139 patients (average age 49) with symptomatic Achilles tendinopathy, analyzing tendon and paratendon microcirculation using noninvasive laser Doppler and spectrophotometry (59). Overall, females were found to have better tendon and paratendon microcirculation compared to males. Specifically, the symptomatic females were found to have increased Achilles tendon and paratendon oxygen saturation and reduced postcapillary venous filling pressures compared to symptomatic males (59). The authors report that a decrease in tendon oxygen saturation implies downregulation of tendon metabolism (59). While the study did state that 19% of females were taking oral contraceptive drugs, there was no collection of information on endogenous or exogenous hormone concentrations, so it is unclear if either of these variables influences tendon and paratendon microcirculation.
TREATMENT OF TENDINOPATHY
Another study by Knobloch et al. evaluated the response to eccentric training in patients with symptomatic Achilles tendinopathy (94). A total of 75 patients (44 males, 31 females) with a mean BMI of 26 ± 2 were evaluated. Initial pain scores on the visual analogue scale (VAS) were similar between females and males (5.6 ± 2.2 versus 5.4 ± 2.1). The study found that after 12 weeks of eccentric training, females had a significantly higher pain score on VAS (4.4 ± 2.6 versus 3.0 ± 2.1, P = .023). The Victorian Institute of Sport Assessment A (VISA-A) scores also improved in males by 27% (63 ± 12 to 86 ± 13), which was significant compared to a 20% improvement in females (60 ± 14 to 75 ± 11) (P < .05 for sex difference). Overall, females in this study were found to benefit less than males with symptomatic Achilles tendinopathy from 12 weeks of eccentric training (94). One limitation of the study was that endogenous or exogenous hormone concentrations were not measured and this might influence the females’ response to treatment.
Silbernagel et al. evaluated the 5 year outcome of patients with symptomatic Achilles tendinopathy who were treated with exercise (95). The patients consisted of 18 males and 16 females (average age of 51 ± 8.2 years) with Achilles tendinopathy and duration of pain for more than 2 months. The exercise program consisted of progressive Achilles tendon-loading strengthening, mainly eccentric exercises, monitored by a physical therapist for 12 weeks to 6 months. Overall, 80% of the patients treated with this exercise regimen fully recovered in regard to function and symptoms measured by various questionnaires. There were no sex differences in 5 year outcomes for patients with Achilles tendinopathy who were treated with exercise (95).
In terms of operative management of tendinopathy, Maffulli et al. studied the outcomes of 45 males and 41 females who underwent surgery for Achilles tendinopathy (96). The patients had unilateral Achilles tendinopathy, had failed conservative management for 3 to 6 months, including rest from sport or treatment with nonsteroidal anti-inflammatory drugs, physiotherapy, and injections, and had no prior surgeries on the affected tendon. The mean BMI in males (24.1 ± 3.8 kg/m2) was not significantly different from the mean BMI in females (26.8 ± 4 kg/m2) (96). However, the body fat percentage was higher in females (26.2) compared to males (18.1) (P < .01). The patients underwent surgical management with tenotomies and excision of degenerative areas. The females had more complications (superficial infections of the surgical wound) than the males (19.5% versus 6.7%). Five female patients underwent additional surgery compared with three male patients. Only 24 of 41 female patients (58.5%) reported excellent or good results compared to 39 of 45 males (86.7%), and the female patients took 8.3 months on average to return to activity compared to 4.7 months for the males. Overall, this study found that surgery for Achilles tendinopathy leads to worse results for females compared to males (96). Possible explanations for why females had worse outcomes include longer interval between referral and surgery, time between symptom onset and surgery, and higher body fat compared to males (96).