Lower extremity tendinopathy has an incidence rate of 10.52 per 1000 person-years and a prevalence rate of 11.83 per 1000 person-years in a Dutch general practice population. The mean age of the tendinopathy patients was higher than the mean age of the general practice population. There were no statistically significant differences between the tendinopathy patients and the general practice population regarding gender, use of medication, or co-morbidities.
This is the first study to investigate the incidence and prevalence of adductor related tendinopathy, jumper’s knee, and plantar fasciopathy in a general practice population. The incidence and prevalence for Achilles tendinopathy in a general practice population has been studied once before; our results are similar to the numbers found by De Jonge et al. in the Netherlands in 2011 [2]. The incidence of greater trochanteric pain syndrome was higher than the incidence of 1.8 per 1000 per year found by Lievense et al. [10]. However, in their study only 54 % of the originally selected patients responded to the questionnaire designed to verify the patients’ symptoms, which could introduce a bias and might explain the difference with our results.
To put the numbers into perspective, the total incidence and prevalence of locomotor system symptoms seen by Dutch general practitioners are 267 and 397 per 1000 persons per year, respectively [20]. The numbers found in our study indicate that the incidence of lower extremity tendinopathy represents 3.0 % of all new locomotor system symptoms seen by general practitioners. In addition, the incidence found for tendinopathy in the current study was higher than the incidence of osteoarthritis in the Dutch general practice population in 2012 (8.4 per 1000 person-years) [21]. While prevention of osteoarthritis is already high on international research agendas [22], the prevention of tendinopathy has received little attention. The negative impact that tendinopathy can have on the ability to work and quality of life of patients calls for more research into preventive measures, especially because the treatment can be difficult [3, 4].
In the current study, the mean age of tendinopathy patients was significantly higher than the mean age of the general practice population. Earlier studies have found tendinopathy to be more prevalent among older people [11, 12]. The exact mechanism why older tendons seem to be more prone to damage remains to be elucidated. One theory attributes the effect to the accumulation of chronic repetitive damage over time [23]. Another hypothesis is that age-related changes in tendon structure and biomechanics could decrease the loading capacity and regenerative capacity of the tendons [24].
We found no significant difference in the percentages of men and women when we compared the tendinopathy patients to the practice population. Research among athletes shows different outcomes per tendinopathy. The male gender is considered a risk factor for jumper’s knee [13, 25]. Earlier, the male gender was found to be a risk factor for Achilles tendinopathy as well [26]. However, in athletes over 40 years of age, Longo et al. did not find a difference in risk between men and women [27]. Plantar fasciopathy does not seem to have a male or female predisposition [28].
Although in the current study the prevalence of diabetes among the tendinopathy patients was twice as high as the prevalence of diabetes in the general practice population, this difference was not statistically significant. This conflicts with earlier research, in which diabetes was found to be a risk factor for tendinopathy [29]. It is possible that our relatively small study population explains this difference in outcomes. There is evidence that diabetes can alter tendon structure, possibly through an excess of advanced glycation end products as a result of hyperglycaemia [17]. In this study, we did not look into the levels of blood glucose in the patients with diabetes. In general, Dutch patients who are being checked by their general practitioner or practice nurse are well regulated. However, we cannot exclude the possibility that poorly regulated or not yet diagnosed patients with diabetes were in the dataset. Gaida et al. have questioned whether the higher risk of tendinopathy associated with diabetes is caused by a disturbance in glucose metabolism per se. They proposed that the higher risk might have to be attributed to the overweight associated with diabetes [30, 31]. The influence of overweight on tendinopathy has been explained in two different ways. One of the theories is that the extra weight leads to an increased loading of the tendons. However, this theory does not explain why non-weight bearing tendons also more often develop tendinopathy in overweight persons [11]. Another theory is that lipocytes have an effect on tendon structure by their metabolic activity [30]. In a recent review on tendinopathy in athletes, Scott et al. state there is evidence for both a mechanical effect and a systemic effect, but the relative contributions of the two mechanisms should be further investigated [31]. In this study, no exact data on BMI of the tendinopathy patients were available.
There were no significant differences in the prevalence of hypertension between the tendinopathy patients and the practice population. Only few patients had dyslipidaemia, so we could not draw conclusions on the association between dyslipidaemia and tendinopathy. We did not have data on how well controlled the patients with hypertension and dyslipidaemia were. Future research could clarify whether developing tendinopathy is related to levels of control of lipids and tension.
Although the use of corticosteroids and fluorquinolones has been identified as a risk factor for developing tendinopathy [14, 15], in this study only few patients were treated with corticosteroids or fluoroquinolones before the start of the symptoms, so we could not draw conclusions on the association between the use of these medications and tendinopathy. The percentage of tendinopathy patients using statins was not significantly different from the percentage of people using antilipaemic drugs in the total practice population. Marie et al. investigated reports on statin-induced tendinous disorders and concluded that these complications are very rare, given the large number of statin prescriptions [16]. The mechanism behind these complications is unknown, but in a rat study De Oliveira et al. described an association between statin treatment and alterations in tendon metabolism [32].
Several factors could have influenced the outcomes of this study. An important factor is the help-seeking behavior of patients and the organization of (para)medical care in the Netherlands, which could have led to an underestimation of the actual incidence and prevalence of lower extremity tendinopathy in the general population. People with musculoskeletal problems do not always seek professional help. Picavet et al. state that half of the people with musculoskeletal complaints visit a health care professional, and 33 to 42 % of people visit a general practitioner for their complaints [33]. In addition, since 2006 patients do not need to be referred by their general practitioner to visit a physical therapist. Podotherapists are directly accessible since 2011, and in the studied time frame patients did not need to be referred by their general practitioner to visit a sports physician either. People with tendinopathy symptoms could therefore have gone directly to one of these healthcare professionals, instead of visiting their general practitioner. Another factor which could have influenced the outcomes, is the use of ICPC codes. Although a wide combination of ICPC codes was used to identify the cases, it is possible that some cases were missed. A general practitioner could have accidentally given the wrong ICPC code to a consult. In the current study, one case of Achilles tendinopathy was found under the ICPC code L15 (knee complaints).
A factor that could have led to an overestimation of the actual incidence and prevalence of lower extremity tendinopathy, is the inclusion of the greater trochanteric pain syndrome. Although most cases of greater trochanteric pain syndrome are caused by gluteal tendinopathy [34–36], there is a possibility that in some patients the pain was caused by e.g. primary trochanteric bursitis or referred pain from degenerative joint disease.
As this study focused on the epidemiology in primary care, we followed the clinical description and diagnosis as performed by the general practitioners. This entails that the diagnoses were not confirmed by medical imaging as general practitioners rarely order diagnostic imaging when a tendinopathy is suspected. As this was not the scope of this study, validation of these clinical diagnoses by adding additional investigations like medical imaging should be object of future research.
A strength of this study is that it provides insight into the incidence and prevalence of lower extremity tendinopathy among the general practice population, which was currently lacking. It also provides an easily applicable search strategy that allows to investigate multiple tendinopathies at the same time. Limitations of this study are the retrospective design and the relatively small study population, which might hinder extrapolation of the results. However, the numbers for Achilles tendinopathy in the current study were similar to those found by De Jonge et al., who collected data from different geographical locations in the Netherlands [2].
