Osgood-Schlatter Disease: History
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Osgood-Schlatter disease is the most common osteochondritis of the lower limb in sport-practicing children and adolescents. Its manifestation usually coincides with the appearance of the secondary ossification center of the tibia and is linked to the practice of sports with an explosive component. 

  • Osgood-Schlatter
  • knee pathology
  • patellar tendon
  • patellar tendonitis

1. Introduction

Osgood-Schlatter disease (OSD), also known as Lannelongue disease [1], is a type of osteochondrosis first described by Osgood and Schlatter in 1903 [2]. It consists of the onset of a traction apophysitis as a consequence of repeated contractions of the femoral rectum part of the quadriceps [3] (see Figure 1) and may be bilateral [4]. OSD is one of the most common overuse of the lower limb injuries among children and adolescents [5] and is usually a self-limiting pathology [6]. Its manifestation coincides with the development of the secondary ossification center of the anterior tibial tuberosity (apophyseal phase), which usually occurs at around age 9 in girls and 11 in boys. However, symptoms usually first appear between ages 8 and 12 among the former, and between 12 and 15 among the latter [7]. Despite this, cases in adults have been reported [8]. OSD has been associated with other pathologies and alterations, such as compartment syndrome, meniscal and patellar tendon injuries [9] or hyperactivity and attention deficit [10]. In addition, nearly 40% of patients reported pain after long-term follow up, which may lead to consequences such as the chronification of knee pain and the appearance of tendinosis, which, in turn, will end up conditioning the application of surgical techniques [11].
Figure 1. Illustration of the typical features of Osgood-Schlatter disease.

2. Epidemiology

The prevalence of OSD ranges from 6.8% to 33% [12][13][14], affecting 1 in 10 athletic adolescents [3], and depends on factors such as the degree of development, the sport discipline or the presence of preventive programs [6]. For example, Lucena et al. found a prevalence of 9.8% among males and females (mean age 13.7 years) [8], while Kujala et al. reported a prevalence of 12.9% (mean age: 13.1 years) [9]. Furthermore, it seems that symptoms increase as bone maturation progresses and that the onset does not depend on the hours of sports practice [15]. Symptoms can persist until adulthood in 10% of cases [16]. Additionally, between 20% and 30% of all cases are bilateral [17].

2.1. Gender

The ratio of cases between males and females is 14:1 [18]. Furthermore, Kaneuchi et al. found different prevalence peak ages according to gender. When no gender distinction was made, the peak age was found to be 12 (prevalence of 13.8% for boys and 11.4% for girls). However, among girls, the peak was between 9 and 10 (9.2–10.9%), while among boys it was 14 (10.3%). This fact could be explained due to the fact that girls reach the bone maturation stage of the tibial tuberosity two years earlier than boys [15]. Furthermore, some authors suggest that the risk of developing OSD is higher among females during the epiphyseal stage, particularly among sports practitioners [14].

2.2. Practice Level

Lucena et al. [8] calculated a prevalence of 13% among adolescents who practiced sports and 6.7% among those who did not. In comparable groups, Kujala et al. [9] found a prevalence of 21% and 4.5%, respectively. The previous findings seem to indicate that the incidence is higher among the sport-practicing adolescent population.

2.3. Sports

OSD is the knee pathology with the highest incidence among adolescent soccer players [19] and accounts for 13.6% of all knee pathologies in soccer players aged 12 to 15 [20]. Furthermore, it is bilateral in 20–30% of cases [21][22]. It has also been reported among practitioners of other sports that feature explosive, anaerobic and acyclic components and continuous changes of direction, such as basketball, sports gymnastics, volleyball, karate, taekwondo, baseball and running, as well as among people who practice multiple sports [23][24][25][26].

2.4. Bilaterality of the Disease

Although the etiology is not clear and the causes are still unknown, a common hypothesis is that the asynchronous development of bone and soft tissue during the maturation stage (especially of the femoral rectum part of the quadriceps) generates imbalances [27]. Alterations in traction forces are considered a trigger for OSD because the force levels that increase considerably in certain growth phases can generate imbalances. This increases stress in the joint and generates bilateral asymmetry between limbs, which exacerbates the incidence of this pathology [28].

3. Etiopathology

The appearance of OSD seems to be multifactorial and encompasses mechanical, functional, morphological, environmental and psychosocial factors [29][30].

3.1. Mechanical Factors

Most authors believe that the main cause is sustained traction of the patellar tendon and the repetitive strain caused by a strong and violent pull of the muscle and the patellar tendon applied on the apophyseal cartilage of the anterior tibial tuberosity [31], along with change that happen during a growth spurt [32]. The stress loads transmitted from the quadriceps to the cartilage through the quadriceps and patellar tendons end up causing a cartilaginous avulsion, which, as the ossification center tends to consolidate, will evolve towards the creation of bone tissue. Thus, for example, a higher incidence of OSD has been found in the support leg due to the tractional loads applied when the quadriceps contracts eccentrically [25]. Occasionally, bone fragmentation may be observed in the late evolutionary stages [16]. In patients affected by OSD, Enomoto et al. observed a lower deformation capacity of the patellar tendon per unit of tractional force [33]. This highlights the mechanical and anatomical causes associated with specific situations (patella alta, patella infera, shortening of the rectus femoris or quadriceps muscle tightness/inflammation in the tendon) as key elements in the appearance of OSD due to segment avulsion [34][35].
Despite all this evidence, some authors also determined that OSD is a tendinous injury and not an avulsion fracture. It appears, according to this other causal factor theory, that it begins in the apophyseal stage and looks like an apophysiolysis compared to an epiphysiolysis, only representing a precondition before the impact of pathologic stress forces without signs of osteonecrosis [36].

3.2. Functional Factors

Firstly, the strength level decompensation between the quadriceps and the hamstrings should be highlighted, given the existing agonist–antagonist relation between both muscles [37][38]. Several other highly influential factors are the type of movement pattern (jumping actions, sprints, kicks and changes of direction), increase in muscle mass and strength levels which appear in the pubertal period (especially among boys), flexibility reduction in the quadriceps muscle [8] and application of intensive (high training loads in a short time) and highly specific (repetition of movement patterns in which high inertial loads are generated) training. Furthermore, it appears that increased tension in the rectus and biceps femoris, gastrocnemius and soleus may also play a role in the etiopathology [1].

3.3. Morphological Factors

The main risk factors for the support leg appear to be height, weight, body mass index (BMI), loss of flexibility in both legs, height of the internal longitudinal arch of the support foot (risk increases with taller arch), previous diagnosis of Sever’s pathology [39], reduction of the ankle dorsal flexion of 10° or less [40], tibial rotations (an increase in the condyle-malleolar angle and tibial external rotation) [41][42], concomitant genu valgum and pronated foot [43] and lateral patellofemoral maltracking [44]. In patients analyzed with Nuclear Magnetic Resonance (NMR) techniques, Demirag et al. [29] found that when the patellar tendon was inserted more proximally and in a larger area of the tibia, the risk of OSD increased. Furthermore, Green et al. [45] recently found a direct relationship between a greater posterior tibial slope angle and a higher incidence of OSD and Pan et al. [46] demonstrated a higher Insall–Salvati Index in non-operative OSD patients.

3.4. Environmental Factors

The appearance of OSD may be induced by factors related to the management of training loads, such as the intensity level during physical exercise, volume [47] and its modification [48][49], early specialization [50] and even with certain dietary deficiencies, such as vitamin D deficiency, particularly in countries with few hours of sun [51][52]. It also seems that the incidence is greater during the winter, especially in cold countries. Vitamin D plays an essential role in calcium phosphate homeostasis, and its deficiency leads to disruption in the growth plate organization. For these reasons, some authors have theorized about the possibility that fragility in the tibial tuberosity could appear in adolescents with vitamin D deficiency, which would compromise the enthesis’ mechanical response. Although this theory has yet to be confirmed, when children with OSD and vitamin D deficiency took a supplement, symptoms disappeared [52].

3.5. Psychological Factors

Reassurance and family education seem to be key components of successful treatment, management and recovery of OSD. The occasionally long duration of OSD symptomatology—sometimes over a year—could have repercussions on the way the patients perceive the injury and recovery. In most sports, it is known that long-term injuries, in which the patient experiences pain, produce worsened sleep, increased anxiety, heightened catastrophizing and low mood, especially among young athletes [53][54]. In this regard, the support of family and the health professionals who treat the athlete is essential. In a study conducted among health professionals treating OSD, 85% of those surveyed considered that psychological factors were important for returning to activity [30].

4. Symptomatology and Diagnosis

The main symptom of OSD is pain of variable intensity which increases when the site is pressed, especially in positions such as kneeling [55]. Furthermore, inflammation and hypersensitivity are commonly found in the anterior tibial tuberosity, where the patellar tendon inserts. This can be observed especially during physical and sports practice and might manifest as a limp. During the acute phase, symptoms usually evolve gradually from light and occasional to severe and continuous pain [8][16]. Thickening of the patellar tendon insertion can be noticed upon palpation, and is often accompanied by pain, particularly when resisted knee extensions or counter-resisted flexions are performed [23]. The pain is usually linked to an increase in blood flow to the area, which over time may cause neo-vascularization [56]. Guldhammer et al. [57] found that the median duration of OSD was 90 months (interquartile range, 24–150 months), with 42.9% of patients reporting daily pain. According to Kaya et al. [58], approximately 50% of patients fully recovered 2 years after being diagnosed, though levels of extensive strength continued to be lower. The differences between the studies could be explained by factors such as the type of sport practiced, patient age at the time of the event, methodology used and various environmental and cultural factors. Despite this, some cases may become chronic and complications such as pseudoarthrosis, genu recurvatum, patella alta, fragmentation–migration of bone fragments and a reduced knee flexion [4] or even osteochondromatosis may appear [59].
OSD diagnosis is mostly clinical and based on symptoms [32]. However, it should be confirmed by complementary radiological tests (X-ray, ultrasound or MRI), which allow OSD to be differentiated from other types of pathologies, such as fractures, tumors and infections, tendinitis or Hoffa’s disease [15][23][60].

4.1. Conventional Radiology

Usually, this is the first-choice complementary technique to rule out other pathologies, especially if its presentation is severe or atypical [61]. A sagittal plane of the knee with thigh rotation of 10–20° allows for easy identification of irregularities and separations of the apophysis from the tibial tuberosity, especially in early stages. In more advanced stages, it allows to identify bone fragmentation [40]. In general, X-rays allow for the establishment of three different levels of involvement: Grade (I), slight tuberosity elevation; Grade (II), radio lucidity of the tuberosity; and Grade (III), tuberosity fragmentation. On the other hand, some cases are asymptomatic, despite structural alterations being observed during radiological examination [62].

4.2. Ultrasound

Ultrasound is used in OSD diagnosis and monitorization given it is non-invasive, reliable, fast and low cost. It allows to visualize the fragmentation of the ossification center, patellar tendon injuries, the presence of edema and the appearance of possible reactive bursitis [15][38][63].

4.3. Nuclear Magnetic Resonance (NMR)

Possibly the most sensitive technique for diagnosis, since it enables the visualization of cartilage and the detection of edema, even before an ossification center tear occurs [64]. Furthermore, it is key for the early detection of the pathology [65]. Unfortunately, its high cost usually limits its use to cases in which the previous techniques prove insufficient. Hirano et al. [66] described five stages of OSD based on this technique: Stage 0—NMR is normal, although the patient may present certain symptoms; Stage 1 or early stage—no signs of inflammation visible in radiological exploration; Stage 2 or progressive stage—the torn secondary ossification center can be observed; Stage 3 or terminal stage—the ossicle has been completely separated and thickening of the tendon appears; and Stage 4 or healing proliferation of new bone tissue is observed.
Recently, other objective methodologies, such as algometry or thermography, have been used as diagnostic tools, with promising results [67].

This entry is adapted from the peer-reviewed paper 10.3390/healthcare10061011

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