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Overuse Injuries in Sport: a Comprehensive Overview R Aicale et al. Journal of Orthopaedic Surgery and Research (2018) 13:309 https://doi.org/10.1186/s13018-018-1017-5 REVIEW Open Access Overuse injuries in sport: a comprehensive overview R. Aicale1*, D. Tarantino1 and N. Maffulli1,2 Abstract Background: The absence of a single, identifiable traumatic cause has been traditionally used as a definition for a causative factor of overuse injury. Excessive loading, insufficient recovery, and underpreparedness can increase injury risk by exposing athletes to relatively large changes in load. The musculoskeletal system, if subjected to excessive stress, can suffer from various types of overuse injuries which may affect the bone, muscles, tendons, and ligaments. Methods: We performed a search (up to March 2018) in the PubMed and Scopus electronic databases to identify the available scientific articles about the pathophysiology and the incidence of overuse sport injuries. For the purposes of our review, we used several combinations of the following keywords: overuse, injury, tendon, tendinopathy, stress fracture, stress reaction, and juvenile osteochondritis dissecans. Results: Overuse tendinopathy induces in the tendon pain and swelling with associated decreased tolerance to exercise and various types of tendon degeneration. Poor training technique and a variety of risk factors may predispose athletes to stress reactions that may be interpreted as possible precursors of stress fractures. A frequent cause of pain in adolescents is juvenile osteochondritis dissecans (JOCD), which is characterized by delamination and localized necrosis of the subchondral bone, with or without the involvement of articular cartilage. The purpose of this compressive review is to give an overview of overuse injuries in sport by describing the theoretical foundations of these conditions that may predispose to the development of tendinopathy, stress fractures, stress reactions, and juvenile osteochondritis dissecans and the implication that these pathologies may have in their management. Conclusions: Further research is required to improve our knowledge on tendon and bone healing, enabling specific treatment strategies to be developed for the management of overuse injuries. Keywords: Fractures, Stress fracture, Overuse injuries, Osteochondritis dissecans, Tendinopathy Background players to relatively large changes, or spikes, in load dur- The specific definition of overuse injury was most com- ing periods with higher training and match loads [4]. monly based on the concept of an injury occurring in The tendons transfer the force produced from muscular the absence of a single, identifiable traumatic cause [1]. contraction to the bone. In most instances, sports-related Professional soccer players sustain on average 2.0 injur- tendinopathies present well-defined histopathological le- ies per season, which cause them to miss 37 days in a sions, providing an explanation for the chronicity of symp- 300-day season on average [2]. Following the updated in- toms which often occur in athletes with tendinopathies jury etiology model, training and match load contribute, [5–8]. together with intrinsic and extrinsic risk factors, to the The aim of the present article is to investigate the multifactorial and dynamic etiology of injury [3]. Not physiopathology, clinical presentation, diagnostic tools, only excessive loading and insufficient recovery, but also and management of the most common overuse sport in- underpreparedness may increase injury risk by exposing juries. In particular, we focus on tendinopathy, stress re- action, stress fracture, and juvenile osteochondritis * Correspondence: [email protected] dissecans, which are the most frequent lesion caused by 1Department of Musculoskeletal Disorders, School of Medicine and Dentistry, University of Salerno, Salerno, Italy overuse. Furthermore, in the first part of this study, to Full list of author information is available at the end of the article © The Author(s). 2018 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. Aicale et al. Journal of Orthopaedic Surgery and Research (2018) 13:309 Page 2 of 11 better understand the changes of the bone, muscle, and Stress reactions of the musculoskeletal system may be tendon structures, we mention different mechanisms interpreted as possible precursors of stress fractures. present in an overuse situation. Biological tissues, in contrast to artificial products, can Overuse tendinopathy induces in the affected tendon react in numerous and complex ways. This can lead not pain and swelling, and associated decreased load tolerance only to a continual weakening of the tissue, but also to and function during exercise of the limb [9, 10]. Various adaption phenomena in response to overuse. The causes types of tendon degeneration have been described at elec- of such stress reactions are still unclear. tron microscopy, namely (a) hypoxic degeneration, (b) Juvenile osteochondritis dissecans (JOCD) is a frequent hyaline degeneration, (c) mucoid or myxoid degeneration, cause of pain in adolescents, both athletes and (d) fibrinoid degeneration, (e) lipoid degeneration, (f) cal- non-athletes. JOCD is characterized by delamination and cification, and (g) fibrocartilaginous and bony metaplasia localized necrosis of the subchondral bone, with or with- [11]. Healing of tendinopathic tendons relies on the intrin- out the involvement of the overlying articular cartilage sic ability of tenocytes to respond to the stimulus induced [28–31]. The etiology remains unclear, but repetitive by the injury to the surrounding tissue matrix [12, 13]and microtrauma, such as that typical of overuse injury, is con- consists of a cellular response including apoptosis (pro- sidered the significant factor leading to JOCD [28, 29]. grammed cell death), chemotaxis, proliferation, and differ- entiation [14]. The mechanism underlying the precise The role of inflammation and molecular factors in sequence of these events, which balance the effectiveness overuse injuries of healing and any subsequent predisposition to repetitive The effects of an altered inflammatory response damage, remains obscure. In this model, the question arises as to why the healing The essence of tendinopathy is a “failed healing re- response is successful in some individuals but fails in sponse.” This model suggests that, after an acute insult to others. More importantly, can we identify factors which the tendon, an early inflammatory response that would may increase the risk of this ineffective healing re- normally result in successful injury resolution veers to- sponse? For example, the incidence of tendinopathy is ward an ineffective healing response [15], with degener- increased in individuals with obesity and decreased insu- ation and proliferation of tenocytes, disruption of collagen lin sensitivity, as seen in patients with type 1 and type 2 fibers, and subsequent increase in non-collagenous matrix diabetes mellitus (T1/T2DM) [10, 32–34]. Evidence for a [7, 16–19](Table1). chronic, low-grade inflammatory state in obesity is rep- Poor training technique and a variety of risk factors may resented principally by marked increases in plasma levels predispose players to lower limb overuse injuries affecting of proinflammatory cytokines such as tumor necrosis the bone, including stress reactions to full-fledged stress factor (TNF)-a and interleukin (IL)-6, and proinflamma- fractures. The underlying principle of the bone response tory chemokines such as monocyte chemoattractant pro- to stress is Wolff’s law, whereby changes in the stresses tein (MCP)-1 [34]. imposed on the bone lead to changes in its internal archi- Patients with type 1 and type 2 diabetes exhibit a less tecture [20, 21]. Stress fractures, defined as microfractures effective healing response [35]. Recently, it has been of the cortical bone tissue, affect thousands of athletes per demonstrated the presence of an independent relation- year [22, 23]. Certain subpopulations, including runners, ship between impaired insulin sensitivity and the devel- gymnasts, and female athletes, exhibit higher rates of opment of chronic low-grade inflammation through a stress fractures [24, 25]. If left untreated, a stress fracture protein, the levels of which are normally physiologically can progress to a complete fracture of a bone, which may inhibited by insulin, called FOXO1, a key upregulator of require surgical fixation [26]. In addition, factors contrib- the proinflammatory cytokine IL-b [35]. uting to stress fractures increase the risk for osteoporosis, Considering the influence that a prolonged state of a substantial long-term health concern [27]. low-grade systemic inflammation may have on the heal- ing process after acute tendon injury, it must be appreci- Table 1 Types of tendon collagens ated that tendon healing is a delicate and prolonged Types of MW Quantity (%) Localization process even under optimal physiological conditions [10, collagens 34]. Even minor disruptions to any of the noted healing Type I 95.000
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