Tendon microinjuries become painful in tendinosis due to specific physiological processes.
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INSUFFICIENT LEANING
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The retrieved literature acknowledges that tendinosis involves pain associated with tendon degeneration and microinjuries, but it lacks detailed direct evidence explaining the specific physiological processes that convert tendon microinjuries into pain.
<h4>Background</h4>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.<h4>Methods</h4>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.<h4>Results</h4>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.<h4>Conclusions</h4>Further research is required to improve our knowledge on tendon and bone healing, enabling specific treatment strategies to be developed for the management of overus
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 status released display-pdf yes is-olf no is-manuscript no is-preprint no is-journal-matter no is-scanned no is-retracted no Received 2018 Jun 21; Accepted 2018 Nov 21; Collection date 2018. Background The specific
Recently, it has been demonstrated the presence of an independent relationship between impaired insulin sensitivity and the development of chronic low-grade inflammation through a protein, the levels of which are normally physiologically inhibited by insulin, called FOXO1, a key upregulator of the proinflammatory cytokine IL-b [ 35 ]. Considering the influence that a prolonged state of low-grade systemic inflammation may have on the healing process after acute tendon injury, it must be appreciated that tendon healing is a delicate and prolonged process even under optimal physiological conditions [ 10 , 34 ].
Even minor disruptions to any of the noted healing stages could result in a much more prolonged and complicated resolution of injury. Similarly, if several minor disruptions to this process occur (in the form, for example, of microtraumas), complete healing and resolution of injury become progressively unlikely [ 10 ]. The acute inflammatory phase noted in the first few days after a tendon injury is marked by the migration of inflammatory cells such as macrophages and monocytes [ 36 ].
Examining the incidence of tendinopathy among patients with type 2 diabetes, unilateral or bilateral tendinopathy was found in 32% of the diabetic patients studied versus 10% of controls [ 39 ]. Also, when the incidence of unilateral tendinopathy among diabetic patients was examined more closely, 45% were found to occur in the right shoulder compared with just 27% in the left shoulder [ 33 ]. Molecular factors in overuse injury A lack of exposure to adequate levels of physiological stress over a prolonged time period or “underloading” may paradoxically predispose to overload injury [ 34 ]. An underloaded tendon may become unable to cope with increased demands imposed on it.
In the four principal soccer leagues in England, there are an average of 3.5 Achilles tendon-related injuries per week in the preseason and an average of one injury per week in the competitive season [ 89 , 90 ]. Tendinopathies may result from excessive loading of the tendon and subsequent mechanical breakdown of the loaded tendon [ 91 ]. Theoretically, repeated microinjuries may occur, and the tendon may be able to heal a certain level of microinjury. However, as training and heavy loading of the tendon continues, this healing process may be overwhelmed, and a further injury ensues.
They can be divided into palpation tests (tendon thickening, crepitus, pain on palpation, the Royal London Hospital (RLH) test, the painful arc sign) and tendon loading tests (pain on passive dorsiflexion, pain on single heel raise, and pain on hopping). Plain radiography can be used to diagnose associated or incidental bony abnormalities [ 99 ]. Ultrasound is an effective imaging method since it correlates well with the histopathologic findings despite being an operator-dependent [ 100 ]. MRI studies should be performed only if the ultrasound scan remains unclear.
There may be a history of intermittent knee effusion following a practice or game session [ 29 ]. The examination may reveal mild effusion or limitation of motion of the knee. Findings may also vary depending on the stage of the disease [ 147 ]. In the early stages, with the articular cartilage over the femoral condyle still intact, the signs are non-specific. In the later stages, when the articular cartilage is eroded, the fragment may separate and become an intra-articular loose body. This can cause pain, effusion, and locking.
Degenerative tendinopathy results from the accumulation of minor injuries following unsuccessful tendon repair during acute tendon injuries. The process of tendon repair is prolonged and varies between individuals, making it susceptible to reinjury. Moreover, treating chronic tendinopathy often requires expensive and extensive rehabilitation, along with a variety of combined therapies to facilitate recovery. This condition significantly affects the quality of life of affected individuals, underscoring the urgent need for more efficient and cost-effective treatment options. Although traditional treatments have improved significantly and are being used as substitutes for surgical interventions, the findings have been inconsistent and conflicting. This review aims to clarify these issues by exploring the strengths and limitations of current treatments as well as recent innovations in managing various forms of degenerative tendinopathy.
Each phase involves specific cellular activities and biochemical pathways essential for effective healing ( Figure 2 ) [ 3 , 7 ]. Eccentric exercise (EC) can benefit many patients, but it may not be appropriate for everyone due to individual differences in tendon condition, pain tolerance, and other health factors [ 5 , 7 , 11 ]. Some patients may experience adverse effects or inadequate improvement, requiring alternative or additional therapies. The variability in patient outcomes emphasizes the need for personalized treatment plans in managing degenerative tendinopathy.
These morphological changes are associated with a progressive decline in tendon quality and function [ 30 ]. Early detection and prediction of Achilles tendinopathy (AT) remain challenging due to the absence of definitive biomarkers. Nevertheless, some studies have reported that a lower shear modulus in tendons is associated with improved clinical outcomes, with significant progress observed up to six months post-treatment.
Lateral Elbow Tendinopathy/Tennis Elbow/Lateral Epicondylitis (LET) Overuse of the extensor carpi radialis brevis (ECRB) tendon can lead to microinjuries, resulting in lateral epicondylitis (LET), commonly referred to as tennis elbow. This condition is frequently reported in tennis players, with approximately 75% of them experiencing tennis elbow pain due to constant grip and wrist extension. LET is characterized by persistent elbow pain. Fortunately, the prognosis of LET is generally good, as the majority of patients report spontaneous recovery.
The ECM of healthy tendons is predominantly composed of collagen (COL). COL1 constitutes 90% of the tendon ECM, while the remainder consists of COL III, V, XI, XII, and XIV. In addition to collagen, there are a variety of other non-collagenous
For example, a study by Yu et al. investigated the effects of aging on the activity of MMPs and TIMPs, revealing a significant upregulation of MMP-2 and MMP-9 levels in aging tenocytes compared to TIMP-1 and TIMP-2. This imbalance suggests that aging may compromise tendon structure and impair healing processes by promoting an overactive MMP-mediated matrix degradation. Such findings underscore the need for further investigation into therapeutic strategies aimed at restoring the MMP/TIMP equilibrium to preserve tendon health in aging populations [ 53 , 55 ].
In addition to maintaining the balance between matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs), several therapeutic strategies have been proposed to support extracellular matrix (ECM) recovery following tendon injury. One such approach is targeted exercise, which enhances the tendon’s ability to tolerate increased mechanical loads, improves its mechanical properties, and stimulates anabolic processes, thereby facilitating ECM homeostasis.
However, it has been shown that even short-term beneficial effects of NSAIDs may be patient specific. Heinemeier et al. observed that one-week ibuprofen treatment in individuals with Achilles tendinopathy did not initiate a reparative response in the affected tendon tissue, and any potential pain relief was moderate [ 97 ]. Long-term NSAID use has been reported to potentially impair bone and tendon functions [ 96 ]; thus, their use in tendinopathy remains controversial owing to limited efficacy in promoting tendon healing [ 98 ]. For example, Malmgaard et al.
These molecular processes convert a typically prolonged inactive early-to-middle healing phase into a more biologically active phase, resulting in significant improvement in tendon biomechanical properties [ 146 ]. Another important component of PRP, IGF-1, is known to exert anabolic effects by enhancing deoxyribonucleic acid (DNA) content and promoting collagen synthesis. It plays a crucial role in adult tendon growth in response to mechanical loading [ 147 ]. In addition, IGF-1 does not function by decreasing the migration of inflammatory cells.
It regulates numerous processes, such as the recruitment and regulation of proteins via DNA methyltransferases, histone deacetylases, DNA replication and transcription, and the action of miRNAs on target genes. Despite their significance in the initiation, progression, and regulation of inflammation, the epigenetic mechanisms underlying tendon pathologies remain largely unexplored. Investigating the interactions between epigenetic processes and tendon-specific inflammatory genes may pave the way for novel therapeutic strategies to treat tendon disorders [ 198 ].
In a study of 20 osteoarthritis patients treated with autologous concentrated adipose tissue, one patient experienced tendonitis-like swelling two months post-procedure, and two patients withdrew from the study due to persistent pain, opting for knee replacement [ 133 ]. In a trial of 43 patients with non-insertional Achilles tendinopathy, both SVF and PRP treatments significantly reduced pain, with SVF demonstrating faster recovery and better outcomes in tendon thickness and blood flow [ 134 ].
Enthesitis is a cardinal feature of spondyloarthropathies. The Achilles insertion on the calcaneus is a commonly evaluated enthesis located at the hindfoot, generally resulting in hindfoot pain and possible tendon enlargement. For decades, diagnosis of enthesitis was based upon patient history of hindfoot or posterior ankle pain and clinical examination revealing tenderness and/or enlargement at the site of the tendon insertion. However, not all hindfoot or posterior ankle symptoms are related to enthesitis. Advanced imaging, including magnetic resonance imaging (MRI) and ultrasound (US), has allowed for more precise evaluation of hindfoot and posterior ankle conditions. Use of US in diagnosis has helped confirm some of these cases but also identified other conditions that may have otherwise been misclassified without use of advanced imaging diagnostics. Conditions that may result in hindfoot and posterior ankle symptoms related to the Achilles tendon include enthesitis (which can include retrocalcaneal bursitis and insertional tendonopathy), midportion tendonopathy, paratenonopathy, superficial calcaneal bursitis, calcaneal ossification (Haglund deformity), and calcific tendonopathy. With regard to classification of these conditions, much of the existing literature uses confusing nomenclature to describe conditions in this region of the body. Some terminology may imply inflammation when in fact there may be none. A more uniform approach to classifying these conditions based off anatomic location, symptoms, clinical findings, and histopathology is needed. There has been much debate regarding appropriate use of tendonitis when there is no true inflammation, calling instead for use of the terms tendinosis or tendonopathy. To date, there has not been clear examination of a similar overuse of the term enthesitis in conditions where there is no underlying inflammation, thus raising the need for more comprehensive taxonomy.
Abstract The chronic painful tendinosis tendon is generally considered a degenerated and weak tendon. However, this has not been scientifically verified, and is to be considered a hypothesis. We present here a case study involving a high‐level Olympic weightlifter with chronic painful patellar tendinosis who started heavy‐weight training very early after successful treatment with sclerosing injections. A 25‐year‐old super heavy‐weight (+105 kg) Olympic weightlifter with 9 months duration of severe pain (prohibiting full training) in the proximal patellar tendon, where ultrasound and Doppler showed a widened tendon with structural changes and neovascularisation, was given one treatment with ultrasound and Doppler‐guided injections of the sclerosing agent polidocanol. The injections targeted the neovessels posterior to the tendon. The patient was pain‐free after the treatment, and already after 2‐weeks he started with heavy‐weight training (240 kg in deep squats) to try to qualify for the Olympics. Additional very heavy training on training camps, most often without having any discomfort or pain in the patellar tendon, resulted in Swedish records and ninth place at the European Championships 17 weeks after the treatment. Despite beating the national records, he did not qualify for the Olympics. Ultrasound and Doppler follow‐ups have shown only a few remaining neovessels, and little structural tendon changes. This case questions previous theories about the weak tendinosis tendon, and stresses the importance of studies evaluating tendon strength.
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