Calcific tendinopathy is a common pain disorder of unclear origin characterised by the deposition of hydroxyapatite crystals in a tendon, most often in tendons of the rotator cuff of the shoulder. Degenerative changes in collagen fibres have been suggested to be responsible for dystrophic calcification. A local decrease in oxygen tension, not always due to chronic strain, may lead to reduction of pH in a critical region, with fibrocartilaginous metaplasia and resultant calcification. Rotator cuff calcification occurs in 3–8% of healthy shoulders in adults, more frequently in women, during the 4th–6th decades of life, sometimes bilaterally.
In a group of 30 subjects (20 women, 10 men; mean age 51.1, range 27–63 years) with rotator cuff calcification, treated with two-needle US-guided percutaneous treatment, we analysed phospho-calcium metabolism markers (calcaemia, phosphorus, magnesium, 25-OH vitamin D, 1,25(OH)2-vitamin D, calciuria, phosphaturia and PTH). 28 patients showed a low level of 25-OH vitamin D (mean value: 16.96 ng/mL, 3–26 ng/mL), calcitriol at or above the upper limits (mean value: 62.77 pg/mL), and PTH concentration in line with the 25OHD levels, most frequently at the upper normal limits. Urinary levels of calcium and phosphorus were at or below the lower limits.
Vitamin D, as well as enhancing intestinal absorption of calcium, plays an important role in the regulation of bone mineralisation, stimulating both RANKL and osteoprotegerin expression. A transient hyperparathyroidism secondary to vitamin D deficiency may be at the origin of heterotopic calcifications in patients with rotatory cuff tendinopathy. Administration of 25OHD, by reducing transient increases of PTH and directly acting on connective tissue cells, could probably reduce the phenomenon or even prevent it.
Tendinopathy is of distinct interest as it describes a painful tendon disease with local tenderness, swelling and pain associated with sonographic features such as hypoechogenic texture and diameter enlargement. Recent research elucidated microcirculatory changes in tendinopathy using laser Doppler flowmetry and spectrophotometry such as at the Achilles tendon, the patellar tendon as well as at the elbow and the wrist level. Tendon capillary blood flow is increased at the point of pain. Tendon oxygen saturation as well as tendon postcapillary venous filling pressures, determined non-invasively using combined Laser Doppler flowmetry and spectrophotometry, can quantify, in real-time, how tendon microcirculation changes over with pathology or in response to a given therapy. Tendon oxygen saturation can be increased by repetitive, intermittent short-term ice applications in Achilles tendons; this corresponds to 'ischemic preconditioning', a method used to train tissue to sustain ischemic damage. On the other hand, decreasing tendon oxygenation may reflect local acidosis and deteriorating tendon metabolism. Painful eccentric training, a common therapy for Achilles, patellar, supraspinatus and wrist tendinopathy decreases abnormal capillary tendon flow without compromising local tendon oxygenation. Combining an Achilles pneumatic wrap with eccentric training changes tendon microcirculation in a different way than does eccentric training alone; both approaches reduce pain in Achilles tendinopathy. The microcirculatory effects of measures such as extracorporeal shock wave therapy as well as topical nitroglycerine application are to be studied in tendinopathy as well as the critical question of dosage and maintenance. Interestingly it seems that injection therapy using color Doppler for targeting the area of neovascularisation yields to good clinical results with polidocanol sclerosing therapy, but also with a combination of epinephrine and lidocaine.
Tendinopathy of the flexor carpi ulnaris tendon is a rare entity. Recent research revealed the role of a neurovascular ingrowth at the point of pain in various tendinopathic locations, such as at the Achilles and patellar tendon, in plantar fasciitis as well as in supraspinatus and tennis elbow tendinopathy. However, beyond the elbow no such neovascularisation has been reported to date.
We present a 35‐year old tennis player suffering tremendous pain (visual analogue scale (VAS) rating of 9/10) at the flexor carpi ulnaris tendon with adjacent calcification in close proximity to the pisiform bone. The patient was assessed with power Doppler and laser Doppler quantification of neovascularisation at the point of pain.
Power Doppler and laser Doppler quantification of neovascularisation at the point of pain identified higher capillary blood flow at three points over the painful vs the non‐painful tendon (146/240/232rU vs 93/74/70rU at the non‐affected side). Sclerosing therapy using polidocanol under power and laser Doppler guidance was initiated, with immediate decrease of capillary blood flow by 25% with resolution of the neovascularisation in power Doppler. Immediately following sclerosing, the patient's reported pain level on the VAS was reduced from 9/10 to 4/10. Following a short period of rest, eccentric training of the forearm muscle was initiated over 12 weeks with functional complete recovery and complete resolution of wrist pain.
Sclerosing therapy using polidocanol under power‐ and laser‐Doppler guidance can decrease capillary blood flow by 25% with resolution of the neovascularisation. Subsequent eccentric training of the forearm muscle over 12 weeks can result in complete resolution of wrist pain.
Our understanding of the pathogenesis of "tendinopathy" is based on fragmented evidences like pieces of a jigsaw puzzle. We propose a "failed healing theory" to knit these fragments together, which can explain previous observations. We also propose that albeit "overuse injury" and other insidious "micro trauma" may well be primary triggers of the process, "tendinopathy" is not an "overuse injury" per se. The typical clinical, histological and biochemical presentation relates to a localized chronic pain condition which may lead to tendon rupture, the latter attributed to mechanical weakness. Characterization of pathological "tendinotic" tissues revealed coexistence of collagenolytic injuries and an active healing process, focal hypervascularity and tissue metaplasia. These observations suggest a failed healing process as response to a triggering injury. The pathogenesis of tendinopathy can be described as a three stage process: injury, failed healing and clinical presentation. It is likely that some of these "initial injuries" heal well and we speculate that predisposing intrinsic or extrinsic factors may be involved. The injury stage involves a progressive collagenolytic tendon injury. The failed healing stage mainly refers to prolonged activation and failed resolution of the normal healing process. Finally, the matrix disturbances, increased focal vascularity and abnormal cytokine profiles contribute to the clinical presentations of chronic tendon pain or rupture. With this integrative pathogenesis theory, we can relate the known manifestations of tendinopathy and point to the "missing links". This model may guide future research on tendinopathy, until we could ultimately decipher the complete pathogenesis process and provide better treatments.
Achilles tendinopathy is a common condition, which can become chronic and interfere with athletic performance. The proteinase inhibitor aprotinin (as injection) has been found to improve recovery in patellar tendinopathy1 (evidence level 1b2) and Achilles tendinopathy.3 Internationally this therapy is being used based on this limited knowledge base.
To evaluate whether aprotinin injections decrease time to recovery in Achilles tendinopathy.
A prospective, randomised, double blind, placebo controlled trial was performed comparing saline (0.9%) plus local anaesthetic injections and eccentric exercises with aprotinin (30 000 kIU) plus local anaesthetic injection and eccentric exercise. Three injections were given, each a week apart. In total, 26 patients, with 33 affected tendons, were enrolled for this study.
At no follow up point (2, 4, 12, or 52 weeks) was there any statistically significant difference between the treatment group and placebo. This included VISA‐A scores4 and secondary outcome measures. However, a trend for improvement over placebo was noted.
In this study on Achilles tendinopathy, aprotinin was not shown to offer any statistically significant benefit over placebo. Larger multicentre trials are needed to evaluate the efficacy of aprotinin in Achilles tendinopathy.
Tendinopathy is a common and significant clinical problem characterised by activity‐related pain, focal tendon tenderness and intratendinous imaging changes. Recent histopathological studies have indicated the underlying pathology to be one of tendinosis (degeneration) as opposed to tendinitis (inflammation). Relatively little is known about tendinosis and its pathogenesis. Contributing to this is an absence of validated animal models of the pathology. Animal models of tendinosis represent potential efficient and effective means of furthering our understanding of human tendinopathy and its underlying pathology. By selecting an appropriate species and introducing known risk factors for tendinopathy in humans, it is possible to develop tendon changes in animal models that are consistent with the human condition. This paper overviews the role of animal models in tendinopathy research by discussing the benefits and development of animal models of tendinosis, highlighting potential outcome measures that may be used in animal tendon research, and reviewing current animal models of tendinosis. It is hoped that with further development of animal models of tendinosis, new strategies for the prevention and treatment of tendinopathy in humans will be generated.
collagen; connective tissue; tendinitis; tendinosis; tendon
The efficacy of platelet-rich plasma (PRP) in the treatment and healing of chronic tendinopathy through stimulation of cell proliferation and total collagen production has been demonstrated by both in vitro and in vivo studies. The aim of this study is to evaluate the effectiveness of ultrasound (US)-guided autologous PRP injections in patellar and Achilles tendinopathy.
Materials and methods
Autologous PRP was injected under US-guidance into the Achilles and patellar tendons (30 Achilles tendons, 28 patellar tendons) in 48 prospectively selected patients (30 males, 18 females, mean age 38 ± 16 years, range 20–61 years). All patients were previously evaluated according to the Victoria Institute of Sport Assessment (VISA) scale, which assessed pain and activity level, and they all underwent US of the tendon before treatment and at follow-up after 20 days and 6 months. Statistical analysis was performed with Chi-square and Wilcoxon tests.
20 days after PRP injection the patients presented a non-significant improvement of clinical symptoms. At the 6-month follow-up VISA score increased from a mean value of 57–75.5 (p < .01). US evaluation revealed a reduction of hypoechoic areas in 26 tendons (p < .01) associated with a widespread improvement of fibrillar echotexture of the tendon and reduced hypervascularity at power Doppler.
PRP injection in patellar and Achilles tendinopathy results in a significant and lasting improvement of clinical symptoms and leads to recovery of the tendon matrix potentially helping to prevent degenerative lesions. US-guidance allows PRP injection into the tendon with great accuracy.
Platelet-rich plasma; Achilles tendon; Patellar tendon; Jumper's knee; Achilles tendinopathy
A tendinopathy is a clinical condition characterized by activity-related pain, focal tendons tenderness, and intratendinous imaging changes. This study characterizes a surgically induced tendinopathy in a goat model with a noninvasive in vivo longitudinal followup based on physical examination and US. Cross-sectional area (CSA) is the most objective feature for the evaluation of tendinopathy in correlation with clinical findings. The deep digital flexor tendon (DDFT) of the left hind limb of six goats was isolated and scarified by a modified splitting. Pain and lameness at walk and trot were evaluated. External width and thickness of tendon region were measured by calipers. CSA and the ratio lesion/tendon CSA were obtained at days 0, 7, 21, 42, and 84 by US. The highest value of global functional score was obtained at day 7, then decreased until day 40 and was not significantly different from day 0 at the end of the study. The external width recovered a normal value at the end of the study, but the external thickness was still significantly increased (P < 0.05). Peritendinous oedema was observed at day 7, but intratendinous lesions were visible only at day 21 as a focal hypo to anechoic area. At day 84, two tendons still presented visible lesions. US examination was reproducible, specific, and provided complementary information to the global functional score. A standardized focal tendinopathy was induced in goats. This experimental model of focal tendinopathy could be used to study the effect of different treatments.
Several members of the ADAMTS (A Disintegrin And Metalloproteinase with ThromboSpondin motifs) family have been identified as aggrecanases, whose substrates include versican, the principal large proteoglycan in the tendon extracellular matrix. We have characterized the expression of ADAMTS-4 in human Achilles tendon and tendon-derived cells. ADAMTS-4 mRNA levels were higher in ruptured tendon compared with normal tendon or chronic painful tendinopathy. In tissue extracts probed by Western blotting, mature ADAMTS-4 (68 kDa) was detected only in ruptured tendons, while processed ADAMTS-4 (53 kDa) was detected also in chronic painful tendinopathy and in normal tendon. In cultured Achilles tendon cells, transforming growth factor-β (TGF-β) stimulated ADAMTS-4 mRNA expression (typically 20-fold after 24 h), while interleukin-1 induced a smaller, shorter-term stimulation which synergised markedly with that induced by TGF-β. Increased levels of immunoreactive proteins consistent with mature and processed forms of ADAMTS-4 were detected in TGF-β-stimulated cells. ADAMTS-4 mRNA was expressed at higher levels by tendon cells in collagen gels than in monolayer cultures. In contrast, the expression of ADAMTS-1 and -5 mRNA was lower in collagen gels compared with monolayers, and these mRNA showed smaller or opposite responses to growth factors and cytokines compared with that of ADAMTS-4 mRNA. We conclude that both ADAMTS-4 mRNA and ADAMTS-4 protein processing may be differentially regulated in normal and damaged tendons and that both the matrix environment and growth factors such as TGF-β are potentially important factors controlling ADAMTS aggrecanase activities in tendon pathology.
ADAMTS, A Disintegrin And Metalloproteinase with ThromboSpondin motifs; Ct, threshold cycle; DMEM, Dulbecco's modified Eagle's medium; EGF, epidermal growth factor; FCS, fetal calf serum; FGF, fibroblast growth factor; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; IL-1β, interleukin-1β; PDGF, platelet-derived growth factor; TGF-β, transforming growth factor-β; TNF, tumour necrosis factor; ADAMTS; Aggrecanase; Tendon; Transforming growth factor-β
Surgical reattachment of tendon and bone such as in rotator cuff repair, patellar-patella tendon repair and anterior cruciate ligament (ACL) reconstruction often fails due to the failure of regeneration of the specialized tissue ("enthesis") which connects tendon to bone. Tendon-to-bone healing taking place between inhomogenous tissues is a slow process compared to healing within homogenous tissue, such as tendon to tendon or bone to bone healing. Therefore special attention must be paid to augment tendon to bone insertion (TBI) healing. Apart from surgical fixation, biological and biophysical interventions have been studied aiming at regeneration of TBI healing complex, especially the regeneration of interpositioned fibrocartilage and new bone at the healing junction. This paper described the biology and the factors influencing TBI healing using patella-patellar tendon (PPT) healing and tendon graft to bone tunnel healing in ACL reconstruction as examples. Recent development in the improvement of TBI healing and directions for future studies were also reviewed and discussed.
Chronic rotator cuff tears are often associated with pain or poor function. In a rat with only a detached supraspinatus tendon, the tendon heals spontaneously which is inconsistent with how tears are believed to heal in humans.
We therefore asked whether a combined supraspinatus and infraspinatus detachment in the rat would fail to heal and result in a chronic injury in the supraspinatus tendon.
We acutely detached the supraspinatus and infraspinatus tendons in a rat model. At 4, 8, and 16 weeks post-detachment, biomechanical testing, collagen organization, and histological grading were evaluated for the detached supraspinatus and infraspinatus tendons and compared to controls.
In the detached supraspinatus tendon, area and percent relaxation were increased at all time points while the modulus and stiffness were similar to those of controls at 4 and 8 weeks. Collagen disorganization increased at late time points while cellularity increased and cells were more rounded in shape. In the detached infraspinatus tendon, area and percent relaxation were also increased at late time points. However, the modulus values initially decreased followed by an increase in both modulus and stiffness at 16 weeks compared to control. In the detached infraspinatus, we also observed a decrease in collagen organization at all time points and increased cellularity and a more rounded cell shape.
Due to the ongoing changes in mechanics, collagen organization and histology in the detached supraspinatus tendon compared to control animals at 16 weeks, this model may be useful for understanding the human chronic tendon tear.
This rat rotator cuff chronic model can be used to test hypotheses regarding injury and repair mechanisms that cannot be addressed in human patients or in cadaveric studies.
Electronic supplementary material
The online version of this article (doi:10.1007/s11999-009-1206-y) contains supplementary material, which is available to authorized users.
OBJECTIVE: To establish if computed tomography (CT) imaging, which has proved helpful in detecting intra-articular tophi in gout, can also be used to document gouty enthesopathy and tendinopathy. METHODS: Three patients with tophaceous gout and clinical involvement of the Achilles tendon (two cases) or patellar tendon (one case) were assessed with CT examination and plain radiographs. RESULTS: In the first two cases, CT images revealed linear or nodular high attenuation opacities within the substance of the Achilles tendons and their calcaneal insertion. In case 3, dense linear opacities were seen within the patellar tendon and within its tibial insertion. No such opacities of the tendons and entheses were seen on standard radiographs of these patients. CONCLUSIONS: CT appears to be the imaging method of choice for demonstrating monosodium urate deposits in entheses and tendons in tophaceous gout.
Tendons and ligaments within the upper and lower limbs are some of the more common sites of musculoskeletal injuries during physical activity. Several extrinsic and intrinsic factors have been shown to be associated with these injuries. More recently, studies have suggested that there is also, at least in part, a genetic component to the Achilles tendon, rotator cuff and anterior cruciate ligament injuries. However, specific genes have not been suggested to be associated with rotator cuff or anterior cruciate ligament injuries. Sequence variants of the tenascin C (TNC) gene, on the other hand, have been shown to be associated with Achilles tendinopathies and Achilles tendon ruptures, whereas a variant of the collagen V α 1 (COL5A1) gene has also been shown to be associated with Achilles tendinopathies. Both genes encode for important structural components of tendons and ligaments. The COL5A1 gene encodes for a component of type V collagen, which has an important role in regulating collagen fibre assembly and fibre diameters. The TNC gene, on the other hand, encodes for TNC, which regulates the tissue's response to mechanical load. To date, only variants in two genes have been shown to be associated with Achilles tendon injuries. In addition, although specific genes have not been identified, investigators have suggested that there is also a genetic component to both rotator cuff and anterior cruciate ligament injuries. In future, specific genotypes associated with increased risk of injury to specific tendons and ligaments can prevent these injuries by identifying individuals at higher risk.
Pathologic processes intrinsic and extrinsic to the tendons have been proposed as the underlying cause of rotator cuff disease, but the precise etiology is not known. Tear formation is, in part, attributable to the accumulation of subrupture tendon fatigue damage. We review the molecular, mechanical, and structural changes induced in tendons subjected to controlled amounts of fatigue loading in an animal model of early tendinopathy. The distinct tendon responses to low and moderate levels of loading, as opposed to high levels, provide insight into the potential mechanisms for the therapeutic benefits of exercise in the treatment of rotator cuff tendinopathy. The progression of damage accumulation leading to fiber rupture and eventual tendon tearing seen with higher loading illustrates the progression from tendinopathy to full-thickness tearing. We hope that this more realistic animal model of tendon fatigue damage will allow better assessment of biologic, mechanical, tissue-engineering, and rehabilitation strategies to improve repair success.
Rotator cuff tear; tendon fatigue damage; biologic; healing
There are several treatment modalities for calcifying tendinitis of the shoulder. If the pain becomes chronic after several months of conservative treatment, open or arthroscopic removal is usually recommended. Recently, extracorporeal shock wave therapy has shown encouraging results in treating calcific deposits.
Materials and methods
We report a retrospective study to compare the outcome after arthroscopic extirpation (group I, 22 cases) with the effect of low extracorporeal shock wave therapy (group II, 24 cases) in patients with a chronic homogeneous calcific deposit in the supraspinatus tendon. Patients included in the study had undergone unsuccessful conservative therapy in the previous six months with no evidence of subacromial impingement of the rotator cuff independent of the calcium deposit or rupture of the rotator cuff detected by sonography or magnetic resonance imaging. AP and LL radiographies were performed for all of the patients at least one week before the treatment and 24 months after the treatment. To keep the possibility of spontaneous resorption low, the deposit had to be sharply outlined and densely structured on the radiograph (types I and II in the Gärtner classification). In group II, the patients underwent an average of three treatment sessions of extracorporeal shock waves therapy with 1,500 impulses/session of 0.10–0.13 mJ/mm2.
Preoperative symptoms (P = 0.09), sex (P = 0.17), operated (P = 0.11) and dominant (P = 0.33) limbs, and age (P = 0.99) of the two groups did not show a significative difference between groups. According to the University of California Los Angeles (UCLA) rating system, the mean score in group I improved from 9.36 (±5.2) to 30.3 (±7.62) points after 24 months, with 81.81% reporting good or excellent results (P < 0.001). In group II the mean score after 24 months rose from 12.38 (±6.5) to 28.13 (±9.34) points, with 70.83% reporting good or excellent results (P < 0.001). Radiologically, after two years of follow up, there was no calcific deposit in 86.35% (P < 0.001) of the patients of group I and in 58.33 % (P < 0.001) of the patients of group II. According to the UCLA scores, there was no significant difference between the groups at two years of follow-up (P = 0.38).
We conclude that shock wave therapy is equivalent to arthroscopy, and so shock wave therapy should be preferred because of its noninvasiveness.
Arthroscopy; Shock waves; Calcification; Tendinitis; Shoulder
The impetus for the use of patellar straps in the treatment of patellar tendinopathy has largely been based on empirical evidence and not on any mechanistic rationale. A computational model suggests that patellar tendinopathy may be a result of high localized tendon strains that occur at smaller patella–patellar tendon angles (PPTAs).
Infrapatellar straps will decrease the mean localized computational strain in the area of the patellar tendon commonly involved in jumper’s knee by increasing the PPTA.
Controlled laboratory study.
Twenty adult males had lateral weightbearing and nonweightbearing radiographs of their knees taken with and without 1 of 2 infrapatellar straps at 60° of knee flexion. Morphologic measurements of PPTA and patellar tendon length with and without the straps were used as input data into a previously described computational model to calculate average and maximum strain at the common location of the jumper’s knee lesion during a simulated jump landing.
The infrapatellar bands decreased the predicted localized strain (average and maximum) in the majority of participants by increasing PPTA and/or decreasing patellar tendon length. When both PPTA and patellar tendon length were altered by the straps, there was a strong and significant correlation with the change in predicted average localized strain with both straps.
Infrapatellar straps may limit excessive patella tendon strain at the site of the jumper’s knee lesion by increasing PPTA and decreasing patellar tendon length rather than by correcting some inherent anatomic or functional abnormality in the extensor apparatus.
The use of infrapatellar straps may help prevent excessive localized tendon strains at the site of the jumper’s knee lesion during a jump landing.
infrapatellar straps; patellar tendon strain; patellar tendinopathy; patella–patellar tendon angle; computational model
Objectives. Histological examination of pathological tendon generally does not reveal signs of inflammation. However, the inflammatory cytokine IL-6 has been shown to be expressed in ruptured rotator cuff tendon. The aim of this study was to investigate the expression of IL-6 family members in painful posterior tibialis tendon (PTT) and in painful and ruptured Achilles tendon (AT) compared with normal tendon.
Methods. AT samples were obtained from cadavers (normal) or from patients undergoing surgical procedures to treat chronic painful tendinopathy or ruptured tendon. PTT samples were obtained from patients undergoing surgery for other reasons (normal) and from patients with PTT dysfunction (painful). Total RNA was extracted and mRNA expression was analysed by quantitative real-time PCR.
Results. Collagen type I α-chain I (COL1A1) expression was increased in both painful PTT and AT compared with normal. Ciliary neurotrophic factor levels were increased in painful PTT only. In the painful AT, cyclooxygenase-2 (COX2) and IL-6 expression increased compared with normal. In the ruptured AT, levels of VEGF A, COX2, oncostatin-M, leukaemia inhibitory factor and IL-6 expression were higher compared with both normal and painful AT. IL-6R expression decreased in both painful and ruptured AT compared with normal.
Conclusion. Painful AT and PTT show different expression patterns, indicating a substantial difference between those two tendinopathies. Inflammatory markers are up-regulated in painful and particularly in ruptured AT, pointing towards a role of inflammation not only in rupture healing, but also in Achilles tendinopathy.
gene expression; tendinopathy; tendon rupture; OSM; LIF; CNTF; IL-6; Achilles tendon; posterior tibialis tendon
The terminology of Achilles tendon pathology has become inconsistent and confusing throughout the years. For proper research, assessment and treatment, a uniform and clear terminology is necessary. A new terminology is proposed; the definitions hereof encompass the anatomic location, symptoms, clinical findings and histopathology. It comprises the following definitions: Mid-portion Achilles tendinopathy: a clinical syndrome characterized by a combination of pain, swelling and impaired performance. It includes, but is not limited to, the histopathological diagnosis of tendinosis. Achilles paratendinopathy: an acute or chronic inflammation and/or degeneration of the thin membrane around the Achilles tendon. There are clear distinctions between acute paratendinopathy and chronic paratendinopathy, both in symptoms as in histopathology. Insertional Achilles tendinopathy: located at the insertion of the Achilles tendon onto the calcaneus, bone spurs and calcifications in the tendon proper at the insertion site may exist. Retrocalcaneal bursitis: an inflammation of the bursa in the recess between the anterior inferior side of the Achilles tendon and the posterosuperior aspect of the calcaneus (retrocalcaneal recess). Superficial calcaneal bursitis: inflammation of the bursa located between a calcaneal prominence or the Achilles tendon and the skin. Finally, it is suggested that previous terms as Haglund’s disease; Haglund’s syndrome; Haglund’s deformity; pump bump (calcaneus altus; high prow heels; knobbly heels; cucumber heel), are no longer used.
Achilles paratendinopathy; Insertional tendinopathy; Haglund; Terminology; Tendinosis; Retrocalcaneal bursitis
Chronic mid-portion Achilles tendinopathy is generally difficult to treat as the background to the pain mechanisms has not yet been clarified. A wide range of conservative and surgical treatment options are available. Most address intratendinous degenerative changes when present, as it is believed that these changes are responsible for the symptoms. Since up to 34% of asymptomatic tendons show histopathological changes, we believe that the tendon proper is not the cause of pain in the majority of patients. Chronic painful tendons show the ingrowth of sensory and sympathetic nerves from the paratenon with release of nociceptive substances. Denervating the Achilles tendon by release of the paratenon is sufficient to cause pain relief in the majority of patients. This type of treatment has the additional advantage that it is associated with a shorter recovery time when compared with treatment options that address the tendon itself. An evidence-based philosophy on the cause of pain in chronic mid-portion Achilles tendinopathy is presented.
Level of evidence V.
Achilles; Mid-portion; Painful; Cause of pain; Tendon
Nitric oxide (NO) is a small free radical generated by a family of enzymes, the nitric oxide synthases (NOSs). Following injury to a tendon, NO is induced by all three isoforms of NOS and NOS activity is also upregulated in tendinopathy. In animal models when NOS activity is inhibited by competitive inhibitors of NOS, tendon healing is reduced. When additional NO is added, tendon healing is enhanced. In humans, in three randomised clinical trials, we have shown that NO delivered via a transdermal patch enhances the subjective and objective recovery of patients with tennis elbow, Achilles tendinosis and supraspinatus tendinosis.
Achilles tendinopathy is understood to be a failed healing response. Operative management is utilised following the failure of non-operative methods.
We present a case of Achilles tendon rupture, sustained whilst isometrically loading the Achilles tendon during an eccentric loading exercise programme. Conclusion: Bilateral surgical exploration and debridement had previously been performed after conservative management of bilateral Achilles tendinopathy had been unsuccessful.
The aging population is at an increased risk of tendon injury and tendinopathy. Elucidating the molecular basis of tendon aging is crucial to understanding the age-related changes in structure and function in this vulnerable tissue. In this study, the structural and functional features of tendon aging are investigated. In addition, the roles of decorin and biglycan in the aging process were analyzed using transgenic mice at both mature and aged time points. Our hypothesis is that the increase in tendon injuries in the aging population is the result of altered structural properties that reduce the biomechanical function of the tendon and consequently increase susceptibility to injury. Decorin and biglycan are important regulators of tendon structure and therefore, we further hypothesized that decreased function in aged tendons is partly the result of altered decorin and biglycan expression. Biomechanical analyses of mature (day 150) and aged (day 570) patellar tendons revealed deteriorating viscoelastic properties with age. Histology and polarized light microscopy demonstrated decreased cellularity, alterations in tenocyte shape, and reduced collagen fiber alignment in the aged tendons. Ultrastructural analysis of fibril diameter distributions indicated an altered distribution in aged tendons with an increase of large diameter fibrils. Aged wild type tendons maintained expression of decorin which was associated with the structural and functional changes seen in aged tendons. Aged patellar tendons exhibited altered and generally inferior properties across multiple assays. However, decorin-null tendons exhibited significantly decreased effects of aging compared to the other genotypes. The amelioration of the functional deficits seen in the absence of decorin in aged tendons was associated with altered tendon fibril structure. Fibril diameter distributions in the decorin-null aged tendons were comparable to those observed in the mature wild type tendon with the absence of the subpopulation containing large diameter fibrils. Collectively, our findings provide evidence for age-dependent alterations in tendon architecture and functional activity, and further show that lack of stromal decorin attenuates these changes.
Tendon; Aging; Biglycan; Decorin; Proteoglycan; Extracellular matrix
Although presumed, damage in the remaining (intact) rotator cuff tendons in the presence of an isolated supraspinatus tendon tear or multiple tendon tear has not been well studied. This study utilized an animal model of multiple rotator cuff tendon tears to investigate alterations in the remaining (intact) tendon mechanical properties at 4 and 8 weeks post-injury. Twenty-four animals served as uninjured controls, while seventy-two were divided among the tendon detachment groups (supraspinatus tendon detachment, supraspinatus+infraspinatus tendon detachment, supraspinatus+subscapularis tendon detachment). We found the remaining (intact) rotator cuff tendons have decreased mechanical properties in the presence of rotator cuff tears. Remaining (intact) subscapularis and infraspinatus tendon cross-sectional area increased, while tendon modulus decreased after both one and two tendon tears. Additionally, the remaining (intact) tendon cross-sectional areas continued to increase with time post-injury. These alterations could potentially lead to further tendon damage and tear progression.
High resolution colour Doppler ultrasound shows intratendinous Doppler activity in patients with chronic Achilles tendinopathy. Treatment of this neovascularisation with sclerosing therapy seems to relieve the pain. However, the procedure often has to be repeated.
To investigate the effect of electrocoagulation of the neovessels on tendon pain and tendon vascularity in patients with chronic Achilles tendinopathy.
Colour Doppler ultrasound guided electrocoagulation was used on vessels in the ventral portion of the Achilles tendon in 11 patients (seven men, four women, mean age 41 years) with painful chronic mid‐portion Achilles tendinosis. A unipolar coagulation device was used.
One patient dropped out after two months (dissatisfied with the results). The remaining 10 patients (91%) were satisfied. These 10 patients were still satisfied at six months of follow up and had returned to their previous level of activity. All 10 patients were “cured” after one treatment. The patient who dropped out received two treatments because of lack of progress. There was significantly reduced pain (Likert pain scale, 0–10) during activity, from a median of 7 (range 4 to 10) at baseline to 0 (0 to 8) at six months' follow up (p<0.005); and at rest, from 1.5 (1 to 5) to 0 (0 to 8) (p = 0.005). In all patients, vascularisation was unchanged at the six months follow up, with no significant change in semiquantitative or quantitative colour scoring.
Coagulation in the area with vessels entering the tendon appears to be effective treatment for painful chronic mid‐tendinous Achilles tendinopathy. No effect on the intratendinous Doppler activity could be detected, suggesting that the effect is independent of changes in blood flow. Localisation of hyperaemia appears to be the key to the pathology and for targeting the treatment. One explanation could be that the effect is obtained by destruction of nerves accompanying the vessels.
Achilles tendinopathy; colour Doppler; coagulation therapy
Injection of Dexamethasone (Dex) is commonly used in clinics to treat tendon injury such as tendinopathy because of its anti-inflammatory capabilities. However, serious adverse effects have been reported as a result of Dex treatment, such as impaired tendon healing and tendon rupture. Using both in vitro and in vivo approaches, this study was to determine the effects of Dex treatment on the proliferation and differentiation of human tendon stem cells (hTSCs), which can directly impact tendon healing. We found that Dex treatment stimulated cell proliferation at lower concentrations (< 1000 nM), whereas a high concentration (1000 nM) decreased cell proliferation. Moreover, at all concentrations used (5, 10, 100, and 1000 nM), Dex treatment induced non-tenocyte differentiation of hTSCs, as evidenced by a change in cell shape, a nearly complete suppression of collagen type I expression, and an upregulation of non-tenocyte related genes (PPARγ and Sox-9), which was especially evident when higher concentrations (> 10 nM) of Dex were used. Implantation of Dex-treated hTSCs for a short time (3 weeks) resulted in the extensive formation of fatty tissues, cartilage-like tissues, and bony tissues. These findings suggest that Dex treatment in clinics may cause a paradoxical effect on the injured tendons it is supposed to treat: by inducing non-tenocyte differentiation of hTSCs, Dex treatment depletes the stem cell pool and leads to the formation of non-tendinous tissues (e.g. fatty and cartilage-like tissues), which make tendon susceptible to rupture.
Dexamethasone; tendinopathy; tendon stem cells; proliferation; differentiation