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Tendon Lesions and Soft Tissue Rheumatism-Great Outback Or Great Opportunity?

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Tendon Lesions and Soft Tissue Rheumatism-Great Outback Or Great Opportunity? Annals ofthe Rheumatic Diseases 1996; 55: 1-3 ARD Ann Rheum Dis: first published as 10.1136/ard.55.1.1 on 1 January 1996. Downloaded from Annals of the Rheumatic Diseases Leader Tendon lesions and soft tissue rheumatism-great outback or great opportunity? In 1979, Dixon described soft tissue rheumatism as 'the This group of diseases make up a high proportion of great outback ofRheumatology, a vastfrontier land, iUl-defined rheumatological practice in the UK, but traditionally little and little explained, itsfeatures poorly categorised andfarfrom effort has been made to understand their underlying internationally agreed.' Has much changed in the past 15 pathology. There are a number of reasons for this. Soft years? tissue lesions are not life threatening, unlike the much rarer immunological and inflammatory rheumatological diseases. Soft tissues are rarely biopsied, so samples are difficult Soft tissue rheumatism in 1995 to obtain and current animal models do not necessarily Musculoskeletal symptoms without frank arthritis are very reflect the chronic degenerative lesions found in aging common. Most of us suffer such symptoms each year. patients. However, while there is lack of pathological They usually occur in one region, in an individual who is information on many of these lesions, there are usually otherwise well. These regional musculoskeletal disorders, adequate clinical features to allow identification of which have commonly been overlooked in the planning individual conditions. and provision of health care, are disorders of major and Perhaps the biggest hindrance to progress in our increasing importance. understanding of soft tissue rheumatism has been a Soft tissue rheumatism accounts for up to 25% of negative attitude to the affected tissues, which are still http://ard.bmj.com/ all hospital consultations for the rheumatic disorders.' thought of as inert, homogeneous structures. This is Shoulder pain is prevalent and often under reported, with certainly true of diseases where tendon tissues are symptoms or disability in at least 20% of the elderly principally involved. hospital population.2 Data from United Kingdom general practitioners suggest that, each year, approximately 1:170 of the adult population will present to their general Tendon diseases practitioner with a new episode of shoulder pain.3 Lateral The biological function of a tendon is to pull and transmit on September 23, 2021 by guest. Protected copyright. epicondylitis is estimated to affect four adults per 1000 muscle power. Rupture-partial or complete-is its worst each year, particularly those aged 35-54 years. Most functional failure, but it may also fail by adhering within experience a recurrence of symptoms within 18 months.4 its sheath or by stenosis ofthe sheath. Tendon function can Soft tissue rheumatism is certainly still confusing. In be impaired locally by trauma and in systemic disease, by clinical practice it is often difficult to ascertain the under- inflammation and fibrosis, by impairment ofblood supply, lying disorder. Different tissues such as muscle, ligament, or by atrophy or degeneration and calcification, and some- tendon, and tendon sheaths can be affected, and often times, in systemic disease, by metabolic deposits. minor injury and inflammation cause much pain and The role of tendons is often considered to be passive, dysfunction. Disorders can be classified by clinico- the tissue relatively inert and very much secondary to other pathological process (tendinitis), by anatomical region joint structures such as bone, cartilage, and synovium- (shoulder pain), or by aetiology (repetitive strain syndrome). tissues which have received the greater share of attention. The heterogeneity of soft tissue rheumatism poses con- These misconceptions are belied by recent studies investi- siderable problems in arriving at a sensible programme of gating human tendon lesions, that demonstrate that these treatment and system of management. For example, more tissues are metabolically active, interesting, and worthy of than 40 treatments have been proposed for lateral epi- research. condylitis, reflecting the lack of consensus about how to treat this and other soft tissue conditions.5 Soft tissue rheumatism also remains costly; the lesions HISTOLOGICAL STUDIES are chronic and have been estimated to result in the loss In shoulder tendon lesions, changes occur in the appear- of up to 1 1 million working days annually.' Most cases of ance of human tendon collagen fibres and the distribution lateral epicondylitis are managed in primary care, although of tendon cells and arterioles. There is an increase in cells the condition causes considerable loss from work and resembling chondrocytes and arteriole intimal hyperplasia, industrial compensation. Labelle et al6 reported that, particularly in older specimens.7 Analysis of spontaneously among industrial workers, an average of62 days per patient ruptured tendons shows degenerative changes that include is lost from work. changes in collagen fibre size and orientation, with an 2 Cawston, Riky, Hazleman increased deposition of proteoglycan between the fibres. of different populations of tenocytes and the factors that The tenocytes have enlarged vacuoles that can contain control tendon cell matrix metabolism (synthesis and lipids, and sometimes cell necrosis is found. In certain turnover). Ann Rheum Dis: first published as 10.1136/ard.55.1.1 on 1 January 1996. Downloaded from cases calcium is deposited. These changes are not present in all tendons, although they can occur together in some specimens.8 Similar changes are found in human tendons GROWTH FACTOR AND CYTOKINE STUDIES removed at operation for rotator cuff degeneration and Growth factors in general have anabolic effects on tissues, lateral epicondylitis.9 These studies have used routine increasing matrix synthesis and reducing matrix break- histological techniques for descriptive investigations; other down. Cytokines such as interleukin-1 (IL-1) and tumour studies have investigated these lesions biochemically. necrosis factor a often have the opposite effect, decreasing matrix synthesis and upregulating the proteinases that promote matrix breakdown."6 Recent studies have shown BIOCHEMICAL STUDIES that tendons in vitro respond to IL-1 by altering the Biochemical studies have shown that diseased supra- synthesis of matrix components and proteinases such as spinatus tendons have an increased concentration of the matrix metalloproteinases.'7 "' The production of dermatan sulphate and chondroitin sulphate and a three excessive enzyme activity can exceed that oflocal inhibitors fold increase in hyaluronan,'0 showing that a change in such as the tissue inhibitors of metalloproteinases and so proteoglycan synthesis has occurred. There is also an lead to tissue collagen breakdown.'6 19 Knowledge of the increase in cell numbers, a reduced collagen content, response ofaging human tenocytes to cytokines would help possibly caused by an increase in collagen degradation, and determine the role of these factors in the pathological in the majority (88%) an increased collagen type III changes found in diseased tendons. content is present'" (table). These changes are consistent with inflammation and a fibroproliferative response, presumably in an attempt to repair the tendon defect, Tendon disease mechanism although it is not known if this process is primary or These multidisciplinary studies suggest a common disease secondary to the tendon rupture. mechanism (figure), whereby various traumas to the tendon (for example impingement, trauma, hypoxia) induce growth factors that stimulate the tendon fibroblasts, CELLULAR STUDIES changing the pattern of matrix synthesis. This alteration, Normal tendons adapt to their mechanical environment with the deposition of tenascin20 and new synthesis of and this has profound implications for tendon physiology glycosaminoglycan,8 may be a protective response to com- and pathology. A highly specialised 'fibrocartilage' develops pression or shear forces. Whatever the cause, these changes in regions of tendons exposed to compression.'2 These are accompanied by cell rounding and an upregulation of regions differ biochemically and structurally from tension proteinases that result in the loosening and then net loss bearing regions of tendon and have characteristics some- ofpart of the collagen fibrillar network. In normal tendons where between that of classic tendon regions and articular these responses are followed by the tendon replacing this cartilage.'3 Although type I collagen remains the principal altered matrix, and a normal tendon structure reforms. matrix component, the cellular activity in these com- http://ard.bmj.com/ pressed regions includes the synthesis of both type II collagen and aggrecan.'4 These studies demonstrate that tendon cells are metabolically responsive, capable ofrepair, Normal Overuse ? ,,---+| tendon and maintain the matrix composition by a balance between Microtrauma ? anabolic and catabolic processes.'5 The ability of aging tenocytes to synthesise macromolecules and to remodel Hypoxia ? on September 23, 2021 by guest. Protected copyright. and repair tendon defects is consequently of major Cell rounding, importance in human tendon degeneration and injury, but Adaptation! i Cell/matrix repair matrix synthesi much more needs to be known about the varied responses I_ and degradatio)n response ? Biochemical changes in supraspinatus 'tendinitis't Cytokines Normal Degenerate Growth factors ? supraspinatus supraspinatus
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