Skeletal Radiol (1990) 19:1-3 Skeletal Radiology

Osteoarthritis revisited

Iain Watt and Paul Dieppe

Department of Radiology and Rheumatology, Royal Infirmary, Bristol, UK

Abstract. Current research challenges the concept that osteoarthritis is an inevitably progressive disease. Evidence suggests that many factors are involved and that the radiological features represent a spectrum of bone and joint response to disease, rather than reflect disease as such.

Key words: Osteoarthritis - Pathogenesis

Some time ago it was questioned whether osteoarthritis (OA) was one disease or many [23]. Since then much support has been forthcoming for the postulate that OA is a heterogeneous condition [22]. Careful studies of clinical and radiological features, together with the use of other imaging modalities, such as radionuclide scintigraphy, are now providing new insights into the many faces of OA [18, 201.

OA is strongly associated with increasing age [3]. Ageing causes many changes in joint architecture, includ- ing an increase in joint congruity, reduced cartilage volume and proteoglycan content, and reduced bone mass. Age alone also results in radiographic features including joint space narrowing and marginal osteophy- tosis which have been hitherto considered cardinal signs of OA [16]. However, it is clear from biochemical and pathological studies that age alone is an insufficient cause for OA, and that enormous differences exist between the old joint and the osteoarthritic one [2].

How then can osteoarthritis be recognised, character- ised, investigated and subsetted? The way forward in- cludes meticulous analysis of individual clinical and radio- graphic features, coupled with learning from further imaging modalities so that specific patterns can be recognised and delineated. Time-honoured theories of OA are held in question by such studies.

Address reprint requests to." I. Watt, Departments of Radiology and Rheumatology, Royal Infirmary, Bristol BS2 8HW, UK

In addition to age association a striking feature of OA is its limited articular distribution. Why should the distal interphalangeal joints and the carpometacarpal joint of the thumb be affected, while other hand joints are predominantly spared? Why are hips and knees affected more often then shoulders and ankles? Almost certainly the aetiology of OA involves a complex set of genetic and environmental influences. It is clearly multifactorial. Joint shape and biomechanical influences must be in- cluded in the determinance.

Recently a hypothesis has been advanced to explain the distribution of OA in terms of primate evolution and joint shape [13]. It is suggested that many joints have not adapted sufficiently to the change of function associated with an upright posture. Fundamental changes have occurred in the position and function of the acetabulum and in remodelling of the femoral condyles associated with prolonged bipedal weight-bearing and the ability to lock the knee into full extension in such a position. Minor degrees of dysplasia have been emphasised in association with OA at the hip [21] and, more recently, the knee [4]. Minor abnormalities of joint shape, perhaps reflecting a lack of design, may have a wider significance in the pathogenesis of OA than has been hitherto suspected.

Articular use and abuse are generally regarded as significant in the pathogenesis and localisation of OA. However, it has proved difficult to explain OA on a simple mechanical basis, and attempts to relate it directly to overuse or indeed certain activities have proved largely unsuccessful. A recent hypothesis has been advanced that under-utilisation of part of a joint's range of movement may contribute to the preselection of that joint to involvement by OA [1].

A need remains for simple clinical and epide- miological studies of OA looking at joint distribution and associations. These then must be related to outcome so that the significance of putative subsets can be es- tablished. Current studies indicate that several patterns of joint involvement may occur, each with different associ- ations [5]. Patients presenting with disease of the hip, as

�9 1990 International Skeletal Society

2 I. Watt and P. Dieppe: Osteoarthritis revisited

opposed to the knee, have different age, sex, racial and other demographic features suggesting that they may be quite different conditions [12]. Hip disease in Caucasians has a male bias and a probable association with facet joint arthritis in the cervical and lumbar spine. Knee OA has a strong female bias in association with obesity, hyperten- sion, and an increased risk of hand OA. In addition, there exists a severe form of OA of the hand with marked inflammatory features and erosive changes [24]. Only in the very elderly does the disease tend to become more generalised, affecting all of the vulnerable (underdesigned or underused?) joint sites. It is possible that clinically and radiologically, several different types of disorder are presenting, all of which result in a similar end stage of joint response to injury.

In parallel to further elaboration of these clinical subsets, some of the time honoured radiological and pathological features by which OA has been classified need revising, including the relevance of crystals to arthritis. For example, patients with calcium pyrophos- phate dihydrate deposits were at first thought to represent a distinct group [17]. However, it has become apparent that crystal deposits are not always associated with disease and that three quite separate aspects of pyro- phosphate deposition are recognised - radiological evidence of crystal deposition (chondrocalcinosis), at- tacks of synovitis caused by crystal shedding (pseudo- gout), and an associated structural change in joints (pyrophosphate associated arthropathy).

It is now clear that chondrocalcinosis is an age-related phenomenon [25] which may be accelerated by local joint damage, which in turn may be associated with a develop- ment of a hypertrophic bone response. For example, meniscectomy often results in premature chondrocalci- nosis in the operated knee. This is associated with more severe and a more markedly hypertrophic form of OA [9]. However this is only one of a number of markers of outcome in this type of patient [10]. Because of its strong age relationship it is easy to make a false association of chondrocalcinosis with other age-related phenomena including OA and osteophyte formation. It may be most appropriate to regard pyrophosphate deposition as part of normal ageing and an "opportunistic" event. How- ever, when premature or in association with OA, it can probably act as a modifying factor. It appears that the patient prone to chondrocalcinosis may also have a tendency to a certain type of response to joint injury [6]. Similar conclusions are justified in relation to the pre- sence of abundant intra-articular hydroxyapatite crystals in OA. This has been associated with a specific type of rapidly destructive atrophic osteoarthritis of the shoulder [19]. However, is it apparent that the phenomenon is not specifically related to the shoulder and occurs in a wide spectrum of joint changes at other sites [7]. Elderly females with pre-existing joint disease appear to be particularly susceptible to the phenomenon of sudden large joint atrophic destructive arthritis associated with apatite crystals in the synovium and synovial fluid. So called "analgesic hip" or Postel arthropathy is probably a form of this condition [11]. The crystals are probably a

marker and result of joint damage rather than the cause. Apatite crystals are certainly not disease-specific and are frequently seen in conjunction with other particles includ- ing pyrophosphate [8]. Crystals in joints may be viewed as a reflection of patient age and tissue response to injury. They may modify the expression of joint disease, but do not indicate specific disorders in their own right.

Scintigraphic studies of OA have also produced fascinating new insights. Conventional bone scintigrams, using technetium-labelled diphosphonates, often indicate abnormal activity at sites radiographically shown to be affected by OA. This phenomenon has been studied in detail in the hand and knee joints. In a study of 14 patients with hand OA followed over a 5-year period it was found that scintigraphic change could be present at a time when the joint was clinically and radiologically normal [14]. However, such activity was an excellent predictor of subsequent radiological change. Similarly, joints with radiographic evidence of severe joint damage were often normal scintigraphically. These joints generally remained unchanged during the duration of the study. Different joints in the same patient could be shown to be going through different phases of activity in which scintigraphic abnormality preceded radiographic changes. These in- cluded some joints showing evidence of stabilisation or even healing in terms of increase in joint space width and remodelling of subchondral bone [15].

These observations suggest that OA, whilst affecting a predictable set of joints, can behave as a "monarthritis multiplex" with the ability to heal as well as to progress. Scintigraphic studies of the knee have emphasised also the heterogeneity of disease [20]. They show that osteophyte, synovium, and subchondral bone can all go through phases of activity at different times during the evolution of the disease. Scintigraphic patterns described may have radiographic and even MRI correlates indicating a pos- sible spectrum of disease from aggressive destructive variants to more benign conditions such as painful rim osteophytosis of the knee in middle aged women [20]. MRI has emphasised the soft tissue component of the disease including meniscal damage, as well as confirming the principal subsets of bone change as revealed by scintigraphy [18]. It is apparent that within OA are several disease processes involving the whole joint organ, not purely the hyaline cartilage. Similarly, a wide spectrum of different patterns of outcome exists within, as well as between, individual joint sites.

How then should osteoarthritis be perceived? Clearly the time honoured radiographic signs of joint space narrowing and rim osteophytosis do not represent "dis- ease" but are often age-related phenomena. Even when disease is present, it has become apparent that the processes involved may have differing degrees of severity and activity in the various tissue components of the joint organ. One of the outstanding challenges is to relate the different clinical patterns observed to evidence of activity in cartilage, bone and synovium and to outcome. Os- teoarthritis is not a disorder with a slow, inevitable progression. Some joints go through phases of change, then stabilise and remain unchanged for years. Others

I. Watt and P. Dieppe: Osteoarthritis revisited 3

progress slowly for m a n y years and then suddenly deteriorate in dramat ic fashion. Heal ing also occurs, as can be demons t ra ted pathological ly, radiographical ly and scintigraphically. This intrinsic ability o f the joint organ to repair damage is a key feature o f the pa tho logy o f OA. Heal ing can occur even in the mos t severely damaged joint. I f this p h e n o m e n o n were to be under- s tood, then means might be made available to manipula te the processes, encouraging more joints to heal. I f healing could be predicted, then lesser emphasis on surgical salvage would be needed.

Some o f the features highlighted, including inflam- mat ion and crystal deposition, are beginning to provide new insights into the processes involved in OA. However little is still k n o w n about the processes that p rovoke the changes o f OA, despite this being one o f man ' s c o m m o n - est afflictions. It would seem that we are looking at a dynamic response o f a joint organ to injury or to underdesign. Sometimes a posi t ion stabilises, other times it progresses and joint integrity breaks down. Fur ther unders tanding requires a multidisciplinary approach. M u c h m a y be learnt f rom the chaologists with their use o f fractals to explain why apparent ly stable situations suddenly and unpredic tably become chaotic. The mat ter is becoming urgent. We live with an ageing popula t ion in which the f requency of O A is increasing if we live long enough we may all get it!

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