Osteoarthritis (OA) is a chronic disorder of synovial joints in which there is progressive softening and disintegration of articular cartilage accompanied by new
growth of cartilage and bone at the joint margins (osteophytes), cyst formation and sclerosis in the subchondralbone, mild synovitis and capsular fibrosis. It differs from simple wear and tear in that it is asymmetrically distributed, often localized to only one part of a joint and often associated with abnormal loading rather than frictional wear. In its most common form, it is unaccompanied by any systemic illness and, although there are sometimes local signs of inflammation, it is not primarily an inflammatory disorder. It is also not a purely degenerative disorder, and the term ‘degenerative arthritis’ – which is often used as a synonym for OA – is a misnomer. Osteoarthritis is a dynamic phenomenon; it shows features of both destruction and repair. Cartilage softening and disintegration are accompanied from the very outset by hyperactive new bone formation, osteophytosis and remodelling. The final picture is determined by the relative vigour of these opposing processes. In addition, there are various secondary factors which influence the progress of the disorder: the appearance of calciumcontaining crystals in the joint; ischaemic changes (especially in elderly people) which result in areas of osteonecrosis in the subchondral bone; the appearance of joint instability; and the effects of prolonged anti-inflammatory medication.
The most obvious thing about OA is that it increases in frequency with age. This does not mean that OA is simply an expression of senescence. Cartilage does ‘age’, showing diminished cellularity, reduced proteoglycan concentration, loss of elasticity and a decrease in breaking strength with advancing years. These factors may well predispose to OA, but it is significant that the progressive changes which are associated with clinical and radiological deterioration are restricted to certain joints, and to specific areas of those joints, while other areas show little or no progression with age (Byers et al., 1970). Primary changes in cartilage matrix might (theoretically) weaken its structure and thus predispose to cartilage breakdown; crystal deposition disease and ochronosis are well-known examples. ‘Inheritance’ has for many years been thought to play a role in the development of OA. A number of studies have demonstrated a significant increase in the prevalence of generalized OA in first-degree relatives of patients with OA as compared with controls (Kellgren,1963) and others have
This is borne out in clinical practice: patients with ‘secondary’ OA of the knee following meniscectomy have been found also to have a higher than usual incidence of ‘primary’ OA in other joints (Doherty et al. occurring in any condition which causes a disparity between the mechanical stress to which articular cartilage is exposed and the ability of the cartilage to withstand that stress. generalized factors (genetic.g.. in deformities that affect the lever system around a joint) or to a reduction of the articular contact area (e. OA is. more process than disease. Knowlton et al. This may be due to increased load (e. with joint incongruity or instability). metabolic or endocrine) alter the physical properties of cartilage and thereby determine who is likely to develop OA. 1990). Articular cartilage may be damaged by trauma or previous inflammatory disorders. one should bear in mind that OA of large joints is often attributable to anatomical variations.g.g. e. 1983).. whether similar processes operate in ‘primary’ (‘idiopathic’) OA is unknown. This could explain the appearance of ‘secondary’ OA in patients with rheumatoid diseases. either by altering the shape of the articular surface or by an increase in bone density (e. In most cases the precipitating cause of OA is increased mechanical stress in some part of the articular surface. At the molecular level. Both factors operate in varus deformity of the knee and in acetabular dysplasia – common precursors of OA. and it is these that are inherited rather than any tendency to develop OA as a primary abnormality. following fracture healing) which reduces the shock-absorbing effect of the supporting cancellous bone. 1989.published similar observations for OA of the hip (Lanyon et al.
. Enzymes released by synovial cells and leucocytes can cause leaching of proteoglycans from the matrix.g. genetic defects in type II collagen have been demonstrated in some cases (Palotie et al. while secondary factors such as anatomical defects or trauma specify when and where it will occur. However. Changes in the subchondral bone may also increase stress concentration in the overlying cartilage.. but it is unlikely that this is a major aetiological factor in the majority of cases. 2000). acetabular dysplasia and other forms of epiphyseal dysplasia. Perhaps primary.. and synovial-derived interleukin-1 (IL-1) may suppress proteoglycan synthesis. From the foregoing outline it should be apparent that the division of osteoarthritis into ‘primary’ (when there is no obvious antecedent factor) and ‘secondary’ (when it follows a demonstrable abnormality) is somewhat artificial. ultimately.
As the cartilage becomes less stiff. or osteophytes. as well as increased vascularity and reactive sclerosis in the zone of maximal loading. while the cartilage is still morphologically intact. of the normally smooth and glistening cartilage. that so clearly distinguish osteoarthritis (once called ‘hypertrophic arthritis’) from ‘atrophic’ disorders such as rheumatoid disease. (2) subarticular cyst formation. repair and remodelling. At a slightly later stage there is loss of proteoglycans and defects appear in the cartilage. With progressive disintegration of cartilage. The result: focal trabecular degeneration and cyst formation. There is softening and fraying. with (3) sclerosis of the surrounding bone. are an increase in water content of the cartilage and easier extractability of the matrix proteoglycans. the underlying bone becomes exposed and some areas
. secondary damage to chondrocytes may cause release of cell enzymes and further matrix breakdown. cartilage at the edges of the joint reverts to the more youthful activities of growth and endochondral ossification. thus amplifying the changes in a cycle that leads to tissue breakdown. When it loses its integrity these forces are increasingly concentrated in the subchondral bone. and (5) capsular fibrosis. giving rise to the bony excrescences. or fibrillation. Articular cartilage has an important role in distributing and dissipating the forces associated with joint loading.
The cardinal features are: (1) progressive cartilage destruction. Initially the cartilaginous and bony changes are confined to one part of the joint – the most heavily loaded part.Pathogenesis The initial stages of OA have been studied in animal models with induced joint instability and may not be representative of all types of OA. Cartilage deformation may also add to the stress on the collagen network. The earliest changes. What cartilage remains is still capable of regeneration. (4) osteophyte formation. The term chondromalacia (Gr = cartilage softening) seems apt for this stage of the disease. similar findings in human cartilage have been ascribed to failure of the internal collagen network that normally restrains the matrix gel. but it is used only of the patellar articular surfaces where it features as one of the causes of anterior knee pain in young people. As the articular surfaces become increasingly malapposed and the joint unstable.
The cyst itself contains amorphous material. according to the degree of destruction. sometimes there is marked inflammation or fibrosis of the capsular tissues. however. A feature of OA that is difficult to appreciate from the morbid anatomy is the marked vascularity and venous congestion of the subchondral bone. As in all types of arthritis. as a rule. especially on the deep aspect of any cyst. or burnished. sometimes of extraordinary degree. small areas of osteonecrosis are quite common. At a distance from the damaged area the articular cartilage looks relatively normal. looks only mildly inflamed. to ivory-like smoothness (eburnation). Often within this area of subchondralsclerosis. bluish cartilage. This can be shown by angiographic studies and the demonstration of increased intraosseous pressure. of chondrocytes – 20 or more to a batch. from local areas of osteonecrosis or from the forceful pumping of synovial fluid through cracks in the subchondral bone plate. it is thick and red and covered by villi. The subchondral bone shows marked osteoblastic activity.
. The histological appearances vary considerably. however. are one or more cysts containing thick. the clefts become more extensive and in some areas cartilage is lost to the point where the underlying bone is completely denuded. In later stages. or clones. sometimes. Beneath the damaged cartilage the bone is dense and sclerotic. but at the edges of the joint there is remodelling and growth of osteophytes covered by thin. Sometimes small tufts of fibrocartilage may be seen growing out of the bony surface.may be polished. the cartilage shows small irregularities or splits in the surface. Early on. (1971). The osteophytes appear to arise from cartilage hyperplasia and ossification at the edge of the articular surface. Most striking. however. its origin is mysterious – it could arise from stress disintegration of small trabeculae. and immediately subjacent to the surface. and the appearance of clusters. while in the deeper layers there is patchy loss of metachromasia (obviously corresponding to the depletion of matrix proteoglycans). gelatinous material. It is also apparent from the intense activity around osteoarthritic joints on radionuclide scanning. The joint capsule usually shows thickening and fibrosis. The synovial lining. is the increased cellularity. The capsule and synovium are often thickened but cellular activity is slight. The biochemical abnormalities corresponding to these changes were described by Mankin et al.
1973. the female-to-male ratio for OA of the hip is about 1:1 in northern Europe but is nearer 2:1 in southern Europe where there is a high incidence of acetabular dysplasia in girls. Men and women are equally likely to develop OA. However. affecting both sexes and all races. and in the different joints. for example the knee. Reports of prevalence rates vary. depending on the method of evaluation. Autopsy studies show OA changes in everyone over the age of 65 years. in the different sexes within any group. This may simply reflect the fact that some joints are more prone to predisposing abnormalities than others. A similar explanation may account for certain geographical and ethnic differences in prevalence. That they have no inherent resistance to OA is shown by the fact that they often develop the condition in other joints. For example. Even more striking is the virtual absence of hip OA in southern Chinese and African blacks (Hoagland et al.. Osteoarthritis of the finger joints is particularly common in elderly women. Perthes’ disease and slipped femoral epiphysis are uncommon in these populations. hip. knee and spine) than in others (the elbow.
. in some degree. It is not always easy to spot minor degrees of dysplasia and careful studies may have to be undertaken if these are not to be missed.
Risk Factor Joint dysplasia Disorders such as congenital acetabulardysplasia and Perthes’ disease presage a greater than normal risk of OA in later life. Solomon. Radiographic surveys suggest that the prevalence rises from 1 per cent below the age of 30 years to over 50 per cent in people above the age of 60. It is a truly universal disorder. Osteoarthritis is much more common in some joints (the fingers. 1976). wrist and ankle). this may simply be because predisposing disorders such as developmental displacement of the hip. but more joints are affected in women than in men. affecting more than 70 per cent of those over 70 years.Prevalence Osteoarthritis is the commonest of all joint diseases. there are significant differences in its rate of occurrence in different ethnic groups. everyone who lives long enough will have it somewhere.
1989). This applies to mid-shaft fractures. 1992. hormonal and metabolic factors which may also influence cartilage metabolism independently of any effect due to bone density. Kulkala et al. Obesity The simple idea that obesity causes increased joint loading and therefore predisposes to OA may be correct – at least in part.. Boxers are certainly prone to developing OA of the hands but this may be due to trauma. The same applies to footballers with OA of the knees and baseball pitchers with OA of the shoulder.. Occupation There is good evidence of an association between OA and certain occupations which cause repetitive stress. More convincing evidence of a causative relationship comes from recent studies which have shown a significant increase in the risk of hip and knee OA in athletes (Harris et al.. Hart et al.. research has shown that moderate angular deformities of the tibia (up to 15 degrees) are not associated with an increased risk of OA (Merchant and Dietz.
. 1994. 1994).
Bone density It has long been known that women with femoral neck fractures seldom have OA of the hip. This negative association between OA and osteoporosis is reflected in more recent studies which have demonstrated a significant increase in bone mineral density in people with OA compared to those without (Hannan et al. More controversial is the relationship of OA to sporting activity. for example OA of the knees in workers engaged in kneebending activities (Felson. in the knee or ankle after a tibial fracture). However. 1972) and OA of the hands in cotton mill workers (Lawrence. malunion close to a joint may well predispose to secondary OA.The particular trait responsible for this is not known (see above under Aetiology).
Family history Women whose mothers had generalized OA are more likely to develop the same condition. OA in the upper limbs in people working with heavy vibrating tools (Schumacher et al. Contrary to popular belief. What is less certain is whether malunion of a long-bone fracture predisposes to OA by causing segmental overload in a joint above or below the healed fracture (for example. 1994). The association is closer in women than in men and therefore (as with bone density) it may reflect other endocrine or metabolic factors in the pathogenesis of OA. so too lesser injuries which result in joint instability.Trauma Fractures involving the articular surface are obvious precursors of secondary OA. 1991).. 1961). this may not be simple cause and effect: bone density is determined by a variety of genetic.
It is often quite widespread. although with time relief is less and less complete.
Swelling may be intermittent (suggesting an effusion) or continuous (with capsular thickening or large osteophytes). and. muscular fatigue. In the late stage the patient may have pain in bed a night. congenital dysplasia. on the interphalangeal joints (especially in women) or on any joint that has suffered a previous affliction (e. is often the most distressing symptom. Joint involve -ment follows several different patterns: symptoms centre either on one or two of the weightbearing joints (hip or knee).
Stiffness is common. restriction of walking distance. though not the most dramatic. bone pressure due to vascular congestion and intraosseous hypertension. the symptoms of OA follow an intermittent course. It starts insidiously and increases slowly over months or years. but be aware that the deformity may actually have preceded and contributed to the onset of OA.g. Pain is the usual presenting symptom. There are several possible causes of pain: mild synovial inflammation.
Loss of function. with periods of remission sometimes lasting for months.Symptomps
Patients usually present after middle age. A limp.
Deformity may result from capsular contracture or joint instability. It is aggravated by exertion and relieved by rest. difficulty in climbing stairs. characteristically it occurs after periods of inactivity. Typically. or progressive inability to perform everyday tasks or enjoy recreation may eventually drive the patient to seek help. perhaps most important of all. but with time it becomes constant and progressive. or it may be referred to a distant site – for example. pain in the knee from OA of the hip. A family history is common in patients with polyarticular OA. capsular fibrosis with pain on stretching the shrunken tissue. osteonecrosis or intra-articular fracture).
Other joints should always be examined. wrists. the first metatarsophalangeal or knee joints can be just as obvious. or use a walking stick. and muscle wasting suggests longstanding dysfunction.
Limited movement in some directions but not others is usually a feature.
Function in everyday activities must be assessed. a stiff lumbar spine or an unstable knee making it more difficult to cope with restricted movement in an osteoarthritic hip). It is also helpful to know whether problems in other joints add to the difficulties in the one complained of (e. or rise easily from a chair. This may be due to an effusion. X-ray appearances do not always correlate with either the degree of pain or the patient’s actual functional capacity.
Instability is common in the late stages of articular destruction. does he or she limp. but it may be detected much earlier by special testing. Instability can be due to loss of cartilage and bone. but deformity of the hip can be masked by postural adjustments of the pelvis and spine. synovial thickening or osteophytes may be felt. and is sometimes associated with pain at the extremes of motion. but hard (‘knobbly’) ridges around the margins of the distal interphalangeal. knees and toes). they may show signs of a more generalized disorder. Can the patient with an arthritic knee walk up and down stairs.g.Signs
Joint swelling may be the first thing one notices in peripheral joints (especially the fingers. and in superficial joints fluid. Tell-tale scars denote previous abnormalities. asymmetrical capsular contracture and/or muscle weakness.
Crepitus may be felt over the joint (most obvious in the knee) during passive movements.
Deformity is easily spotted in exposed joints (the knee or the large-toe metatarsophalangeal joint).
Local tenderness is common.
patients may respond to a simple analgesic such as paracetamol. Other measures. If this fails to control pain. the age of the patient and his or her functional needs.
. Common sense measures such as weight reduction for obese patients. therefore. but not all patients require drug therapy and those who do may not need it all the time. wearing shock-absorbing shoes. and pain may subside spontaneously for long periods. If other measures do not provide symptomatic improvement. as yet. a non-steroidal anti-inflammatory preparation may be better. avoiding activities like climbing stairs and using a walking stick are worthwhile. (3) relieve pain. and (4) modify daily activities.
Load reduction Protecting the joint from excessive load may slow down the rate of cartilage loss. the stage of the disorder. the severity of the symptoms. (2) protect the joint from ‘overload’. such as massage and the application of warmth. (2) some forms of OA actually become lesspainful with the passage of time and the patient may need no more than reassurance and a prescription for pain killers. which should be directed at maintaining joint mobility and improving muscle strength.Management
The management of OA depends on the joint (or joints) involved.
Physical therapy The mainstay of treatment in the early case is physical therapy.
Analgesic medication Pain relief is important. but care should be taken to avoid activities which increase impact loading. (3) at the other extreme. The programme can include aerobic exercise. It is also effective in relieving pain. may reduce pain but improvement is short-lived and the treatment has to be repeated. the recognition (from serial x-rays) that the patient has a rapidly progressive type of OA may warrant an early move to reconstructive surgery before bone loss compromises the outcome of any operation. Treatment is.
EARLY TREATMENT There is. The principles are: (1) maintain movement and muscle strength. no drug that can modify the effects of OA. Three observations should be borne in mind: (1) symptoms characteristically wax and wane. symptomatic.
.g. Joint replacement Joint replacement. is nowadays the procedure of choice for OA in patients with intolerable symptoms. Refinements in techniques. marked loss of function and severe restriction of daily activities. total joint replacement by modern techniques promises improvement lasting for 15 years or longer. cartilage tags. joint replacement operations are highly dependent on technical skills. instability and deformity (particularly of one of the weightbearing joints). fixation devices and instrumentation led to acceptable results from operations on the hip and knee.g. High tibial osteotomy is still considered to be a viable alternative to partial joint replacement for unicompartmental OA of the knee. in all parts of the world. at different times. appropriate instrumentation and postoperative care – requirements that cannot always be met. Pain relief is often dramatic and is ascribed to (1) vascular decompression of the subchondral bone. If appropriate radiographic images suggest that symptoms are due to localized articular overload arising from joint malalignment (e. arthroplasty and arthrodesis.
LATE TREATMENT Progressive joint destruction. usually requires reconstructive surgery. interfering osteophytes or a torn or impinging acetabular or glenoid labrum) may give some improvement. These operations should be done while the joint is still stable and mobile and x-rays show that a major part of the articular surface (the radiographic ‘joint space’) is preserved. held the field: realignment osteotomy. Three types of operation have. and (2) redistribution of loading forces towards less damaged parts of the joint. implant design. realignment osteotomy was widely employed. Realignment osteotomy Until the development of joint replacement surgery in the 1970s. This may be done either by arthroscopy or by open operation. elbow and ankle are less successful but techniques are improving year by year. For OA of the hip and knee in middle-aged and older patients. in one form or another. with increasing pain. acetabular and femoral head dysplasia). After load redistribution.INTERMEDIATE TREATMENT Joint debridement (removal of loose bodies. ensuring that this approach has not been completely abandoned. fibrocartilage may grow to cover exposed bone. and intertrochanteric femoral osteotomy is sometimes preferred for young patients with localized destructive OA of the hip. Similar operations for the shoulder. a corrective osteotomy may prevent or delay progression of the cartilage damage. or may not be cost-effective. varus deformity of the knee) or incongruity (e.
g. This is most likely to apply to small joints that are prone to OA.
Rehabilitation of Osteoarthritis
.Arthrodesis Arthrodesis is still a reasonable choice if the stiffness is acceptable and neighbouring joints are not likely to be prejudiced. e. the carpal and tarsal joints and the large toe metatarsophalangeal joint.