Iijima T, Tada H, Hidaka Y, et al. Prediction of postpartum onset of Patient advice Counseling patients about the need for improved disease control prior to con ception, potential complications to both mother and fetus, and the risk of \202 ares in t he post- partum period should be discussed. Screening for compli- cations should be underta ken regularly during pregnancy, and the risks and bene \201 ts of drug therapies, both in preg- nancy and whilst breastfeeding, discussed. rheumatoid arthritis. Ann Rheum Dis 1998; 57: 460 \200\2233. Kong NC. Pregnancy of a lupus patients \200\223 a challenge to the nephrologist. Nephrol Dial Transplant 2006; 21: 268 \200\22372. Mok CC, Wong RW. Pregnancy in systemic lupus erythematosus. Postgrad Med J 2001; 77: 157 \200\22365. Ostensen M, Forger F, Nelson JL, Schuhmacher A, Hebisch G, Villiger PM. Pregnancy in patien ts with rheumatic disease: anti- in \202 ammatory cytokines increase in pregnancy and decr ease post partum. Ann Rheum Dis 2005; 64: 839 \200\22344. Ostensen M, Villiger PM. The remission of rheumatoid arthritis dur- Monitoring in pregnancy Monitoring of both mother and fetus should be under- taken regularl y. In the mother, disease activity and disease complications such as renal involvement shou ld be sought. Additionally, close monitoring for complications of preg- nancy, such as thro mbo-embolic disease and pre-eclampsia, particularly in those patients with SLE, APLS, vascu litis, and systemic sclerosis, should be undertaken. In the fetus, close monitoring to dete ct IUGR, fetal abnormalities and abnormalities in uterine blood \202 ow waveform should b e regularly performed. ing pregnancy. Semin Immunopathol 2007; 29: 185 \200\22391. Petri M, Allbritton J. Fetal outcome of lupus pregnancy: a retrospec- tive case-control stu dy of the Hopkins Lupus Cohort. J Rheumatol 1993; 20: 650 \200\2236. Ruiz-Irastorza G, Khamashta MA, Gordon C, et al. Measuring systemic lupus erythematosis act ivity during pregnancy: valida- tion of the lupus activity index in pregnancy scale. Arthri tis Rheum 2004; 51: 78 \200\22382. Yee CS, Farewll V, Isenberg DA, et al. Revised British Isles Lupus Assessment Group 2004 In dex: a reliable tool for assessment of systemic lupus erythematosis activity. Arthritis Rhe um 2006; 54: 3300 \200\2235. Resources Internet sites Systemic lupus erythematosis and pregnancy. Available at: http://w ww.uklupus.co.uk/fact13.html and http:// www.uklupus.co.uk/preg.html Rheumatoid arthritis a nd pregnancy. Available at: http:// www.rheumatoid.org.uk/article.php?article_ id=83 and ht tp://www.arc.org.uk/arthinfo/ patpubs/6060/6060.asp This page intentionally left blank 371 Chapter 12 Osteoarthritis and related disorders Osteoarthritis 372 Osteoarthritis-related disorders 380 OSTEOARTHRITIS 372 Osteoarthritis Osteoarthritis (OA) is a mechanically driven, but biochemically-mediated disease of synovia l joints. The ACR classi \201 cation criteria for OA Hand OA Pain, aching or stiffness in the handa and 3 of the following: \200 Bony swelling of \211 2 distal interphalangeal (DIP) joints . Bony swelling of 2 or more of 10 selected joints*. <3 swollen metacarpophalangeal (MCP) j oints. Deformity of 2 or more of 10 selected joints*. De \201 nition In clinical practice, as in epidemiologic studies, OA is diag- nosed where there is joint pain, together with characteris- tic radiographic changes, in the absence of an alternative cause. Surprisingly, one of the most useful de \201 nitions of OA is to be found on Wikipedia: \200 \200 \200 Osteoarthritis (OA, also known as degenerative arthritis or degenerative joint disea se, and sometimes referred to as \200\230arthrosis \200\231 or \200\230osteoarthrosis \200\231), is a condition in which low-grade in \202 ammation results in pain in the joint s, caused by wearing of the cartilage that covers and acts as a cushion inside joints. As t he bone surfaces become less well protected by carti- lage, the patient experiences pain up on weight bear- ing, including walking and standing. Due to decreased movement because of t he pain, regional muscles may atrophy and ligaments may become more lax. OA is the most com mon form of arthritis. The word is derived from the Greek word \200\230osteo \200\231 mean ing \200\230of the bone \200\231, \200\230arthro \200\231 meaning \200\230joint \200\231 , and \200\230itis \200\231 meaning in \202 ammation, although many sufferers have little or no in \202 ammation \200 Knee OA: using history and examination Pain in the kneea and 3 of the following: \200 \200 \200 \200 \200 \200 Age >50 years. Morning stiffness <30 min. Crepitus on active motion. Bony tenderness. Bony enlargement. No palpable warmth of synovium. Hip OA: using history, examination and laboratory \201 ndings Pain in the hipa and: \200 Internal rotation \211 15 and either ESR \211 45 mm/h or hip \202 exion \211 115 i f ESR unavailable. Or \200 A more unwieldy, but widely quoted de \201 nition is from the American Academy of Orthoped ic Surgeons (1995): Internal rotation >15 with pain, morning stiffness \211 60 minutes, >50 years old. \200 Osteoarthritis diseases are a result of both mechanical and biologic events that des tabilize the normal coupling of degradation and synthesis of articular cartilage chondrocyt es, extracellular matrix and subchondral bone. Although they may be initi- ated by multiple factors such as genetic developmen- tal, metabolic, and traumatic factors, osteoarthritis diseases are manifest by morphologic, biochemical, molecular and biomechanical changes of b oth cells and matrix which leads to a softening, \201 brillation, ulceration and loss of articular cartilage, sclerosis and eburnation of subchondral bone, osteophytes and subchond ral cysts. When clinically evident, osteoar- thritis diseases are characterized by joint pa in, tenderness, limitation of movement and variable degrees of in \202 ammation without sy stemic effects. aOn most days of the previous month. bRight and left 2nd and 3rd proximal interphalangeal j oints, 2nd and 3rd DIPJ, and 1st carpometacarpal joints. Patterns of OA Primary \200 \200 \200 \200 Nodal (hand). Erosive (hand). Generalized (hand + knee/hip). Diffuse idiopathic skeletal hy perostosis (DISH). Secondary \200 \200 \200 \200 \200 Localized (e.g. fracture, infection). Diffuse (e.g. secondary to rheumatoid arthritis). Cal cium pyrophosphate dihydrate (CPPDD) deposition. Metabolic (e.g. haemochromatosis; ochronos is). Neuropathic [e.g. tabes dorsalis, diabetes mellitus (DM)]. Bone dysplasias. Classi \201 cation The American College of Rheumatology (ACR) criteria were developed to d ifferentiate OA from other, especially in \202 ammatory, arthritides in specialist practic e. Epidemio- logical studies usually classify occurrence of OA on the basis of radiographic changes alone. However, the presence of pain in addition to osteophytes or joint space nar rowing is now generally accepted. Epidemiology OA is the commonest arthropathy, typically affecting joints most exposed to me chanical load, including the hand, knee, hip, and 1st MTP joints. \200 Spondylosis The term given to the (degenerative) process causing reduced intervertebral dis c space. Synovial facet joints are typically secondarily affected by an OA process; however , primary OA of facet joints can occur. The degree to which costovertebral and costotransve rse joints are affected by OA is not well documented. The prevalence of radiographic changes alone in anyone >50 years old is notable: hip 8%; ha nd 15%; knee 30%. About 50% of these people will have pain over a 1-year period. Robust UK incidence data is lacking. Incidence data from the United States of America shows an age- a nd sex-standardized incidence for symptomatic knee OA of CHAPTER 12 Osteoarthritis and related disorders 373 160 \200\223240 per 100 000 patient-years, rising to 1% in those over age 70 years. This co mpares to 47 \200\22388 per 100 000 patient-years for hip OA (compared to 10 \200\22330 per 100 000 in Sweden) and 100 per 100 000 patient-years for hand OA. Serial radiographic surv eys, including the Framingham, Goteberg, and Tecumseh cohorts show higher rates of incident radiographic change alone, from 2.7 to 11.9%, depending on the joint and de \201 nition u sed. The number of joint replacement operations (and prob- ably the prevalence and incidenc e of underlying OA) are increasing in the UK, due to demographic population changes and the NHS evolving from a supply limited to a demand led service. In 2007, 137 000 hip and knee replacements were performed in England and Wales, contributing to a cost of over 3 bn per annum for OA management. In general, Caucasians have a high rate of OA with lower rates in Afro-Caribbean and Asian populations, which is thought to be primarily genetically determi ned. OA prevalence might be modi \201 ed by environmental factors, e.g. the higher prevale nce of knee OA in indige- nous Chinese population thought to be in \202 uenced by the tend ency to squat. The prevalence of OA probably peaks around 70-year-old; however, a recent st udy in the very elderly (85 \200\22397 years of age) suggests all who survive to this age d evelop radiographic change of one or more joint. Function is often well preserved. There is a female preponderance of up to 2:1 for knee and hand OA, but a less consistent gender dif ference for hip OA. Occupational and mechanical factors are relevant. For example, knee ben ding and obesity are important factors determining knee OA; farming is associated with hip OA and occupations where there is intensive use of a precision grip, a risk for hand OA. Genetic factors The genetic associations observed so far have been small and rarely replica ted in more the one cohort. \200 Some genetic associations might explain a minority of disease (e.g. ADAM12 for knee OA, fri zzled related protein 3 in hip OA). Large collaborative studies, such as arcOGEN (funded by Arthritis Research Campaign) and TREAT_OA (funded by The European Union FP-7 program) are likely to provide a de \201 nitive estimate of the genetic effects on OA within the next 5 years. Environment Damage to structures in and around the joint that result in altered joint biome chanics, whatever the cause, has a consistent effect on promoting the development and progr ession of OA. \200 Early changes include reduced muscle power and ligamentous changes. This has led to the rec ent sugges- tion that entheseal changes may be central to the patho- physiology of OA. Howe ver, no longitudinal epidemiological studies with high-resolution imaging have addressed th is hypothesis. Although there has been no de \201 nitive demonstration of the sequence of initiation of pathological processes in OA, other hypotheses include: \200 the central importance of subchondral bone changes as an initiating factor; the widespread assumption that cartilage changes are the earliest event;. the widespread acceptance that o steophytes are a reaction to early changes within the joint. There is evidence that cartilage becomes less elastic, at least in part due to the accumula tion of advanced glycosylation end-products and reduced matrix \202 uid pressurization. F inally, chondrocytes are sensitive to mechanical loading. This provides a potential link be tween altered loading and joint pathology. Etiology and pathophysiology Most OA can be classi \201 ed into primary or secondary varia nts. Secondary OA occurs earlier with more predict- able severity in a damaged joint e.g. a fter cruciate ligament injury in the knee or congenital hip dysplasia. Primary OA is more c ontentious, but there is some evidence for both genetic and environmental contributions. \200 Celular, matrix, and immunobiology Mechanical stress is required for joint maintenance, but pathological stresses may lead to microtrauma and in \202 am- matory changes. Although th ere are far fewer \200\230features of in \202 ammation \200\231 compared with the in \202 ammatory arthritides, in \202 ammation is found in OA. \200 The prevailing dogma is that that OA is a failure of compensation for an imbalance within t he degradative and reparative connective tissue processes within the whole joint, leading t o failure of the joint. However, while biochemical markers suggest a degree of synthetic ac tivity of type II collagen and other matrix components in OA models, and sometimes subjects , there has been no clear demonstration of meaningful reconstruction of cartilage damage on ce established. The caveat to the above comes from anecdotes report- ing improved joint spa ce on non-weight-bearing \201 lms. However, this is more likely to represent a lack of ap po- sition of weight-bearing surfaces, rather than cartilage regeneration. Similarly, recen t work on surgical joint distraction has only demonstrated \201 brocartilage, not true hy aline cartilage, formation. Overall, it seems plausible that the degree of connective tissu e matrix turnover in normal joints may not be struc- turally relevant and, therefore, that decompensation of matrix turnover is not the most universally relevant model of OA. Arthroscopic and histological studies together with high-resolution musculoskeletal ultraso und (US) have suggested that low-grade in \202 ammation is an important feature of OA. Als o, recent magnetic resonance (MR) imaging studies have suggested that changes consistent wi th in \202 amma- tory lesions have are consistently identi \201 ed in OA joints (e.g. joi nt \202 uid and increased bone marrow signal). In OA, in \202 ammation is characterized by raised levels of IL-1 and TNF-A in the joint and activation of inducible nitric oxide sy nthase and cyclo-oxygenase 2. These changes are associated with changes in expression of ma trix metalloproteinases (MMPs) and tissue inhibitors of MMPs (TIMPs), favoring excessive pr oteolysis. Risk factors The most clinically relevant way to consider the risk factors for OA is whethe r they are constitutive (and therefore cannot be modi \201 ed) or potentially modi \201 a ble. OSTEOARTHRITIS 374 Constitutive risk factors Age, gender, race, familial factors, genetically determined osteo phytic response/evolution, congenital, and/or devel- opmental deformities. History to help guide therapeutic decisions Knowledge of previous disease and full assessme nt of gastrointestinal and cardiovascular risk factors is required in any patient being con sidered for treatment with non-steroidal anti-in \202 ammatory drugs is important. Potentially modi \201 able risk factors Obesity, joint malalignment, or previous injury, c o-existent inflammatory arthritis, adjacent muscular weakness, occupational factors, hormon al status (e.g. HRT is protec- tive) and bone mass (high baseline bone mass and greater los s in OA). Depression Depression commonly co-exists with OA, as with other painful arthropathies, and may require separate assess- ment and treatment (e.g. initially with the HADS question- nai re tool). Key features on examination Signs of generalized OA are often found in those presenting wit h a single painful joint, so while initial examination may focus on the presenting problem, examination of all poten- tially involved joints should be undertaken, including hands, kn ees, and hips. \200 Clinical features OA can present with one or more affected joints. It is always important t o assess pattern and extent of disease, including hand (distal/proximal interphalangeal/1st carpo- metacarpal joints), knee, and hip involvement. Key features in history There are consistent features to the history associated with severi ty and duration of disease. \200 Index joint examination should be as per the REMS model: look, feel, move, and assess funct ion. Observe any wasting of surrounding muscles; bony enlargement of the articular margins, including Heberden \200\231s nodes (DIPJ). These may be red (known as \200\230hot Heberde n \200\231s \200\231) at presentation (See Figure. 12.1). Also observe Bouchard \200\231s n odes (PIPJ) occurring at PIPJ and OA of the 1st carpometacarpal joints typically gives squa ring. Valgus/varus deformities, especially at the knee and ankle, can be seen; as can use o f sticks or orthoses; uneven wear of shoes. OA can result in cool effusions (especially kne e). There are few OA-speci \201 c signs from examination of joint movement, but crepitus, and pain on movement or weight-bearing is typical. Restriction of extension and internal ro tation is an early feature of hip OA. In small hand joint OA, \201 nger \202 exion can be reduced and associated with \201 xed \202 exion deformities. Active and pas- sive mo vement ranges are usually the same unless severe intra-capsular in \202 ammation restricts active movement. Functional assessment should include writing and assess- ment of walking (often the latter previously examined by the observant clinician who uses the arrival of th e patient in the clinic as an opportunity to scrutinize). In early/mild disease there is typically joint use-related pain and pain can be episodic. I n late/severe disease there may be refractory or pain disturbing sleep at night. Early morn ing stiffness is usually short-lived or absent. Any such stiffness clearly involves affecte d joints, rather than being generalized. There is usually impairment of function especially when OA involves the major weight bearing joints. Ideally history-taking should be by appr opriate open questioning to allow the patient to encapsulate the problem from their perspec tive. Screening questions from The GALS assessment (see p. 9) might be expected to unmask a n OA in all but the most trivial symptomatic cases: \200 \200 Do you have any pain or stiffness in your arms, legs, neck, or back? Do you have any proble ms with washing or dressing? Do you have any problems with stairs or steps? \200 Problems identified from the initial history can be explored further with respect to affected joints: \200 \200 Did you have pain most days last month? Do you get pain with using the joint (e.g. when sta nding or walking for a knee or hip)? If so, how far can you walk? Is the joint stiff in the morning? For how long? Do you get pain at night? Does pain affect your work/leisure activi ties? \200 \200 Eliciting a history of risk factors Some risk factors will have relevance to development of OA in all joints, whereas other risk factors will be joint-speci \201 c. \200 For knee OA ask about previous injuries or meniscal ( \200\230cartilage \200\231) problems or operations in the past, and occupational overuse (e.g. Do you do bend your knees or lift heavy weights repeatedly at work?). Ask if there is a family history of OA. If the patient is unsure, ask about hip or knee replacement operations, and if their relatives \200\231 h and deformities included the DIP or MCP joints. Hormonal status has some relevance. Ask (a postmeno- pausal female) when they last menstruated and whether they \200\231re taking HRT. Figure 12.1 OA of small hand joints with a degree of loss of digital extension owing to bon y deformities: Heberden \200\231s and Bouchard \200\231s nodes. CHAPTER 12 Osteoarthritis and related disorders 375 Investigations A typical clinical presentation where referral for consider- ation of surger y is not required would not usually require investigation. The high age-associated prevalen ce leads to OA being a common coincidental diagnosis in patients with other arthropathies. Laboratory OA is typically not associated with high acute phase response, although a modest elevation in ESR is consistent with the diagnosis. \200 Tests may be necessary to discriminate other arthritides (or assess for their presence). Bo th RF and anti-CCP antibodies may be useful in this respect. Endocrine and metabolic tests might be indicated where OA is thought to be secondary or CPPDD arthritis a possibility [e. g. transferrin saturation (>50%) and very high ferritin in haemachromatosis; elevated parat hyroid hormone in primary hyperparathyroidism]. Polarized light microscopy of aspirated joi nt \202 uid should be examined for CPPDD and gout crystals. Other cal- cium-containing cr ystals might be detected if pathology support is suf \201 ciently expert. Figure 12.3 Weight-bearing AP knee radiograph showing characteristic loss of medial compart ment tibio-femoral joint space loss in advanced OA. Other imaging Experience using US to characterize changes in OA joints is increasing in som e units. MR is mainly employed to assess internal joint derangement, particularly where sur gical intervention is planned, and assess osteonecrosis in appropriate situations. \200 High resolution musculoskeletal US can be useful if Imaging Radiographs Where radiographs are indicated, appropriate \201 lms to request are: \200 \200 Hand: anteroposterior (AP) view (See Figure. 12.2). Knee: weight-bearing AP, lateral, and p atella skyline view (photon beam parallel to articular side of patella and can be done at v arying degrees of knee \202 exion) (See Figure. 12.3). Hip: supine AP pelvis view with 10 internal hip rotation. Consider lateral or false pro \201 le view if AP not diagnostic, but clinical features suggestive of articular disease, i.e. reduced painful extension or i nternal rotation on passive movement (See Figure 12.4). Characteristic changes on plain rad iographs: include osteophytes, joint space narrowing, and subchondral changes: sclerosis an d cysts. (a) Radiographic variants \200 Erosive osteoarthritis: a more destructive variant characterized by more profound disruptio n to joint anatomy. Needs to be discriminated from psoriatic arthritis and CPPDD arthritis though extensive involve- ment of small hand joints in CPPDD disease is unusual. Secondary collapse of the femoral head in advanced hip OA. (b) Figure 12.4 (a) Plain radiograph of left hip joint, and below it, (b) a high-resolution Dua l Energy X-ray Absorptiometry image (iDXA, GE Healthcare), showing joint space narrowing. Figure 12.2 Generalized small hand joint OA involving DIP and PIP joints (AP view). OSTEOARTHRITIS 376 Disease activity assessment Often not used in clinical practice, but extremely helpful for monitoring impact of OA over time. The following are validated questionnaire and assessment tools. \200 \200 \200 \200 \200 VAS: Visual Analog pain score. HAQ: Health Assessment Questionnaire. SF-36: Short Form 36. EQ-5D: EuroQol. WOMAC: Western Ontario & McMaster Universities OA Index. Harris hip score ( used in orthopedic practice). Treatment Objectives of treatment Given the biomechanical in \202 uence on OA and the lack of therapies with a disease-modifying effect, non- pharmacological treatments, and simple analgesia with paracetamol should be regarded as the core treatments. In the UK, the eviden ce was recently reviewed by the National Institute for Health and Clinical Excellence for t heir clinical guideline (NICE, 2008). Core objectives of disease management are: \200 \200 \200 Figure 12.5 3T MRI showing delayed gadolinum uptake in OA cartilage. co-existent in \202 ammatory arthritis is being considered and the sonographer is experien ced in examining joints. MR is important in a knee affected by OA if planning arthroscopy p articularly if additional meniscal damage is a possibility (e.g. knee locking, giving way o n weight bearing and positive examination tests; see p. 178 \200\223183) See Figure 12.5. S ituations where MR of the hip is indicated include con \201 rmation and staging of osteone crosis of the femoral head if appearances are unclear on radiographs, ruling out a labral t ear (may need contrast-enhanced MR) and assessing in \202 ammatory changes (if US not avai lable) if intra-articular glucocorticoid injection is being contemplated. Characteristic pa tterns of tracer localization on bone scintigraphy, particularly for knee OA, are reasonabl y predictive of the need for arthroplasty. In community studies, where high-resolution dual energy X-Ray Absorptiometry (DXA) images have been acquired, images can be scored for the features of osteoarthritis. Relief of pain. Improved function. Slow progression of structural change. Non-pharmacological therapy Involve the multi-disciplinary team, including occupational the rapy, physiotherapy, and podiatry, as appropriate. \200 Education about the disease and effective treatments (see resources below). Exercise therap y should include both aerobic conditioning and strengthening exercise. Compliance and cost effec- tiveness are improved by delivery in groups, which may be combined with other measur es. Weight loss advice for all who are overweight or obese. Foot orthoses for all with sign i \201 cant abnormal lower limb biomechanics, e.g. wedge orthoses for ankle valgus, correc tive bracing for knee valgus/varus. Aids and devices: a stick for use in contralateral hand for knee or hip OA; consider thumb splint for 1st carpomet- acarpal joint OA; a home asses sment may be required where activities and participation limited. Hot and cold packs can be helpful for acute exacerba- tions of joint pain. Transcutaneous electrical nerve stimulati on may be appropriate for some patients with refractory pain. Acupuncture can give addition al, short-lived pain relief as adjunctive therapy. Manual therapy such as manipulation can be considered for hip OA. Complementary therapies are used extensively by patients with OA: \200 \200 Differential diagnosis The main differential diagnosis of OA is with in \202 ammatory arth ritis, although the two commonly co-exist. Psoriatic arthritis (PsA) Erosive OA must be differentiated from PsA (p. 220). Erosive OA d oes not exhibit new bone formation within erosions, exhibits less juxta-articular new bone formation in advanced disease and involves less extensive in \202 amma- tory entheseal cha nges on ultrasound. Gout Gout can involve DIPJ, but it is more in \202 ammatory than OA, usually asymmetrical in its distribution and associated with eccentric soft-tissue swelling. CPPDD disease Chondrocalcinosis may be a feature of knee OA, where it is regarded as an epi phenomenon. CPPDD can present as pseudogout in a single joint or oligoarticular distributio n, or mimicking RA occurring in a symmetrical distribution especially in elderly females. There is considerable, if somewhat inconsistent, evidence for glucosamine sulfate 1500mg da ily in helping pain and loss of function in knee OA, and possibly slowing radiographic chan ge (although the latter has not been replicated in independent studies). The only trial in hip OA did not show any bene \201 t. Chondroitin sulfate also has some supporting evidence for symptomatic bene \201 t in hip and knee OA. One study has shown benefit from combinin g Rheumatoid arthritis If there is hip or knee destruction, then examination of the hands and wrists should establish if changes are likely to be secondary OA related to RA. If there i s any doubt labora- tory investigations should be used. CHAPTER 12 Osteoarthritis and related disorders 377 Articular hip resurfacing is becoming increasingly availa- ble and has potential advantages for younger patients, as less bone is excised and revision is technically less demanding. However, no long-term data is available. Arthroscopy should be restricted to those with lik ely meniscal/ligament pathology. glucosamine and chondroitin in a pre-specified subgroup with moderate to severe knee OA. Th e side effect pro \201 le of glucosamine and chondroitin is excellent (although there are case reports on the potentiation of warfarin with glucosamine). Avocado/soybean unsaponi \201 ables, a Chinese herbal preparation (SKI306X), and rosehip extracts, were also recomme nded by a recent Cochrane review. A comfrey extract ointment and several different ginger p reparations have single RCT evidence showing effectiveness on symptoms. Clinical tips (extracted from UK NICE OA guidelines) \200 Exercise should be a core component of therapy, irrespective of age, co-morbidity, pain sev erity, and disability. Exercise should include local muscle strengthening and general aerob ic \201 tness. Interventions to effect weight loss should be a core treatment for the obe se and overweight. People with biomechanical joint pain or instability should be considered for assessment for bracing/ joint supports/insoles as an adjunct to core therapy. Accurate verbal and written information should be offered to enhance understanding of OA and its ma n- agement, and to counter misconceptions, such as that OA inevitably progresses and cannot be treated. Individual self-management and group programs should emphasize the recommended core treatments, especially exercise. Full dose paracetamol (1 g tds/qds) should be tried before other analgesics or anti-in \202 ammatories. Pharmacological therapy Oral analgesics \200 Paracetamol (up to 1 g qds) is preferred as \201 rst line analgesia, because of its favor able safety pro \201 le. Opioids, such as codeine or dihydrocodeine, or higher strength op ioids may be needed. Non-steroidal anti-in \202 ammatories (NSAIDs) \200 NSAIDs (including \200\230Coxib \200\231 NSAIDs) provide additional symptomatic bene \201 t in some patients. Gastrointestinal and cardiovascular risks must be consid- ered before use NSAIDs. They should be avoided in patients with established ischaemic heart disease or cerebrovascular disease, and used with caution in those with risk factors for these conditi ons. Conventional NSAIDs should be used with gastropro- tection when risk factors exist, su ch as previous peptic ulceration or current aspirin use. Prognosis and natural history OA is a condition with a variable course. Those affected usua lly present with one painful joint, and this episode often improves or resolves. A minority of patients develop progressive disease and require total joint replacement surgery. Those who present with severe pain and advanced disease will usually require operative intervent ion and there is evidence that early surgery helps to prevent the functional deterioration that otherwise occurs. Over time, other joints become involved, so that single joint OA oft en becomes generalized and episodes of pain affect different joints over time in individual s with generalized OA. Topical treatments \200 Certain topical NSAID preparations are effective, but many of the widely available preparat ions have absent or negative evidence of effectiveness. Capsaicin can be effective, especia lly for hand OA, but has a high rate of skin reactions. Intra-articular injections \200 Glucocorticoid injections can give short-term relief (2 \200\2233 weeks) in knee OA and as long as 3 \200\2234 months in hip OA (where \202 uoroscopic or US guidance are required f or their delivery). There is little compelling evidence for the ef \201 cacy of intra-arti cular Hyaluronan. In view of their high cost, further high quality studies are needed to es tablish their role. Monitoring disease activity This is not routinely undertaken, but there are validated tools for research active units and trials (see below). Current controversies \200 \200 \200 \200 \200 Disease modifying OA drugs (DMOADs) There are currently no universally accepted disease- mo difying OA drugs. Single studies have suggested ef \201 cacy for a number of agents and to xicity has prevented develop- ment of others. This is a very active research area. Potentia l DMOADs include: \200 Diacerein (hip). \200 Doxycycline (knee). \200 Licofelone (kne e). \200 Strontium ranelate. \200 Bisphosphonates. \200 Matrix metalloproteinase inhi bitors. Site and nature of the initial insult in OA. Extent of matrix turnover and decompensation. Role of glucosamine sulfate. Ef \201 cacy of disease modifying OA therapy. Cardiovascular risk attributable to OA. Resources on OA Assessment tools OMERACT An organization originally set up to define outcom e measures for rheumatoid arthritis clinical trials recom- mended a core set of outcome mea sures for OA trials in 1997. This included both generic and disease speci \201 c assessmen t tools. Surgery \200 Hip and knee arthroplasty are established effective treat- ments for end-stage disease, wit h an effect size of more than 2- and 10-year arthroplasty survival of over 90% (although ar throplasty has never been subjected to randomized controlled trial). Generic tools Instruments developed to assess health status and quality of life in other co nditions: HAQ, SF-36 and EQ-5D. Download pain tools including Visual analog scale and OSTEOARTHRITIS 378 NHS direct: basic patient information and access to out of hours advice: http://www.nhsdire ct.nhs.uk/ articles/article.aspx?articleId=268 Wheeless \200\231 Textbook of Orthopedics. A vailable at: h t t p : / / w w w . w h e e l e s s o n l i n e . c o m / o r t h o / osteoa rthritis. SF-36 are available from http://www.painworld.zip.com.au/ articles/pain_tools.html Disease speci \201 c tools These tools have been developed and validated to a varying degr ee in OA. \200 WOMAC is probably the best validated tool for assess- ment of knee and hip OA. It measures 3 domains: pain, stiffness, and function, using either visual analog, numerical rating scal e or Likert scales. Lequesne index. Robust tool, but has some overlapping item options lead ing to some scoring ambiguity. Knee OA outcome score (KOOS) was developed for surgical asse ssment and outcome. Australian/Canadian Hand OA Index (AUSCAN). This tool is analogous in s tructure and rigor of development to WOMAC, but is for hand OA. ICD 10 codes Nodal/generalized OA M15.0 M15.1 M15.2 M15.4 M15.9 Primary generalized (osteo)arthrosis Heberden \200\231s nodes (with arthropathy) Bouchard \200\231s nodes (with arthropathy) Erosive (osteo)arthrosis Generalized osteoarthritis Hip OA M16.0 \200\22316.9 Hip OA codes ( \200\230coxarthrosis \200\231). Knee OA M17 \200\22317.9 Knee OA codes ( \200\230gonarthrosis \200\231). Priority scoring tools There are various tools that have been used for assigning priority f or patients to undergo total hip or knee replace- ment surgery. These include the New Zeala nd, NIH, Ontario, and Western Canada criteria. They include a com- bination of pain, and fu nctional and radiographic assess- ment, often with a degree of subjective assessment of ove rall disease state or requirement for surgery. They are not suitable for determining who sh ould receive surgery. Hand OA M18 \200\22318.9 1st CMC joint (and subcodes) References Altman RD & Gold G. Atlas of individual radiographic features in oste- oarthriti s. OARSI: 2007. Available at: http://www.oarsi.org/index2. cfm?section=Publications_and_New sroom&content=atlas Brandt KD, Doherty M, Lohmander LS. Osteoarthritis, 2nd edn. Resources Guidelines NICE Guideline CG59. OA: the care and management of adults with osteoa rthritis. Implementation tools: http:// www.nice.org.uk/CG059#implementation. OA Society In ternational (OARSI) recommendations for the management of hip and knee osteoarthritis. http :// www.oarsi.org/index2.cfm?section=Publications_ and_Newsroom&content=Indexes EULAR evide nced based recommendations for the management of hip and knee OA. MOVE consensus: evidence- based recommendations for the role of exercise in the management of OA of the hip or knee. Oxford: Oxford University Press, 2003. Dickson J, Hughes R, Marsh D. Royal: the New Science of Osteoarthritis \200\223 from Bench to Bedside. London: Royal Society of Medicine Publications, 2008. Doherty M, Jones A, Cawston T. Osteoarthritis. In: Maddison PJ, Woo P, Isenberg D, Glass D (eds) Oxford Textbook of Rheumatology, 3rd edn. Oxford: Oxford University Press (in press). Jordan KM, Arden NK, Doherty M, et al. EULAR recommendations 2003: an evidence based approa ch to the management of knee osteoarthritis: report of a Task Force of the standing committ ee for international clinical studies including therapeutic trials (ESCISIT). Ann Rheum Dis 2003; 62: 1145 \200\22355. NICE Guideline CG59. Osteoarthritis: the Care and Management of Adults with Osteoarthritis. London: HMSO, 2008. Available at: h t t p : / / w w w. n i c e . o r g . u k / g u i d a n c e / i n d e x . j s p ? a c t i o n = byID&o=11926 (accessed 28 March 2008). Moskowitz R, et al. Osteoarthritis: Diagnosis and Medical/Surgical Management, 4th edn. Phi ladelphia: Lippincott Williams & Wilkins, 2007. Patient organizations (UK) Arthritis Care. Head Of \201 ce: Arthritis Care, 18 Stephenson Way, London NW1 2HD. Telephone 020 7380 6500. E-mail: Info@arthritiscare.org.uk Roddy E, et al. Evidence-based recommendations for the role of exercise in the management o f osteoarthritis of the hip or knee- -the MOVE consensus. Rheumatology 2005; 44: 67 \200 \22373. Internet sites Arthritis Care: http://www.arthritiscare.org.uk/. Arthritis Research Campaig n (excellent patient and pro- fessional resources): http://www.arc.org.uk/ arthinfo/patpubs /6025/6025.asp. Patient information: http://www.patient.co.uk/ showdoc/23068795/, or http:/ /www.cks.library. nhs.uk/patient_information_leaflet/osteoarthritis. Clinical knowledge sum maries: osteoarthritis: http:// www.cks.library.nhs.uk/osteoarthritis; Zhang W, Moskowitz RW, Nuki G, et al. OARSI recommendations for the management of hip and k nee osteoarthritis, part I: critical appraisal of existing treatment guidelines and systema tic review of current research evidence. Osteoarthritis Cartilage. 2007; 15: 981 \200\22310 00. Zhang W, Moskowitz RW, Nuki G, et al. OARSI recommendations for the management of hip and k nee osteoarthritis. Part II: OARSI evidenced-based, expert consensus guidelines. Osteoarthr itis Cartilage 2008; 16: 137 \200\22362. This page intentionally left blank OSTEOARTHRITIS-RELATED DISORDERS 380 Osteoarthritis-related disorders Diffuse idiopathic skeletal hyperostosis Diffuse idiopathic skeletal hyperostosis (DISH, Fo restier \200\231s Disease) is a condition where calci \201 cation of the anterior spinal l igament occurs across at least 4 contiguous verte- brae leading to bony excrescences with a n appearance that has been likened to dripping wax. \200 There are no robust European epidemiological data. DISH affects 6 \200\22312% of the adult population in the USA, increasing to 28%of those over 80 years of age. There is a male prep onderance 2:1. Etiology unknown (hence, \200\230idiopathic \200\231), although an associat ion has been described with diabetes. Familial cases have been described. Distinct SNP poly morphisms in a candidate gene associ- ated with ossi \201 cation of the posterior longitud inal liga- ment (OPLL), collagen 6A1 (Col6A1), have been found in Japanese patients with DI SH. Findings have not been reproduced in other populations. The pathophysiology is not well understood. \200 Figure 12.6 Radiographic appearance of DISH. Neuropathic arthropathy Neuropathic arthropathy or \200\230Charcot \200\231s joint \200 \231 is a condition where peripheral (or central) neuropathy leads to secondary, painless, joint destruction. \200 Clinical features DISH may be asymptomatic, or present with variable degrees of pain and di sability. \200 