3Osteoarthritis (OA)a condition of synovial joints with failed repair of joint damage that results from stresses that may be initiated by an abnormality in any of the synovial joint tissuesThe process involves interactive degradation & repair processes of cartilage, bone, & synoviumOA is currently viewed as a disease of the entire joint and, therefore, the failure of the joint as an organOA may be localized to 1 joint, to a few joints, or be generalized.
4The presence of radiographic OA : a definite osteophyte with or without joint space narrowing on plain radiographClinical OA : abnormalities on PE consistent with OA, such as Heberden or Bouchard nodes in the hand, or limited & painful ROM on internal rotation of the hip. Symptomatic OA is usually defined as pain, aching, or stiffness in a joint with radiographic OA
5Plain radiography : it is often not required because both Dx & progression of OA are usually adequately assessed clinically.▪ MRI visualizes the joint as a whole organ, improving understanding of the pathologic processes, natural history, & potential sources of pain in OA. It is not used routinely for the diagnosis or clinical assessment of OA but is of increasing importance in the research environment.▪ Ultrasound : dynamic assessment of joints; it can assess inflammation (synovial hypertrophy & effusions) and damage (erosions & joint space loss); it also may allow guided therapy for OA jointsPlain radiography is the most feasible method of imaging of osteoarthritis (OA) in clinical practice
6Diagnosis of osteoarthritis The diagnosis of osteoarthritis (OA) is complicated by multiple factors.These include a lack of specific physical or laboratory findings and discrepancies between symptoms and the results of radiographic examinations.As a result, OA is frequently diagnosed by an overall clinical impression based upon the patient's age and history, location of the joint abnormalities, and radiographic findings.
8Laboratory TestsNo blood tests are routinely indicated in the workup of a patient with osteoarthritis.unless symptoms & signs suggest RA or other forms of inflammatory arthritis .Examination of synovial fluid ,rule out: inflammatory arthritis or crystalopathy , infection?:a white-cell count below 2000The presence of crystals is diagnostic of either gout or pseudogout.
9Conventional radiography (CR) not required for the routine clinical diagnosis of OA; because:treatment is symptomatic & symptoms are not generally well correlated with the severity of radiographic features of OACR does not often assist in treatment decisions unless joint replacement is being considered
10OA may be an asymptomatic incidental finding on clinical or radiographic examination, or be a progressive, painful, and disabling disorder at different joints in the same personPain, stiffness, and locomotor restriction are the main symptoms of OAOther symptoms include crepitus, joint deformity, or joint swelling (caused by bony remodeling, excessive osteophytosis, or joint subluxation).These symptoms typically begin in just 1 or a few joints in a person of middle or older agePain worse with joint use and relieved by rest (usage or mechanical pain) is often the most troublesome symptom
11**About 50% of persons with radiographically evident OA have symptoms.Pain is the most common reason why a patient with OA consults a physician.A variety of other symptoms can result from OA that affect function and quality of life.Although OA can involve virtually any joint in the body, the most commonly affected joints are hands & feet, hips, & knees.**Clinical features of osteoarthritis
12pain The origin of pain in OA is not completely understood However, hyaline cartilage is aneural, and is not a source of pain in OA.There is no direct pain from cartilage, synovial fluid, or the inner two thirds of menisci.Pain fibers are present in the remaining tissues surrounding the joint, so pain may arise from the nociceptive fibers & mechanoreceptors in the synovium ,subchondral bone, periosteum, capsule, tendons, or ligamentsPain in large joint OA (eg, knee or hip) is also thought to arise from bone marrow lesions, & synovitis/effusion by stimulation of nociceptive fibers and intra-articular hypertension, respectivelyboth central & peripheral sensitization perpetuate & amplify pain in OA
13night pain can be present in OA, which interferes with sleep & leads to fatigue, lack of well-being, & increased pain sensitivity.In some people, the pain has a burning (neuropathic) quality, is widespread around the joint, & associates with tenderness & paresthesiae. Such features also suggest comorbid fibromyalgia, another common pain syndrome in older people.Painful periarticular soft tissue lesions may coexist with large joint OA
14Stages of pain in OA Stage 1 (Early) -Predictable sharp pain, usually brought on by a mechanical insult that eventually limits high-impact activities. There may only be a minimal effect on function.Stage 2 (Mild-moderate)-Pain becomes a more regular feature, & begins to affect daily activities. There may be unpredictable episodes of stiffness.Stage 3 (Advanced)-Constant dull/aching pain, punctuated by short episodes of often unpredictable intense, exhausting pain that results in severe functional limitations.
15OA pain more commonly is most severe over the joint line except for proximal joints (hip, shoulder), which may have the maximal site of pain distal to the originating joint (radiated pain).
16Stiffness may be thought of as a difficulty or during movement caused by a perceived inflexibility of the joint, morning, but may also occur later in the day, typically after periods of inactivity.both morning & inactivity-related stiffness quickly improve & resolve with joint use, whereas the joint pain subsequently worsens with continued use.
17Transmitted crepitus (felt on the adjacent periarticular bone) suggests a full thickness cartilage defect on the affected sideReduced range of movement mainly results from marginal osteophytosis and capsular thickening but synovial hyperplasia and effusion also contribute.Fixed flexion deformities
18Bony swelling, which may be evident in both small (eg, IPJ, first metatarsophalangeal) and large (eg, knee) joint OA, occurs because of a combination of bony remodeling, marginal osteophytosis, and joint subluxationDeformity and instability are signs of marked joint damage.Muscle wasting suggests advanced OA
19HOLISTIC ASSESSMENTdepression, sleep deprivation, hyperalgesia, central sensitization, & catastrophizationjoint pain at other sites as it increases pain severity at the index jointMobility assessment & neuromuscular examinationhip or knee OA may be associate with muscle weakness, impaired joint position sense, & fallsEach of these has the potential to increase the pain severityThe risk of falls may be further increased by postural hypotension, visual or vestibular impairment, and polypharmacy, which are common in the elderly
20ROLE OF INVESTIGATIONS OA is a clinical diagnosis. It may be diagnosed without recourse to laboratory or radiographic investigations in the presence of typical symptoms & signs in the at-risk age group.Peripheral joint OA may be diagnosed confidently on clinical grounds alone if there is:- Persistent usage-related joint pain in 1 or a few joints- Age 45 years- Only brief morning stiffness (30 minutes)
21clinical diagnosisis supported by the poor correlation between radiographically assessed structural changes & symptoms in OA.The ACR clinical classification criteria for knee, hip, & hand OA have a high sensitivity, and at least a moderate to high specificity for discriminating OA from other rheumatic conditions in a hospital setting.
22imaging & laboratory assessments In younger individuals (ie, <45 years in age) in the absence of preceding major joint traumaIf symptoms & signs are atypical; for example, not usual target sites for OA, significant joint inflammation, marked rest &/or night pain, rapidly progressive painIf there is weight loss or constitutional upsetIf there is true locking at the knee, which suggests additional mechanical derangement.
23Prognostic valuethose with more severe joint space narrowing at baseline progressed more rapidly to complete joint space loss over timeGlobal OA severity had a similar but smaller role.OA may be diagnosed on clinical grounds alone in the at-risk populationradiographs being used more for prognostic than diagnostic purposes.
24Risk factors for poor prognosis in OA AgeObesityKnee malalignment (varus-valgus), hindfoot malalignmentLower limb length inequality (1–2 cm)Presence of OA in multiple joints (eg, generalized OA [GOA])Excess or no joint useMuscle wasting and weaknessJoint laxityPoor mental health, lack of self-efficacy, and poor social support
25OA can affect any synovial joint Reproduced from Abhishek A, Doherty M. Disease diagnosis and clinical presentation.
26Simplified clinical approach to identifying OA subsets 11Number of joints involveda. Localized: 1–2 joint regionsb. GOA: 3 joint regions involved, with spine/hands being one of the regions affected (nodal GOA if nodes present)acromegaly, which has typical signs of OA with little restriction in movements,
27Simplified clinical approach to identifying OA subsets 2. Classic or atypical OA (atypical OA: unusual distribution, <45 years, rapid progression)Causes of atypical OA include:a. Prior trauma (common)b. Dysplasia, JIA, Perthes disease & slipped femoral epiphysis of hip, septic arthritisd. Metabolic or endocrine diseases: eg, hemochromatosis,; acromegaly,e. Late AVN: predominantly hips, shoulders, & knees, (more rapid progression)f. Neuropathic joints: rapid clinical progression, marked joint disorganization:g. Apatite-associated destructive arthritis: old age, rapid progression, ( hips, knees, & shoulders )
283. Clinical joint inflammation: usually absent; if present, consider: a. Crystal deposition: CPPD & goutb. Coexistent inflammatory arthritis: eg, RA, SPAc. Erosive OA: targets hand IPJs
29GOA slow accumulation of multiple joint involvement hand joints around middle age , & affect the knees & other joints over the next few decades.multiple Heberden nodes, Bouchard nodesnodal & non-nodalnon-nodal : mainly occurring in menHeberden nodes are often accompanied by less well-defined posterolateral swellings of the proximal IPJs (PIPJs): so-called Bouchard nodes. A form of GOA showing identical joint targeting was subsequently identified in patients without Heberden nodes, which led to GOA being classified as nodal and non-nodal forms,
30Nodal OA Nodal : more common in women Lateral deviation at the IPJs most deviations pointing toward themiddle fingerWithout IPJ instabilityWith reduced range of movement.
35Erosive OA Note the absence of Heberden nodes aggressive subset of hand OAno association with GOAspares the thumb base & MCPJstargets DIPJs more commonlythan PIPJsLateral instability & ankylosis at the IPJs are characteristic
36Erosive OA radial/ulnar instability Erosive OA: marked radial/ulnar instability. Such instability does not usually occurwith the common hand OA
39Psoriatic arthritis Both PsA & OA involveme the DIP joints, Heberden’s nodes : the nodular bony changePsA : more diffuse swelling of the jointPsA :-characteristic nail changes- inflammatory oligoarticular, polyarticular, & or axial disease-enthesitis-dactylitis
40differential diagnosis for hand OA Gout: may be superimposed on preexisting hand OAHemochromatosis: mainly targets MCPJs, and wrists
41Osteoarthritis of knee joint Of the three compartments of the kneemediallateralpatellofemoralthe medial compartment has the greatest susceptibility to OA
42knee OAMost patients have medial compartment tibiofemoral joint (TFJ) OA, PFJ OA, or a combination of bothKnee joint pain is felt anteriorly & the location & pattern of pain indicate the affected compartment(s).Pain from PFJ OA is typically worsened by prolonged sitting, standing up from low chairs, & climbing stairs or inclinesGeneralized knee pain with distal radiation suggests moderate to severe knee OA.Persistent rest & night pain occur in advanced diseaseno posterior knee pain ,unless there is a complicating popliteal (Baker) cyst.a feeling of giving way (especially with PFJ OA &/or quadriceps weakness) & instability, both of which associate with falls
43Pain on patellofemoral compression Tibiofemoral joint-line tenderness is felt anteriorly, on either side of the patella tendon with the knee flexed.Pain on patellofemoral compressiondeformity (fixed flexion and/or varus; less commonly valgus deformity on weight bearing)quadriceps wasting & weaknesship muscle weakness may be presentKnee effusionTibiofemoral joint-line tenderness is felt anteriorly, on either side of the patella tendon with the knee flexed
44Unilateral knee OA: swollen left knee with varus and fixed flexion deformities in a 63-year-old man with a history of knee trauma. On palpation there was marked crepitus,restricted flexion, bony swelling, and a small effusion. The cruciates were intact but there wasminor varus/valgus instability on stress testing.
45Giving way of the kneean internal derangement such as a meniscal tear or a tear of the anterior cruciate ligament?However, it may also reflect weakness of the muscles that support the joint.Night pain reflects either severe symptomatic disease or pain from other causes:inflammatory arthritis,tumors,infection,crystal disease.
46Examination of kneeExamination of the patient should include testing for various possible causes of knee pain .Since arthritis of the hip can cause referred pain to the knee, range of motion of the hip should be assessed .Bursitis (either anserine or trochanteric) should also be ruled out.
47Examination of the knee (meniscal tears) In patients with advanced OA, meniscal tears are nearly universal & anterior cruciate ligament tears are common.Diagnosing them is not likely to change treatment.Repairing meniscal tears in patients with OA is unlikely to improve the disease course or ameliorate pain.meniscal tears are not associated with pain in osteoarthritis.There is no direct pain from cartilage, synovial fluid, or the inner two thirds of menisci. Pain fibers are present in the remaining tissues surrounding the joint.
48Infectious monoarticular OA of a single joint : mild symptoms and a non inflammatory synovial fluid (WBC <2000 cells/mm3) but can also present as an acutely painful synovitis that may mimic infection
49Radiography if knee pain is nocturnal or is not activity-related. If knee pain persists after effective therapy for osteoarthritis, a radiograph may reveal clues to a missed diagnosis.In patients with osteoarthritis, the radiographic findings correlate poorly with the severity of pain & radiographs may be normal in persons with disease.
52Hip Osteoarthritis maximal Pain, deep in the anterior groin may spread to the anteromedial or upper lateral thigh, & occasionally the buttocks.Distal radiation is commonpain may predominate at the knee. Some people present with knee pain without any proximal pain
53Hip OsteoarthritisPain exacerbated by rising from a seated position, & during initial or mid ambulationLimitation of motionWalkingClimbingSteppingStanding
54Hip OsteoarthritisPatient with right hip OA showing fixed flexion & external rotation deformity.(Reproduced from Abhishek A, Doherty M. Disease diagnosis and clinical presentation. In:HenrotinY, Hunter DJ,Kawaguchi H, editors.OARSIOnline Primer
55Hip Osteoarthritispainful restriction in internal rotation & flexion: the tight pack position for the hip and the first movement to be affected
56It may be difficult to differentiate hip OA pain from referred spinal pain or concomitant knee OA intra-articular local anesthetic injection may be required to resolve any diagnostic uncertainty.
57Rapidly destructive hip osteoarthritis mainly in older womenSerial plain radiographs reveal decreasing joint space over several monthstypically unilateralit has been associated with BCP mainly HA crystals, & ( apatite associated destructive arthropathy )MRI often reveals joint effusion & diffusely increased T2 signal in the femoral head, neck, &/or acetabulumIncreased plasma levels of matrix metalloproteinase (MMP)-3 & MMP-9 & urinary excretion of type II collagen breakdown products in the urineIncreased plasma levels of matrix metalloproteinase (MMP)-3 & MMP-9 and urinary excretion of type II collagen breakdown products in the urine in those with rapid hip destruction compared with those with more typical slowly progressive OA supports a distinction between these two disorders
58Hip OA differential diagnosis osteonecrosis (avascular necrosis) of the femoral Head, pain is initially usually night predominant, well localized, unrelated to usage & progressive, becoming worse on usage & more widespread once the femoral bone & overlying cartilage collapse to result in arthropathy.Posterior hip & buttock pain may be caused by lumbar radiculopathy, iliolumbar ligament syndrome, sacroiliac joint pain, and hip extensor or rotator muscle strain
59Early diagnosis▪ Early diagnosis and intervention in OA would improve the likelihood of disease modification & thereby reduce medical costs, morbidity, & disability.▪ Reclassification of the disease as no longer a purely radiographic entity to a disease process that includes preclinical, preradiographic, & radiographic stages would provide a scenario amenable to the development of primary, secondary, and tertiary prevention strategies.
60Early diagnosisJoint injury result in radiographic OA 10 to 20 years later.there is a prolonged preclinical molecular phase of the disease characterized by protein & microRNA biomarker abnormalitiesWithin the first month after joint injury in humans, elevations in the synovial fluid :cartilage proteoglycan fragments,(MMP-3/stromelysin-1), & collagen fragmentsElevations of cartilage components in serum can persist over decades after joint injury
61Early diagnosisThe sustained increased release of cartilage macromolecular fragments after joint trauma is thought to be a harbinger for the development of posttraumatic radiographic OA in patients with injuries.Many of these fragments represent biomarkers within the causal pathway of disease , act to induce & prolong inflammation following joint injuryMany of these fragments are not only biomarkers of early disease pathology but could themselves also act to induce and prolong inflammation following joint injury and therefore represent biomarkers within the causal pathway of disease
62Relationship between radiology & biomarkers Radiology and MRI provide a cumulative historical view of joint destruction, whereas biomarkers provide dynamic information on the current rate of joint destruction or disease activityThe WHO in Priority Medicine for Europe and the World : biomarkers are essential for arthritis in general & osteoarthritis research in particular, and that the lack of adequate markers constitutes a major hurdle for osteoarthritis drug development
63Although OA is present by histologic or radiographic criteria in nearly 80% of people by the age of 80 years, at any age only half have symptoms.Symptoms are often variable & intermittentThere is a modest correlation between the presence of symptoms & the severity of anatomic or radiographic changes.
64Classification criteria and classification trees, while useful for research purposes, have not been validated for clinical diagnosis and should not be relied upon for that purpose.The inclusion of radiographic and/or laboratory features in the assessment for symptomatic idiopathic OA of the knee or hip, but not the hand, improves the diagnostic accuracy, particularly the specificity
65Western Ontario & McMaster Universities Osteoarthritis Index (WOMAC) To assess pain, stiffness, & physical function in patients with hip and/or knee OAThe WOMAC consists of 24 items divided into 3 subscales:Pain (5 items): during walking, using stairs, in bed, sitting or lying, and standingStiffness (2 items): after first waking and later in the dayPhysical Function (17 items): stair use, rising from sitting, standing, bending, walking, getting in / out of a car, shopping, putting on / taking off socks, rising from bed, lying in bed, getting in / out of bath, sitting, getting on / off toilet, heavy household duties, light household duties.standardized questionnaires used by health professionals to evaluate the condition of patients with osteoarthritis of the kneeand hip, including pain, stiffness, and physical functioning of the joints. The WOMAC has also been used to assess back pain, rheumatoid arthritis, juvenile rheumatoid arthritis, systemic lupus erythematosus, and fibromyalgia. It can be self-administered and was developed at Western Ontario and McMaster Universities in A WOMAC test takes about 12 minutes. Reliability for the physical function scale "has been more consistent and stronger. When used in clinical studies, the WOMAC pain and function subscales perform comparably or better than other tests in being responsive to change from experimental interventions, but this varies for the different subscales and types of intervention.
66Osteoarthritis definition OA can be defined by radiographs, clinical examination, or symptomsSymptoms are more common with more severe radiographic OAthe association between radiographic changes & symptoms is not absolute.As more sensitive measures of osteoarthritis such as MRI & biomarkers are developed & validated, definitions of osteoarthritis may change