In the name of GOD

Osteoarthritis diagnosis

Osteoarthritis (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 tissues The process involves interactive degradation & repair processes of cartilage, bone, & synovium OA is currently viewed as a disease of the entire joint and, therefore, the failure of the joint as an organ OA may be localized to 1 joint, to a few joints, or be generalized.

The presence of radiographic OA : a definite osteophyte with or without joint space narrowing on plain radiograph Clinical 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

Plain 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 joints Plain radiography is the most feasible method of imaging of osteoarthritis (OA) in clinical practice

Diagnosis 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.

Laboratory Tests No 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 2000 The presence of crystals is diagnostic of either gout or pseudogout.

Conventional 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 OA CR does not often assist in treatment decisions unless joint replacement is being considered

OA 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 person Pain, stiffness, and locomotor restriction are the main symptoms of OA Other 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 age Pain worse with joint use and relieved by rest (usage or mechanical pain) is often the most troublesome symptom

** 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

pain 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 ligaments Pain 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, respectively both central & peripheral sensitization perpetuate & amplify pain in OA

night 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

Stages 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.

OA 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).

Stiffness 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.

Transmitted crepitus (felt on the adjacent periarticular bone) suggests a full thickness cartilage defect on the affected side Reduced range of movement mainly results from marginal osteophytosis and capsular thickening but synovial hyperplasia and effusion also contribute. Fixed flexion deformities

Bony 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 subluxation Deformity and instability are signs of marked joint damage. Muscle wasting suggests advanced OA

HOLISTIC ASSESSMENT depression, sleep deprivation, hyperalgesia, central sensitization, & catastrophization joint pain at other sites as it increases pain severity at the index joint Mobility assessment & neuromuscular examination hip or knee OA may be associate with muscle weakness, impaired joint position sense, & falls Each of these has the potential to increase the pain severity The risk of falls may be further increased by postural hypotension, visual or vestibular impairment, and polypharmacy, which are common in the elderly

ROLE 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)

clinical diagnosis is 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.

imaging & laboratory assessments In younger individuals (ie, <45 years in age) in the absence of preceding major joint trauma If symptoms & signs are atypical; for example, not usual target sites for OA, significant joint inflammation, marked rest &/or night pain, rapidly progressive pain If there is weight loss or constitutional upset If there is true locking at the knee, which suggests additional mechanical derangement.

Prognostic value those with more severe joint space narrowing at baseline progressed more rapidly to complete joint space loss over time Global OA severity had a similar but smaller role. OA may be diagnosed on clinical grounds alone in the at-risk population radiographs being used more for prognostic than diagnostic purposes.

Risk factors for poor prognosis in OA Age Obesity Knee malalignment (varus-valgus), hindfoot malalignment Lower limb length inequality (1–2 cm) Presence of OA in multiple joints (eg, generalized OA [GOA]) Excess or no joint use Muscle wasting and weakness Joint laxity Poor mental health, lack of self-efficacy, and poor social support

OA can affect any synovial joint Reproduced from Abhishek A, Doherty M. Disease diagnosis and clinical presentation.

Simplified clinical approach to identifying OA subsets 11Number of joints involved a. Localized: 1–2 joint regions b. 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,

Simplified 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 arthritis d. 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 )

3. Clinical joint inflammation: usually absent; if present, consider: a. Crystal deposition: CPPD & gout b. Coexistent inflammatory arthritis: eg, RA, SPA c. Erosive OA: targets hand IPJs

GOA 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 nodes nodal & non-nodal non-nodal : mainly occurring in men Heberden 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,

Nodal OA Nodal : more common in women Lateral deviation at the IPJs most deviations pointing toward the middle finger Without IPJ instability With reduced range of movement.

Thumb base OA

Bouchard’s nodes

Erosive OA Note the absence of Heberden nodes aggressive subset of hand OA no association with GOA spares the thumb base & MCPJs targets DIPJs more commonly than PIPJs Lateral instability & ankylosis at the IPJs are characteristic

Erosive OA radial/ulnar instability Erosive OA: marked radial/ulnar instability. Such instability does not usually occur with the common hand OA

Erosive OA *Gull-wing appearance Central erosion Collapse Osteophyte

Psoriatic arthritis Both PsA & OA involveme the DIP joints, Heberden’s nodes : the nodular bony change PsA : more diffuse swelling of the joint PsA : -characteristic nail changes - inflammatory oligoarticular, polyarticular, & or axial disease -enthesitis -dactylitis

differential diagnosis for hand OA Gout: may be superimposed on preexisting hand OA Hemochromatosis: mainly targets MCPJs, and wrists

Osteoarthritis of knee joint Of the three compartments of the knee medial lateral patellofemoral the medial compartment has the greatest susceptibility to OA

knee OA Most patients have medial compartment tibiofemoral joint (TFJ) OA, PFJ OA, or a combination of both Knee 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 inclines Generalized knee pain with distal radiation suggests moderate to severe knee OA. Persistent rest & night pain occur in advanced disease no 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

Pain on patellofemoral compression Tibiofemoral joint-line tenderness is felt anteriorly, on either side of the patella tendon with the knee flexed. Pain on patellofemoral compression deformity (fixed flexion and/or varus; less commonly valgus deformity on weight bearing) quadriceps wasting & weakness hip muscle weakness may be present Knee effusion Tibiofemoral joint-line tenderness is felt anteriorly, on either side of the patella tendon with the knee flexed

Unilateral 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 was minor varus/valgus instability on stress testing.

Giving way of the knee an 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.

Examination of knee Examination 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.

Examination 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.

Infectious 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

Radiography 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.

Hip Osteoarthritis

Hip Osteoarthritis

Hip Osteoarthritis maximal Pain, deep in the anterior groin may spread to the anteromedial or upper lateral thigh, & occasionally the buttocks. Distal radiation is common pain may predominate at the knee. Some people present with knee pain without any proximal pain

Hip Osteoarthritis Pain exacerbated by rising from a seated position, & during initial or mid ambulation Limitation of motion Walking Climbing Stepping Standing

Hip Osteoarthritis Patient 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

Hip Osteoarthritis painful restriction in internal rotation & flexion: the tight pack position for the hip and the first movement to be affected

It 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.

Rapidly destructive hip osteoarthritis  mainly in older women Serial plain radiographs reveal decreasing joint space over several months typically unilateral it 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 acetabulum Increased plasma levels of matrix metalloproteinase (MMP)-3 & MMP-9 & urinary excretion of type II collagen breakdown products in the urine Increased 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

Hip 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

Early 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.

Early diagnosis Joint 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 abnormalities Within the first month after joint injury in humans, elevations in the synovial fluid : cartilage proteoglycan fragments, (MMP-3/stromelysin-1), & collagen fragments Elevations of cartilage components in serum can persist over decades after joint injury

Early diagnosis The 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 injury Many of these fragments are not only biomarkers of early disease pathology but could themselves also act to induce and prolong inflammation following joint injury 16 21 and therefore represent biomarkers within the causal pathway of disease

Relationship 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 activity The 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

Although 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 & intermittent There is a modest correlation between the presence of symptoms & the severity of anatomic or radiographic changes.

Classification 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

Western Ontario & McMaster Universities Osteoarthritis Index (WOMAC) To assess pain, stiffness, & physical function in patients with hip and/or knee OA The WOMAC consists of 24 items divided into 3 subscales: Pain (5 items): during walking, using stairs, in bed, sitting or lying, and standing Stiffness (2 items): after first waking and later in the day Physical 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 1982. 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.

Osteoarthritis definition OA can be defined by radiographs, clinical examination, or symptoms Symptoms are more common with more severe radiographic OA the 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