Arthritis Presentation 2024 PDF

Arthritis Troy Seely BScPT, MScPT, DPT, FCAPMT Health Conditions and Disease in Rehabilitation RS 3060A © Troy Seely, 2024  Outline 1. Introduce framework for classifying joint disease (arthropathies) 2. Discuss Rheum...

Arthritis Troy Seely BScPT, MScPT, DPT, FCAPMT Health Conditions and Disease in Rehabilitation RS 3060A © Troy Seely, 2024  Outline 1. Introduce framework for classifying joint disease (arthropathies) 2. Discuss Rheumatoid Arthritis – Introduce common deformities – Understand the role of altered mechanics in contributing to the deformity 3. Discuss Osteoarthritis – Review key aspects of articular cartilage pathology – Impact on a patient’s function © Troy Seely, 2024  Joint Disease: Arthropathies Joint disease Differentiated by 3 characteristics: Non- Inflammatory inflammatory 1. Synovial membrane inflammation? No Yes 2. Systemic signs & symptoms? No Yes 3. Normal synovial fluid? Yes No Osteoarthritis Rheumatoid arthritis © Troy Seely, 2024 Rheumatoid Arthritis (RA) Inflammatory Joint Disease - synovial membrane inflammation  - systemic signs & symptoms  - normal synovial fluid  © Troy Seely, 2024  What is Rheumatoid Arthritis? RA is a chronic systemic autoimmune disease. Causes chronic inflammation of connective tissue – mainly seen in joints. 1st tissue affected is synovial membrane Eventually spreads to: a. Articular cartilage b. Fibrous joint capsule c. Surrounding ligaments & tendons Let’s look at key components of © Troy Seely, 2024 synovial joint  Synovial Joint Periosteum: deep layer contains bone-depositing cells (potential source of pain) Ligaments & tendons: (potential Articular Hyaline Cartilage: source of pain) - Reduces friction in joint & distributes - Ligaments hold bones together & forces of weight-bearing prevent undesirable motion - Composed of chondrocytes (cartilage - Tendons control joint motion and cells) & intercellular matrix (collagen, convey low level muscle tone for joint protein polysaccharides & water) stability Synovial membrane: (potential source of pain) - 2 layers Type A cells: ingest & remove bacteria and debris by phagocytosis Type B cells: secrete hyaluronate - binding agent giving synovial Fibrous joint capsule: nerves within fluid its viscous quality sensitive to direction of motion, © Troy Seely, 2024 compression, tension, vibration & pain (potential source of pain)  What is Rheumatoid Arthritis? Because it is systemic, other systems in the human body can also be affected: – Cardiovascular – Pulmonary – Gastrointestinal Infections and osteoporosis are other potential manifestations of the condition. © Troy Seely, 2024  Rheumatoid Arthritis: Epidemiology In 2015, there were ~300,000 Canadians with RA (ie. a cumulative prevalence of 0.9% of the population). RA prevalence has steadily increased over time: – 473 per 100,000 population (0.49%) in 1996 – 784 per 100,000 population (0.9%) in 2015. 3-7 years Median life expectancy is shortened by _____ 20 and ____ Onset usually between ____ 50 years – RA is 3 times more prevalent in women After age 60, men and women affected equally © Troy Seely, 2024  Rheumatoid Arthritis: Etiology The cause of RA is unknown, but it is most likely a combination of genetic and environmental factors. – Some genetic markers have been identified for the disease, but not all persons with RA have these genes. – For an environmental factor, an infectious agent either bacterial or viral could be a cause. © Troy Seely, 2024  Rheumatoid Arthritis: Pathology Rheumatoid factors are autoantibodies that react with immunoglobulin antibodies found in the blood. – The have been found in the synovial fluid and synovial membranes of those with RA. – Approximately 80% of people with RA are ‘rheumatoid factor positive’ (ie. 20% of people with RA are RF negative). It’s hypothesized the interaction between rheumatoid factor and immunoglobulin triggers events that initiate an inflammatory reaction. © Troy Seely, 2024  Pathology of RA: Step by Step 1. An unknown cause initiates immune response. 2. Immune response is abnormal. 3. Inflammation begins in the synovium. 4. The immune response is perpetuated. 5. Progressive joint destruction. © Troy Seely, 2024  Stimulus: antigen (infectious organism) 1. Unknown cause Pathology of Antigen-antibody response RA: Detail producing normal immunoglobulins against the antigen Genetic predisposition to RA Form immune complexes in blood & synovial fluid: Attack self 2. Abnormal immune response Formation of more immune Inflammatory response initiates in 3. Inflammation of synovium synovial membrane of joint complexes & perpetuation of inflammatory response Sustained synovitis 4. Perpetuation of immune response Pannus releases enzymes & Stimulates growth of blood vessels other elements that destroy and fibrous tissue (known as Continued immune response cartilage pannus) into synovial membrane & articular cartilage 5. Progressive joint destruction Chronic inflammatory joint disease Degradation of joint tissues (RA) © Troy Seely, 2024  What is Pannus? Sustained inflammation in the synovium causes fibrin deposition on synovial membrane – Fibrin develops into granulation tissue called pannus, which ultimately becomes scar tissue. The inflammatory cells found in the pannus prevent the synovium from performing its two main functions: – Lubricating the joint and providing nutrients to the avascular articular cartilage. © Troy Seely, 2024 © Troy Seely, 2024  End Stage RA Progression The synovial and joint deformity changes that occur in RA can progress to other presentations: – Erosion of underlying bone – Ankylosis ________________ Abnormal stiffening and immobility due to fusion of bone © Troy Seely, 2024  Clinical Presentation RA The disease begins insidiously and progress slowly: – Fatigue and generalized weakness – Generalized aching and stiffness – Weight loss – Inflammation can be inconsistent (come and go) Morning stiffness Prolonged morning More than 1 + hours stiffness is hallmark symptom of RA Severity & duration directly related to disease severity (vs feeling stiff next morning after © Troy Seely, 2024 exercise)  Clinical Presentation RA Local joint changes occur gradually over time – Earlier Because of swelling Joints become painful & stiff Pain is due to pressure from swelling CARDINAL signs of inflammation - pain (arthralgia) - redness - swelling - heat – Later Due to increased inflammatory exudate in synovial membrane, joint swelling becomes widespread. As number of involved joints increases, likelihood of symmetric involvement increases Pain © Troy Seely, 2024 – Can also be due to sclerosis of subchondral bone & new bone formation  Clinical Presentation RA Location: – Wrist, knee, and joints of the fingers, hands and feet ( although RA can affect any joint ). – The metacarpophalangeal (MCP) and proximal interphalangeal (PIP) joints of the hand are involved early. – Joint deformities in the fingers, hand, and wrist are visible signs of RA. © Troy Seely, 2024  Clinical Presentation RA Characteristic joint changes: – Decreased joint space – Muscle imbalance about the joint – Laxity of supporting soft tissue structures – Damaged or weakening of tendons, ligaments and joint capsule – Cartilage degradation and bone erosion – Unopposed physical forces when using affected joint (altered joint mechanics) Joint changes over time contribute to development of permanent joint deformities © Troy Seely, 2024  Selected Deformities in RA Swan Neck: Fingers Boutonniere: Fingers Volar subluxation and ulnar drift: Wrist & MCPs Loss of ulnar deviation: Wrist Flexion contracture: Wrist Cervical spine instability © Troy Seely, 2024  Swan Neck 1. Initial synovitis Deformity at MCP DIP PIP flexion hyperextension Interosseous & lumbrical pull on dorsal expansion 2. Pain leads to reflex spasm of intrinsics © Troy Seely, 2024 3. Hypermobile PIP pulled volarly by pull of intrinsics  Boutonniere Deformity Synovitis at PIP PIP flexion DIP extension 1. Chronic synovitis of PIP leads to extensor digitorum communis of middle phalanx lengthening © Troy Seely, 2024 2. Lateral bands slide volarly to force PIP into flexion  Volar Subluxation and Ulnar Drift: MCP Joints Volar subluxation and ulnar drift of MCPs: The ulnar deviation occurs as the tendons slip to the ulnar side of the hand. © Troy Seely, 20243  Loss of Ulnar Deviation: Radiocarpal Joints Lose radial ligamentous support Destruction of extensor carpi ulnaris & fibrocartilage disc Proximal row of carpal bones slide to ulna © Troy Seely, 2024  Wrist Flexion Contracture When we make a fist or lift up a heavy object there is a pattern of movement that we tend to adopt at the wrist: __________ Extension of the wrist Early synovitis in carpus leads to flexion contracture: Power grip requires wrist extension Ultimately lose power grip © Troy Seely, 2024  Cervical Spine The C1-C2 articulation is the most common articulation in the spine affected by this condition, because the joints there are purely synovial = primary target for RA. Also, because the C1-C2 articulation are along a horizontal plane ( parallel to the ground ), there is no bony structures to prevent subluxation and they are reliant on ligamentous stability. – These relevant ligamentous structures are at risk in RA. © Troy Seely, 2024  Cervical Spine Atlantoaxial most common level. Odontoid (lack of stability and can even fracture) Ruptured transverse ligament © Troy Seely, 2024 Atlantoaxial joint  Diagnosis of RA In the early stages, diagnosis is challenging because of the subtle, gradual onset of complaints. – These symptoms can wax and wane, delaying the suspected need for an assessment. Early diagnosis of RA can allow for early medical management and help prevent or reduce joint damage. © Troy Seely, 2024  Diagnostic Criteria To use: patient must have at least 1 joint with clinical synovitis (i.e. swelling) AND the synovitis is not better Rheumatoid factor explained by another disease (e.g. psoriatic arthritis, gout) and anti-citrullinated protein are autoantibodies that Classification criteria categories (points): may be present for Joint involvement (number and type): (max 5 points) years before clinical manifestation of RA Blood tests for compounds related to abnormal autoimmune response (max 3 points) Erythrocyte Blood tests for acute-phase reactants (max 1 point) Sedimentation Rate and C-reactive Duration of symptoms (max 1 point) protein are RA if ≥ 6 / 10 nonspecific indicators of Aletaha et al. Rheumatoid Arthritis Classification Criteria general levels of © Troy Seely, 2024 Arthritis and Rheumatism. 62(9):2569-81, 2010 inflammation  Diagnosis of RA Things to consider: – The presence of serum rheumatoid factor supports the diagnosis but can also be found in healthy persons. – Conventional x-rays and MRI investigation can allow for more accurate diagnosis in looking at: Joint changes (x-rays) Lesions of the cartilage, synovium involvement, and joint effusion (MRI) © Troy Seely, 2024  The 51 joints assessed for deformity, tenderness and swelling by NOAR, shown using the recording mannikin Bunn D K et al. Rheumatology 2004;43:1519-1525 © Troy Seely, 2024 Rheumatology Vol. 43 No. 12 © British Society for Rheumatology 2004; all rights reserved  Rheumatoid Arthritis - Summary Unknown cause, likely combination of genetic and environmental factors. Begins with inflammation of synovial membrane. ‘Progressive’ joint involvement: – Synovitis – Pannus formation – Cartilage erosion – Bone erosion and ankylosis © Troy Seely, 2024  Osteoarthritis (OA) Osteoarthritis is a slowly evolving articular disease that originates in the cartilage and affects the underlying bone, soft tissues, and synovial fluid. OA is divided into two classifications: – Primary OA is a disease of unknown cause, and the cascade of joint degeneration is thought to be related to a defect in articular cartilage itself. – Secondary OA has a known cause: trauma, previous infection, lower limb alignment issues, etc.. © Troy Seely, 2024  The Two Main Functions of Cartilage 1. Provides friction-free movement of the two bone ends within the joint. 2. When weight-bearing through the joint: – It disperses load across joint surface. – It absorbs shock/weight to reduce load to bone. To be effective, cartilage is required to: – Be elastic (regain its form after compression) – Have high tensile strength © Troy Seely, 2024 Articular Cartilage © Troy Seely, 2024  Components of Articular Cartilage 1. Chondrocytes 2. Surrounded by a ‘matrix’ Chondrocytes produce two components of the ‘matrix’: - Collagen - Proteoglycans BOTH have mechanical characteristics of elasticity & high tensile strength. The 3rd component of the matrix is water (70-85% of tissue weight) © Troy Seely, 2024  How Proteoglycans Work Within Collagen Proteoglycans are negatively charged: – This causes aggregated proteoglycans to repel one another and spread out – i.e. occupy more volume. The amount of volume that can be taken up by proteoglycans is limited by collagen framework. – This limiting effect of the network of collagen around the proteoglycans provides stiffness to cartilage. © Troy Seely, 2024 How Cartilage Absorbs Compression When cartilage is compressed: – This pushes aggregated proteoglycans together. – i.e. increases their repulsive force (because of negative charges trying to repel each other). – Increasing compressive stiffness. Note: Damaged collagen does not restrain as effectively as healthy collagen © Troy Seely, 2024  Articular Cartilage Maintenance Articular cartilage undergoes normal turnover i.e. matrix components ‘wear out’ (are degraded) and replaced. This balance between replacement and degradation is maintained by chondrocytes: – Synthesize matrix (anabolic repair activity) – Secrete matrix-degrading enzymes (catabolic repair activity) The health of chondrocytes determines joint integrity Condrocyte metabolism in normal cartilage can be modulated by mechanical loading. © Troy Seely, 2024 The interplay between articular cartilage health and mechanical loading is important  Osteoarthritis: Epidemiology It is the single most common joint disease. – Estimated prevalence of ____ 60% in men and ____ 70% in women after age 65 Affects men and women equally to age 55 Joint distribution same for both sexes In older persons (over 55) Hip OA more common in men than women OA of IP joints & thumb more common in women © Troy Seely, 2024  Osteoarthritis: Etiology Modifiable? INTRINSIC JOINT VULNERABILITY Injury (ACL & meniscal) Malalignment (CDH, varus knee) SYSTEMIC FACTORS Proprioceptive defect (CVA) Age Gender EXTRINSIC FACTORS Genetic susceptibility Obesity * Nutritional factors * Physical activity (repetitive) * Arthritis susceptibility © Troy Seely, 2024 ARTHRITIS  Osteoarthritis: Etiology As shown on the previous slide the cause of OA is multifactorial. Recent research has shown other factors that may influence the progression of the presentation: – Smokers with knee OA sustain greater cartilage loss and have more severe knee pain than non-smokers. – There is low or no additional risk of OA from regular, moderate running vs. higher risk of OA from playing in football, soccer, and hockey. © Troy Seely, 2024  OA: Pathogenesis The pathological process of OA initiates in one of two scenarios: 1. Articular hyaline cartilage & subchondral bone are normal, but excessive joint loading causes tissue failure. 2. There is normal applied mechanical loads, but the material properties of cartilage or bone are inferior. © Troy Seely, 2024  OA: Pathogenesis Recall that cartilage is reliant on the balance between replacement and degradation ( ie. anabolic repair activity and catabolic repair activity ). Development of OA is the result of active joint remodeling processes secondary to an imbalance between catabolic and anabolic repair activity. © Troy Seely, 2024  Early Articular Cartilage Changes Earliest changes occur in the matrix of the cartilage = weakening of the collagen network. – Probably due to enzymatic breakdown. Enzymes break down proteoglycans & collagen into individual fragments. – Enzymatic activity interferes with assembly of proteoglycan and collagen subunits. – This affects the mechanics of proteoglycan aggregation, which will affect effective load transfer. © Troy Seely, 2024  Early Articular Cartilage Changes By altering the matrix, there is disruption of the pumping action that regulates normal movement of water and synovial fluid into and out of the cartilage. – Cartilage imbibes too much fluid, which means it is now less able to withstand stresses of weight bearing. This will result in cartilage degeneration and release of breakdown products into the synovial fluid environment. – Early OA changes are difficult to detect on xray. © Troy Seely, 2024  Early Articular Cartilage Changes Nature © Troy Seely, 2024  Later Articular Cartilage Changes Early OA changes progress to the point where articular cartilage: – Demonstrates flaking of its surface layers. – Progresses to development of longitudinal fissures (fibrillation) in its deeper layers. – Later becomes thin or completely absent in areas and leaving subchondral bone unprotected. © Troy Seely, 2024  Later Articular Cartilage Changes With progressive loss of cartilage, inflammation will develop resulting in: – Ligamentous laxity – Progressive muscle weakness This combination of factors results in mechanical stress shifting to other joint structures, including the now exposed subchondral bone. © Troy Seely, 2024  Later Articular Cartilage Changes As the cartilage continues to thin, the joint space narrows and the underlying bone undergoes sclerosis (increase in the density of the bone matrix which can be seen x ray or CT scan). New bone is formed in response to the excessive mechanical load and this new bone also forms at the joint margins (osteophytes). – Small pieces break off causing ‘joint mice’. Irritation of the synovial membrane occurs in later stages causing synovitis and joint effusion. © Troy Seely, 2024  Later Articular Cartilage Changes The joint capsule will become thickened (fibrosis) and may even adhere to underlying bone. This fibrosis and potential adherence can further contribute to limitation in movement which is clinically relevant: – Articular hyaline cartilage has a lack of vascular supply. – It depends on repetitive mechanical loading and unloading for nutritional elements to reach the chondrocytes and the cellular waste to return to the synovial fluid and eventually the blood stream. – These nutritional mechanisms are interrupted by immobilization ( causing further progression of this articular disease ) © Troy Seely, 2024  Later Articular Cartilage Changes Nature © Troy Seely, 2024 © Troy Seely, 2024  Radiography Osteoarthritis Action Alliance © Troy Seely, 2024  Usual Affected Joints Most often: – Hips and knees – Ankles and feet – Hand and wrist – Neck (lower cervical spine) – Lower back (lumbar and sacroiliac joint) © Troy Seely, 2024  OA: Clinical Presentation RA: pain on Likely to occur or increase with motion motion and at rest Cause of OA pain? – Articular cartilage is aneural (so not a source of pain) – Other possible sources: Stretching of nerve endings in periosteum covering osteophytes Microfractures in subchondral bone Stretching of ligaments or muscle spasm in joint instability In later stages of OA, inflammation of the synovium © Troy Seely, 2024 OA: Pain and Age Pain Increased >2 x Vs. other chronic conditions Pain irrespective of age © Troy Seely, 2024 OA: Activity Limitations & Age In same age range see arthritis /condition effect Slow age-related rise in % with activity limitations © Troy Seely, 2024  OA: Clinical Presentation Besides pain, common OA related symptoms include: – Limited range of motion – Crepitus in motion – Joint effusion – Joint malalignment and deformity © Troy Seely, 2024  OA: Clinical Presentation Stiffness of relatively short duration ( less than 30 minutes) can occur after periods of inactivity, including sitting and sleeping. – Morning stiffness usually only lasts 5 to 10 minutes in length. Swelling, if present, is mild and localized to the joint. © Troy Seely, 2024 OA: Activities of Daily Living and Age In same age range see arthritis effect See stronger age-related rise © Troy Seely, 2024  OA Summary Chief pathologic feature: – Degeneration & loss of articular cartilage Modifiable & non-modifiable risk factors. Impacts on pain, function and ultimately health because of its impact on mobility. © Troy Seely, 2024  Contrast OA to RA In Osteoarthritis: – Primarily affects loading joints, and usually begins on one side of body (not as symmetrical as RA) – Brief morning stiffness that is decreased by physical activity. – No systemic symptoms (fatigue, weight loss, etc..) or affiliated conditions – Rheumatoid factor is absent © Troy Seely, 2024