Osteoporosis and Osteoarthritis Quiz

Approach to the Patient with Metabolic Bone Disease & Rheumatic Disease

• This presentation outlines an approach to patients with metabolic bone disease and rheumatic disease.
• A roadmap is presented, highlighting key areas like general approach, osteomalacia/rickets, osteoporosis, rheumatoid arthritis, and spondyloarthropathies.

Clinical Examination of the Musculoskeletal System

• Hands: Swelling, deformity, nail changes, tophi, Raynaud's, rheumatoid nodules, nail dystrophy in psoriatic arthritis.
• Face: Rash, alopecia, mouth ulcers, butterfly rash, scleritis.
• Trunk: Kyphosis, scoliosis, tender spots (fibromyalgia, enthesitis).
• Legs: Deformity, swelling, restricted movement, synovitis, Heberden and Bouchard nodes.
• Feet: Deformity, swelling (gout, dactylitis), redness, acute gout.
• General observation: includes gait, deformity, swelling, redness, and rash are all examined.

Structure of Major Musculoskeletal Tissues

• Bone: Calcified zone, hypertrophic zone, proliferative zone, trabecular bone, cortical bone, osteoblasts, osteocytes, osteoclasts, epiphyseal plate.
• Muscle: Myofilament, myofibril, fascicle.
• Articular cartilage: Chondrocytes, calcified cartilage, subchondral bone, synovium, synovial lining cells, joint capsule, haversian system, blood vessels, collagen lamellae, osteocytes.
• Calcium phosphate travels through blood and goes into kidney.

Bone Remodelling Cycle

• Bone-lining cells, microdamage, osteoclasts (eat old bone), osteocytes (new bone), osteoblasts (formation of new bone), apoptotic osteoclast, resorption, reparation of the bone, osteoclasts dead in 12 days, reversal.

Example of Double Tetracycline Labelling

• Evaluates the creation of new bone.
• Using a double tetracycline marker, the progress of new growth is measured by the disparity between the markers

Cellular and Molecular Regulators of Bone Remodelling

• Renal phosphate excretion, bone marrow stromal cells, FGF23, SOST, Wnt, osteoblast, osteocyte, OPG, M-CSF, RANKL, osteoclast precursor, osteoclast.

Key Regulators of Bone Remodelling

• Mediator: RANKL, Osteoprotegerin, Wnt, Sclerostin, Parathyroid hormone, Thyroid hormone, Oestrogen, Glucocorticoid.
• Source: Osteocytes, stromal cells, activated T cells, lymphocytes, stromal cells, osteocytes, parathyroid glands, thyroid gland, ovaries, adrenal glands, exogenous.
• Effects: Stimulates bone resorption, inhibits bone resorption, stimulates bone formation, activates LRP receptors, blocks effect of Wnt, increases bone resorption and formation, increases bone resorption and formation, inhibits bone resorption, inhibits bone formation.

Investigations of Musculoskeletal Disease

• Imaging: Plain X-rays, bone scintigraphy, MRI, ultrasonography, computed tomography, dual x-ray absorptiometry
• Blood tests: Haematology, biochemistry, immunology
• Other: Tissue biopsy, electromyography, joint aspiration

MRI & Ultrasound Image Showing Synovitis

• Images showing inflammation of the synovial membrane.

Typical Biochemical Abnormalities in Various Skeletal Diseases

• Charts showing the presence and absence of abnormalities in a variety of bone disorders.

Patterns of Joint Involvement in Different Forms of Polyarthritis

• Diagrams showing the areas of the skeleton affected in various forms of arthritis.

Osteoporosis

• Most common bone disease, more than 8.9 million fractures annually.
• One-third of women and one-fifth of men age 50 and above.
• Fracture risks increase over time.
• Common fracture sites include the forearm, spine, humerus, and hip.

Dual-Energy X-ray Absorptiometry (DXA)

• Measures bone density.
• Scores show bone density as T and Z scores.

Risk Factors for Osteoporosis

• Genetic factors: single-gene disorders, receptor mutations, endocrine disease.
• Inflammatory disease: inflammatory bowel disease, ankylosing spondylitis.
• Drugs: glucocorticoids, gonadotrophin releasing hormone agonists, levothyroxine.
• Gastrointestinal disease: malabsorption.
• Lung disease: chronic obstructive pulmonary disease.
• Myeloma, homocystinuria, anorexia nervosa, highly trained athletes, HIV, Gaucher's disease, polygenic inheritance, hyperparathyroidism, Cushing's syndrome.
• Rheumatoid arthritis, aromatise inhibitors, thiazolidinediones, anticonvulsants, alcohol intake, heparin, chronic liver disease, cystic fibrosis, systemic mastocytosis, immobilisation, body mass index <18, smoking.
• Data on Vit D intake and calcium ingestion affect bone reabsorption.
• Osteoporosis occurs due to an imbalance between bone reabsorption osteoblast, and creation of new bone osteoclast.

Fractures

• Tables and diagrams showing fracture rates across different age groups and areas of the body.

Vertebral Fractures

• Data on cumulative survival with and without vertebral fractures.

Pathophysiology of Osteoporosis

• Reduced bone density leads to micro-architectural deterioration and fracture risk, increased risk of falling with age, bone mass increase during growth, fall afterward, bone loss accelerates post-menopause due to estrogen deficiency ,and imbalance in bone remodelling cycle.

Investigations in Osteoporosis

• Lists of investigations to perform to diagnose osteoporosis.

Drug Treatments for Osteoporosis

• Tables comparing various drug treatments' regimens, daily doses, and other factors.

Osteomalacia and Rickets

• OM and rickets are similar; the difference is that rickets occurs in children, OM in adults.
• Disturbed mineralization of osteoid, causing thick osteoid, stress fractures, bow-leggedness, and other skeletal issues.

Causes of Osteomalacia and Rickets

• Deficiency in vitamin D, lack of sunlight exposure, poor diet, malabsorption, familial hyperphosphatemia, kidney damage, and loss-of-function mutations.
• Defects in phosphate and pyrophosphate metabolism, mutations, tumour-induced hypophosphataemic osteomalacia, hypophosphatasia, and high fluoride in water.

Osteomalacia and Rickets (radiographs)

• Radiographic examples illustrating the conditions, particularly pseudofractures and bowing.

Paget's Disease

• Focal areas of increased and disorganized bone remodeling involving one or more skeletal sites.
• Increased bone resorption by abnormal osteoclasts, followed by rapid formation of poorly organized, structurally weak bone.
• Plain radiographs show increased uptake of radionuclide, increased serum levels of alkaline phosphatase, a hallmark sign of the disease.

Clinical Features of Paget's disease

• Axial skeleton is predominantly affected.
• Bone pain and pathological fracture.
• Many patients are asymptomatic.
• Bone deformity and expansion, increased warmth over affected bone.
• Neurological problems: deafness, cranial nerve defects, nerve root pain, spinal cord compression, and spinal stenosis.
• Osteosarcoma, a rare and serious complication.

Paget's disease (radiographs)

• Radiographic image highlighting the intense tracer uptake and deformity of the affected femur, and areas of osteosclerosis and radiolucency with pseudofractures.

Treatment for Paget's disease

• Combination of nonpharmacological (physical therapy) and pharmacological therapy (antiresorptive agents, analgesics).
• Bisphosphonates inhibit osteoclast activity.
• IV zoledronic acid leads to rapid, sustained normalization of alkaline phosphatase.
• Surgery may be needed for impending or complete fractures, joint realignment, and total arthroplasty in severe cases.

Rheumatoid Arthritis

• Common inflammatory arthritis affecting all ethnic groups worldwide.
• Prevalence: 0.8-1.0% in Europe and the Indian subcontinent (lower in Asia).
• Chronic disease with exacerbations and remissions.

Pathophysiology of Rheumatoid Arthritis

• Environmental triggers, genetic predisposition, and immune response lead to inflammation, immune complexes, activation and proliferation of T cells, macrophages and B cells.
• Leading to synovial inflammation, bone erosion, and cartilage destruction.

Criteria for Diagnosis of Rheumatoid Arthritis

• Scoring system based on joint involvement, presence of rheumatoid factors/anti-CCP antibodies, symptoms duration and acute phase reactants.

Clinical Presentation of Rheumatoid Arthritis

• Morning stiffness, symmetrical joint swelling affecting hands, wrists (proximal interphalangeal and metacarpophalangeal joints, and metatarsophalangeal joints), bony erosion and cartilage damage.
• Extra-articular features: rheumatoid nodules, interstitial lung disease, vasculitis, pleuropericarditis, scleritis, episcleritis, leg ulcers, Felty syndrome.

Investigations and Monitoring for Rheumatoid Arthritis

• Clinical criteria, erythrocyte sedimentation rate, C-Reactive protein, ultrasound or MRI, and tests for rheumatoid factor and anti-citrullinated peptide antibodies.
• Monitor disease activity, monitor damage with x-rays, and monitor drug safety.

Calculation of the Disease Activity Score and Algorithm for Management (rheumatoid arthritis)

• Measurement to assess the severity of disease activity and adapt treatment strategies accordingly.
• Factors such as number of swollen and tender joints, erythrocyte sedimentation rate, patient self assessment (on a scale of 0 -100), and are used to categorise patients into a specific category of disease activity.

Osteoarthritis

• Most common type of arthritis, characterised by pain and disability in older adults.
• Focal loss of articular cartilage, subchondral osteosclerosis, osteophyte formation, joint margin remodeling, and affected joint enlargement.
• Increased prevalence with age (45% knee OA, 25% hip OA).

Pathophysiology of Osteoarthritis

• Cartilage degeneration is the defining feature.
• Chondrocytes start dividing and producing nests of metabolically active cells.
• Increased degradation of cartilage matrix components (aggrecan and type II collagen).
• Reduced concentration of aggrecan, making cartilage vulnerable to injury.

Pathologic Features of Osteoarthritic Joint Tissues

• Diagrams illustrating normal vs. osteoarthritic joints, including synovial membrane, cartilage, and subchondral bone.

Risk Factors and Pathological Changes in Osteoarthritis

• Genetic factors, adverse biomechanics, meniscectomy, ligament ruptures, Paget's disease, obesity, trauma, hormonal factors (estrogen deficiency) and aromatase inhibitors, can all lead to osteoarthritis.
• Abnormal nests of proliferating chondrocytes, cartilage fibrillation, osteophytes formation, subchondral sclerosis, and subchondral cysts are all hallmarks of osteoarthritis.

Symptoms and Signs of Osteoarthritis

• Insidious onset, variable, intermittent pain related to movement and weight-bearing, relieved by rest, brief morning stiffness.
• Restricted movement, palpable/audible crepitus, bony swelling, deformation, joint line/periarticular tenderness, muscle weakness, and minimal synovitis.

Investigations for Osteoarthritis

• Plain X-ray of the affected joint, which shows osteophytes and joint space narrowing.
• MRI can be performed to look for nerve compression.
• Biochemical, haematological, and rheumatological tests.
• Synovial fluid analysis is usually normal.

X-Ray Appearances in Knee Osteoarthritis

• Radiographic findings showing almost complete loss of joint space, sclerosis of subchondral bone, and lateral displacement of the patella.

Typical Varus Knee Deformity

• Radiographic image illustrating varus deformity of the knee related to osteoarthritis.

Spondyloarthropathies

• Group of related inflammatory musculoskeletal diseases with shared immunogenetic association with HLA-B27.
• Includes axial spondyloarthritis, ankylosing spondylitis, reactive arthritis, psoriatic arthritis, and arthritis associated with inflammatory bowel disease.

Spondyloarthropathies (Clinical Features)

• Axial skeleton is predominantly affected.
• Non-synovial musculoskeletal lesions (inflammatory in nature).
• Hallmarks is enthesitis (inflammation of a ligament or tendon being inserted into a bone).
• Dactylitis is also possible.

Spondyloarthropathies (Pathophysiology)

• Environmental triggers, genetic predisposition, and immune responses lead to an inflammatory process along ligaments, tendons, and periosteum.
• Key components to look at are the gut flora, microbial products, dendritic cell, antigen, T-cell activation and cytokine production (IL-22, TNF-α, IL-17).

Comparison of Spondyloarthropathies

• Table comparing the characteristics of different types of spondyloarthritis, including sacroiliitis involvement, peripheral arthritis, presence of HLA-B27, extra-articular features, and other names for the condition.

Radiographic Changes in Spondyloarthritis

• X-ray images illustrating typical radiographic changes in ankylosing spondylitis (symmetrical marginal syndesmophytes) and psoriatic spondylitis (coarse, asymmetrical, non-marginal syndesmophytes).
• Sacroiliac joint fusion, and generalised osteopenia.

Reactive Arthritis

• Clinical description of reactive arthritis, including skin changes (keratoderma blennorrhagicum), penile lesions (balanitis circinata), and ocular involvement.

Psoriatic Arthropathy

• Clinical description and appearance of dactylitis and distal interphalangeal pattern, along with accompanying nail dystrophy (pitting and onycholysis).

Test your knowledge on osteoporosis and osteoarthritis with this comprehensive quiz. Explore key concepts such as fracture prevalence, diagnostic methods, and treatment options. Discover the mechanisms behind bone health and the impact of vitamin D and estrogen.