59.1 Osteoarthritis: Hip, Knee & Hand Management

ABFM Family Medicine Certification Study Guide Exam

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1 Chapter 1: Exam Structure, Blueprint & Clinical Decision-Making

1.1 Exam Blueprint, FMCLA vs. One-Day Exam & Board Scoring 1.2 Clinical Reasoning, Test-Taking Strategy & Ambiguity Management 1.3 Evidence-Based Medicine & Clinical Practice Guidelines in Primary Care

2 Chapter 2: Healthcare Systems, Practice Management & Quality

2.1 Practice Management, Billing, Coding & Documentation 2.2 Quality Improvement, Patient Safety & Diagnostic Stewardship 2.3 Interprofessional Team-Based Care & Care Coordination

3 Chapter 3: Ethics, Law, Biostatistics & Health Equity

3.1 Medical Ethics, Informed Consent & Surrogate Decision-Making 3.2 Biostatistics, Clinical Epidemiology & Diagnostic Test Interpretation 3.3 Social Determinants of Health, Health Equity & Cultural Humility 3.4 Physician Wellness, Burnout Prevention & Professionalism

4 Chapter 4: Lifestyle Counseling & Behavior Change

4.1 Alcohol Use Screening & Brief Intervention 4.2 Illicit Drug & Cannabis Counseling 4.3 Tobacco & Vaping Cessation Counseling

5 Chapter 5: Nutrition, Physical Activity & Chronic Disease Prevention

5.1 Dietary Counseling for Obesity & Chronic Disease Prevention 5.2 Exercise Prescription & Physical Activity Counseling 5.3 Genetic Risk Assessment & Family History Counseling

6 Chapter 6: Routine Adult Immunizations

6.1 ACIP Adult Respiratory Vaccines: Influenza, COVID-19, RSV & Pneumococcal 6.2 ACIP Adult Non-Respiratory Vaccines: Tdap, Shingrix, HPV & Hep B 6.3 Immunizations in Special Populations: Pregnancy, Asplenia & Immunocompromise

7 Chapter 7: Pediatric Health Maintenance & Surveillance

7.1 Newborn Examination & Early Postnatal Care 7.2 Well-Child Care, Developmental Surveillance & Milestones 7.3 Pediatric & Adolescent Screening: Vision, Hearing, Anemia & Lead 7.4 Pediatric Oral Health, Dental Screening & Fluoride

8 Chapter 8: Behavioral Health & Safety Screening

8.1 Primary Care Depression, Anxiety & Behavioral Health Screening 8.2 Domestic Violence, Intimate Partner Violence & Firearm Safety 8.3 Occupational Health & Recreational Safety Counseling

9 Chapter 9: Adult Preventive Screening: Cardiovascular & Metabolic

9.1 Cardiovascular Disease & Hypertension Screening 9.2 Type 2 Diabetes Screening & Prediabetes Risk Stratification 9.3 Abdominal Aortic Aneurysm & Osteoporosis Screening

10 Chapter 10: Adult Cancer Screening: Breast & Gynecologic

10.1 Breast Cancer Screening & Risk-Assessment 10.2 Cervical Cancer Screening & ASCCP Algorithms 10.3 Skin Cancer Clinical Assessment & Counseling

11 Chapter 11: Adult Cancer Screening: Colorectal, Lung & Prostate

11.1 Colorectal Cancer Screening Modalities & Intervals 11.2 Lung Cancer Screening with Low-Dose CT 11.3 Prostate Cancer Screening & Shared Decision-Making

12 Chapter 12: Sexual Health, Infectious Disease Screening & Contraception

12.1 Sexual Health Counseling & Risk-Reduction Strategies 12.2 STI Screening: Chlamydia, Gonorrhea, Syphilis & Trichomoniasis 12.3 Bloodborne Infectious Disease Screening: HIV & Hepatitis C

13 Chapter 13: Reproductive Life Planning, Lactation & Preoperative Care

13.1 Preconception Planning & Comprehensive Contraception Management 13.2 Lactation Support & Breastfeeding Counseling 13.3 Preoperative Medical Evaluation & Pre-Participation Sports Exam

14 Chapter 14: Emergent Cardiovascular Conditions

14.1 Acute Coronary Syndromes & Myocardial Infarction 14.2 Acute Chest Pain Risk Stratification & Triage 14.3 Acute or Critical Valvular Heart Emergencies

15 Chapter 15: Cardiac Arrhythmias, Heart Failure & Hypertensive Crises

15.1 Acute Atrial & Ventricular Arrhythmias 15.2 Acute Decompensated Heart Failure & Cardiogenic Shock 15.3 Hypertensive Emergency & Urgency Management

16 Chapter 16: Vascular & Thromboembolic Emergencies

16.1 Pulmonary Embolism & Deep Vein Thrombosis 16.2 Acute Aortic Syndromes & Peripheral Vascular Emergencies 16.3 Critical Limb Ischemia & Acute Arterial Occlusion

17 Chapter 17: Neurologic Emergencies: Stroke & Altered Consciousness

17.1 Acute Ischemic Stroke & Intracranial Hemorrhage 17.2 Syncope Evaluation & Status Epilepticus 17.3 Acute Delirium, Encephalopathy & Severe Confusion

18 Chapter 18: Neurologic Trauma & Acute Cranial Emergencies

18.1 Concussion, Moderate-to-Severe TBI & Intracranial Injury 18.2 Thunderclap & Acute Severe Secondary Headaches 18.3 Acute Ophthalmologic Emergencies

19 Chapter 19: Acute Abdominal, Pelvic & Gastrointestinal Emergencies

19.1 Acute Abdominal & Pelvic Pain Triage 19.2 Upper & Lower Gastrointestinal Bleeding 19.3 Acute Hepatic Failure, Cholangitis & Severe Jaundice

20 Chapter 20: Acute Pulmonary & Airway Emergencies

20.1 Acute Hypoxic Respiratory Failure & ARDS 20.2 Severe Community-Acquired Pneumonia & Empyema 20.3 Acute Severe Epistaxis & Airway Obstruction

21 Chapter 21: Acute Traumatic Injuries & Wound Care

21.1 Major Trauma Resuscitation & Initial Assessment 21.2 Burn Assessment, Inhalation Injury & Resuscitation 21.3 Laceration Management, Complex Wounds & Animal Bites

22 Chapter 22: Acute Orthopedic & Musculoskeletal Emergencies

22.1 Acute Ambulatory Fractures & Initial Splinting 22.2 Compartment Syndrome & Major Orthopedic Trauma 22.3 Septic Arthritis & Acute Microcrystalline Crises

23 Chapter 23: Severe Infections, Sepsis & Systemic Emergencies

23.1 Sepsis, Septic Shock & Initial Fluid Resuscitation 23.2 Necrotizing Soft Tissue Infections & Severe CNS Infections 23.3 Anaphylaxis Diagnosis, Epinephrine Dosing & Airway Protection

24 Chapter 24: Metabolic, Endocrine & Electrolyte Emergencies

24.1 Diabetic Ketoacidosis & Hyperosmolar Hyperglycemic State 24.2 Critical Electrolyte Emergencies: Dyskalemias & Dysnatremias 24.3 Severe Calcium Abnormalities & Acute Adrenal Crisis

25 Chapter 25: Hematologic, Urologic & Dental Emergencies

25.1 Severe Symptomatic Anemias & Coagulopathic Emergencies 25.2 Testicular Torsion, Priapism & Acute Urinary Retention 25.3 Urgent Odontogenic Infections & Dental Trauma

26 Chapter 26: Psychiatric, Behavioral & Obstetric/Gynecologic Emergencies

26.1 Suicidal Ideation, Acute Agitation & Behavioral Emergencies 26.2 Acute Physical & Sexual Assault Care 26.3 Life-Threatening Vaginal Bleeding & Ectopic Pregnancy 26.4 Environmental Heat Stroke & Severe Hypothermia

27 Chapter 27: Acute Head, Neck & Neurologic Symptoms

27.1 Primary Acute Headaches: Migraine, Tension & Cluster 27.2 Concussion & Minor Closed Head Injury Evaluation 27.3 Transient Ischemic Attack Evaluation & ABCD2 Risk Scoring

28 Chapter 28: Acute Cranial Nerves, Hearing & Sensory Symptoms

28.1 Peripheral Neuropathies: Bell's Palsy, Carpal Tunnel & Radiculopathy 28.2 Acute Tinnitus, Sudden Sensorineural Hearing Loss & Cerumen Impaction 28.3 Acute Dizziness, Benign Paroxysmal Positional Vertigo & Vestibular Neuritis

29 Chapter 29: Acute Upper Respiratory Tract Infections

29.1 Acute Viral Rhinosinusitis vs. Bacterial Rhinosinusitis 29.2 Acute Pharyngitis: Group A Streptococcus & Centor Criteria 29.3 Acute Otitis Media, Otitis Externa & Serous Effusion

30 Chapter 30: Acute Lower Respiratory Infections & Cough

30.1 Influenza, COVID-19 & Viral Respiratory Syndromes 30.2 Acute Bronchitis & Lower Respiratory Tract Infections 30.3 Ambulatory Community-Acquired Pneumonia

31 Chapter 31: Allergic, Nasal & Non-Infectious Pulmonary Conditions

31.1 Allergic Rhinitis & Acute Non-Anaphylactic Allergic Reactions 31.2 Acute Dyspnea in Ambulatory Care 31.3 Interstitial Lung Diseases & Sarcoidosis Presentation

32 Chapter 32: Acute Chest, Cardiac & Vascular Symptoms

32.1 Palpitations Evaluation & Arrhythmia Triage in Primary Care 32.2 Deep Vein Thrombosis & Superficial Thrombophlebitis 32.3 Ambulatory Hypotension & Orthostasis Evaluation

33 Chapter 33: Acute Upper Gastrointestinal Conditions

33.1 Peptic Ulcer Disease & Gastritis 33.2 Dysphagia, Esophagitis & Acute Esophageal Disorders 33.3 Acute Nausea, Vomiting & Foodborne Illness

34 Chapter 34: Acute Lower Gastrointestinal Conditions

34.1 Acute Infectious Diarrhea & Gastroenteritis 34.2 Acute Constipation & Functional Bowel Changes 34.3 Ano-Rectal Disorders: Hemorrhoids, Fissures, Abscesses & Pruritus Ani

35 Chapter 35: Inflammatory, Functional & Malabsorptive GI Disorders

35.1 Acute Flares of Inflammatory Bowel Disease 35.2 Irritable Bowel Syndrome: Diagnosis, Subtyping & Management 35.3 Celiac Disease & Malabsorption Syndromes

36 Chapter 36: Acute Abdominal, Hepatic & Biliary Disorders

36.1 Ambulatory Abdominal & Pelvic Pain Triage 36.2 Acute Cholecystitis, Biliary Colic & Pancreatitis 36.3 Acute Liver Injury & Viral Hepatitis

37 Chapter 37: Acute Abdominal Wall, Hernias & Dental Conditions

37.1 Abdominal Wall, Inguinal & Ventral Hernias 37.2 Acute Dental Pain, Odontogenic Abscess & Aphthous Ulcers 37.3 Acute Edema: Unilateral vs. Bilateral Diagnostic Evaluation

38 Chapter 38: Acute Infectious Dermatoses

38.1 Bacterial Skin Infections: Impetigo, Cellulitis & Cutaneous Abscesses 38.2 Fungal Skin Infections: Tinea Corporis, Cruris, Pedis & Onychomycosis 38.3 Viral Cutaneous Infections: Herpes Simplex, Zoster & Molluscum Contagiosum

39 Chapter 39: Inflammatory, Allergic & Autoimmune Dermatoses

39.1 Atopic Dermatitis, Contact Dermatitis & Eczematous Flares 39.2 Non-Infectious Rashes: Urticaria, Drug Eruptions & Erythema Multiforme 39.3 Cutaneous Malignancies & Premalignant Lesions: AK, BCC, SCC & Melanoma

40 Chapter 40: Acute Shoulder, Elbow & Upper Extremity Injuries

40.1 Rotator Cuff Pathology, Tendinopathy & Shoulder Impingement 40.2 Lateral & Medial Epicondylitis, Olecranon Bursitis & Elbow Sprains 40.3 Wrist & Hand Soft-Tissue Injuries: De Quervain, TFCC & Finger Sprains

41 Chapter 41: Acute Knee, Ankle & Lower Extremity Injuries

41.1 Meniscal Tears, Ligamentous Knee Injuries & Patellofemoral Pain 41.2 Ankle Sprains, Ottawa Ankle Rules & Achilles Tendinopathy 41.3 Plantar Fasciitis, Shin Splints & Overuse Syndromes

42 Chapter 42: Acute Ambulatory Fractures & Dislocations

42.1 Distal Radius, Scaphoid & Common Upper Extremity Fractures 42.2 Metatarsal, Clavicle & Common Lower Extremity Fractures 42.3 Joint Dislocation Management: Nursemaid's Elbow & Shoulder Subluxation

43 Chapter 43: Acute Axial Musculoskeletal Pain & Falls

43.1 Acute Low Back Pain: Red Flags, Strain & Disc Herniation 43.2 Acute Cervical Strain, Whiplash & Axial Neck Pain 43.3 Evaluation of Falls in Ambulatory & Older Patients

44 Chapter 44: Acute Inflammatory Arthropathies & Generalized Pain

44.1 Acute Inflammatory Arthritis & Spondyloarthropathies 44.2 Myalgias, Rhabdomyolysis & Post-Viral Pain Syndromes 44.3 Acute Non-Headache Pain Management Strategies

45 Chapter 45: Acute Renal, Urinary & Genitourinary Conditions

45.1 Uncomplicated UTI, Pyelonephritis & Acute Urethritis 45.2 Hematuria Workup & Glomerulonephritis 45.3 Nephrolithiasis & Acute Urinary Tract Obstruction

46 Chapter 46: Acute Male Genitourinary & Prostatic Conditions

46.1 Acute Prostatitis, Epididymitis & Orchitis 46.2 Acute Scrotal Pain: Torsion vs Appendage, BPH & Male Genital Emergencies 46.3 Acute Urinary Retention & Incontinence Evaluation

47 Chapter 47: Acute Women's Health & Early Pregnancy Care

47.1 Early Pregnancy Diagnosis, Dating & Initial Complications 47.2 Abnormal Uterine Bleeding & Acute Menstrual Disorders 47.3 Premenstrual Syndrome & Premenstrual Dysphoric Disorder

48 Chapter 48: Breast Disorders, STIs & Pediatric Elimination

48.1 Palpable Breast Mass, Mastitis & Nipple Discharge 48.2 Sexually Transmitted Infections: Diagnosis, Staging & CDC Guidelines 48.3 Pediatric Enuresis & Encopresis

49 Chapter 49: Systemic Signs, Metabolic Dysregulation & Miscellaneous Infections

49.1 Acute Fever, Sepsis Screening & FUO in Primary Care 49.2 Acute Hyperglycemia & Symptomatic Hypoglycemia 49.3 Electrolyte Abnormalities: Mild-to-Moderate Disturbances 49.4 Vector-Borne, Tick-Borne & Rickettsial Illnesses

50 Chapter 50: Chronic Cardiovascular Diseases: Hypertension & Ischemia

50.1 Essential Hypertension Management: 2025 AHA/ACC Guideline & JNC Strategies 50.2 Chronic Coronary Artery Disease & Post-MI Secondary Prevention 50.3 Chronic Heart Failure: HFrEF, HFpEF & Quadruple GDMT

51 Chapter 51: Chronic Vascular, Valvular & Dyslipidemic Diseases

51.1 Peripheral Arterial Disease & Claudication 51.2 Chronic Valvular Heart Disease & Murmur Evaluation 51.3 Lipid Disorders & ASCVD Risk-Based Statin Therapy

52 Chapter 52: Chronic Respiratory Diseases: Asthma & COPD

52.1 Chronic Asthma Management: GINA Stepwise SMART Therapy 52.2 Chronic Obstructive Pulmonary Disease: GOLD Recommendations 52.3 Solitary Pulmonary Nodule Evaluation & Fleischner Society Criteria

53 Chapter 53: Chronic Metabolic Diseases: Diabetes Mellitus

53.1 Type 2 Diabetes Management: ADA Pharmacotherapy Algorithms 53.2 Type 1 Diabetes: Basal-Bolus Insulin, CGMs & Diabetic Complications 53.3 Diabetic Microvascular & Macrovascular Disease Surveillance

54 Chapter 54: Obesity, Nutrition & Metabolic Bone Diseases

54.1 Medical & Behavioral Management of Obesity & Incretin Mimetics 54.2 Osteoporosis & Metabolic Bone Disease: DEXA, FRAX & Antiresorptives 54.3 Nutritional Deficiencies: Vitamin D, B12, Iron & Malnutrition

55 Chapter 55: Chronic Endocrine Disorders

55.1 Primary & Subclinical Hypothyroidism, Hyperthyroidism & Nodules 55.2 Adrenal Disorders: Addison's Disease & Cushing's Syndrome 55.3 Hypercalcemia, Hyperparathyroidism & Pituitary Disorders

56 Chapter 56: Chronic Kidney Disease & Venous Disorders

56.1 Chronic Kidney Disease: KDIGO Staging & Renoprotective Therapy 56.2 Chronic Venous Insufficiency, Stasis Dermatitis & Lymphedema 56.3 Chronic Electrolyte & Acid-Base Management in CKD

57 Chapter 57: Chronic Gastrointestinal & Hepatic Diseases

57.1 Gastroesophageal Reflux Disease, Barrett's Esophagus & Dyspepsia 57.2 Chronic Liver Disease: MASLD/NAFLD, Cirrhosis & Portal Hypertension 57.3 Viral Hepatitis B & C: Long-Term Monitoring & DAA Therapy

58 Chapter 58: Colorectal Surveillance & Chronic Pancreaticobiliary Care

58.1 Post-Polypectomy Colorectal Polyp Surveillance Guidelines 58.2 Chronic Pancreatitis & Exocrine Pancreatic Insufficiency 58.3 Chronic Nausea, Gastroparesis & Functional GI Disorders

59 Chapter 59: Chronic Musculoskeletal & Rheumatologic Disorders

59.1 Osteoarthritis: Hip, Knee & Hand Management 59.2 Spinal Conditions: Spinal Stenosis, Spondylolisthesis & Compression Fractures 59.3 Chronic Myopathies & Fibromyalgia Syndrome

60 Chapter 60: Chronic Neurologic & Neurodegenerative Disorders

60.1 Dementia: Alzheimer's, Vascular & Lewy Body Disease 60.2 Parkinson's Disease & Essential Tremor 60.3 Epilepsy: Chronic Antiseizure Medications & Post-Stroke Care

61 Chapter 61: Chronic Peripheral Nerves, Pain & Sensory Disorders

61.1 Diabetic & Chronic Peripheral Neuropathies 61.2 Chronic Pain Syndromes & Chronic Daily Headaches 61.3 Chronic Tinnitus, Presbycusis & Persistent Dizziness

62 Chapter 62: Chronic Psychiatric Disorders

62.1 Major Depressive Disorder & Generalized Anxiety Disorder 62.2 Bipolar Disorder: Maintenance Pharmacotherapy & Lithium Monitoring 62.3 Adult & Pediatric Attention-Deficit/Hyperactivity Disorder

63 Chapter 63: Chronic Behavioral Health & Neurodevelopmental Conditions

63.1 Chronic Behavioral Conditions: PTSD, OCD & Somatization 63.2 Autism Spectrum Disorder & Intellectual Disabilities 63.3 Eating Disorders: Anorexia Nervosa, Bulimia & Binge Eating

64 Chapter 64: Chronic Substance Use Disorders & Tobacco Cessation

64.1 Alcohol Use Disorder: Pharmacotherapy & Relapse Prevention 64.2 Opioid & Stimulant Use Disorders: MOUD & Harm Reduction 64.3 Longitudinal Tobacco Cessation Pharmacotherapy

65 Chapter 65: Chronic Dermatologic Conditions

65.1 Acne Vulgaris, Rosacea & Seborrheic Dermatitis 65.2 Chronic Plaque Psoriasis & Biologic Therapies 65.3 Chronic Eczema, Hidradenitis Suppurativa & Cutaneous Lupus

66 Chapter 66: Chronic Reproductive, Infectious & Geriatric Special Care

66.1 Chronic Menstrual Disorders, Infertility & Sexual Dysfunction 66.2 Menopause Management & Hormone Replacement Therapy 66.3 Chronic HIV Infection Management & Primary Care Integration 66.4 Gender-Affirming Primary Care & Hormone Therapy 66.5 Advance Care Planning, Palliative Care & End-of-Life Symptom Control

67 Chapter 67: Continuity Care: Sleep, Fatigue, Cancer, Pregnancy & the Adult Preventive Visit

67.1 Chronic Insomnia & Obstructive Sleep Apnea 67.2 Chronic Malaise, Fatigue & ME/CFS 67.3 Primary Care During Cancer Treatment & Survivorship 67.4 Routine Prenatal Care & Longitudinal Pregnancy Management 67.5 The Periodic Adult Health Examination & Medicare Annual Wellness Visit

59.1 Osteoarthritis: Hip, Knee & Hand Management

Key Takeaways Explain This Topic AI

Osteoarthritis (OA) is fundamentally a whole-organ joint disease characterized by progressive articular cartilage degradation, subchondral bone remodeling with sclerosis and subchondral cysts, marginal osteophyte formation, and low-grade synovial inflammation.

Clinical hallmark is deep, mechanical joint pain aggravated by weight-bearing and relieved by rest, accompanied by morning stiffness lasting <30 minutes (contrasting with rheumatoid arthritis >60 minutes) and brief inactivity stiffness ('gel phenomenon').

Hand OA characteristically features Heberden nodes at distal interphalangeal (DIP) joints, Bouchard nodes at proximal interphalangeal (PIP) joints, and 1st carpometacarpal (CMC) squaring, while strictly sparing metacarpophalangeal (MCP) joints (a key discriminator from RA).

Under 2019 ACR guidelines, first-line strongly recommended interventions include land-based exercise (quadriceps/hip strengthening), weight reduction (5-10% loss cuts joint loading by 30-40%), and topical NSAIDs (topical diclofenac 1% gel, first-line for knee OA with equivalent efficacy to oral NSAIDs but minimal systemic GI/renal toxicity).

Hyaluronic acid viscosupplementation, glucosamine/chondroitin, and routine opioids are strongly recommended against due to lack of meaningful clinical efficacy and substantial adverse event risks; intra-articular corticosteroids provide transient (4-8 weeks) flare relief but must be limited to <=3-4 times annually.

Last updated: September 2026

Pathophysiology & Cellular Mechanisms of Osteoarthritis

Osteoarthritis (OA) is the most prevalent chronic articular disorder worldwide and the leading cause of chronic disability and impaired mobility in older adults. Historically mischaracterized as a passive, non-inflammatory "wear-and-tear" degradation of articular cartilage, contemporary molecular rheumatology defines OA as an active, metabolically driven, whole-organ disease of the synovial joint . The pathological process involves the coordinated degeneration of articular hyaline cartilage, extensive remodeling of subchondral bone, formation of marginal osteophytes, low-grade synovial inflammation (synovitis), thickening of the joint capsule, and degeneration of intra-articular ligaments and menisci.

1. Articular Cartilage Degradation & Chondrocyte Senescence

Normal articular hyaline cartilage is an avascular, aneural, and alymphatic tissue composed of extracellular matrix (ECM)—predominantly type II collagen fibrils and aggregated proteoglycans (aggrecan)—maintained by a specialized, sparse population of chondrocytes . In healthy cartilage, chondrocytes balance low-level matrix synthesis with matrix degradation.

Phenotypic Shift : In OA, mechanical shear stress, advanced glycation end-products (AGEs), and local biochemical cues trigger a phenotypic transition of chondrocytes from a quiescent state to an abnormal "hypertrophic" or catabolic phenotype.

Catabolic Proteases : Hypertrophic chondrocytes markedly upregulate matrix-degrading metalloproteinases, specifically Matrix Metalloproteinase-13 (MMP-13) (which selectively degrades type II collagen triple helices) and aggrecanases belonging to the ADAMTS family ( ADAMTS-4 and ADAMTS-5 ). Degradation of aggrecan causes loss of fixed negative charges (chondroitin sulfate and keratan sulfate glycosaminoglycan side chains), leading to loss of cartilage water-binding capacity and compressive stiffness.

Fibrillation & Erosion : As the collagen meshwork fractures, cartilage undergoes swelling, surface fibrillation , vertical clefting, and progressive full-thickness erosion down to bare subchondral bone.

2. Subchondral Bone Remodeling: Sclerosis, Osteophytes & Geodes

The osteochondral junction experiences profound pathological remodeling during OA progression:

Subchondral Bone Sclerosis (Eburnation) : Increased osteoclast-mediated bone resorption initially occurs, followed by aberrant osteoblast activation and deposition of hypomineralized, dense woven bone ( eburnation ). This thickened, sclerotic subchondral bone is stiffer than normal trabecular bone, reducing its shock-absorbing capacity and transferring excessive peak compressive loads back onto the surviving articular cartilage, accelerating cartilage loss.

Marginal Osteophytes : At joint margins where cartilage meets periosteum and synovium, vascular invasion and elevated concentrations of growth factors—particularly Transforming Growth Factor-beta (TGF-β) and Bone Morphogenetic Proteins (BMP-2, BMP-4) —induce mesenchymal stem cell chondrogenesis followed by endochondral ossification. The resulting bony outgrowths ( osteophytes ) represent an adaptive, biomechanical attempt to broaden joint surface area and redistribute load, but often restrict joint mobility and impinge on adjacent soft tissues.

Subchondral Cysts (Geodes) : Microfractures in the weakened, sclerotic subchondral plate allow pressurized intra-articular synovial fluid to be driven into the subchondral trabeculae during weight-bearing ("hydraulic pumping mechanism"). Alternatively, localized osteonecrosis and focal osteoclastic resorption create cystic cavities filled with fibrous tissue or gelatinous myxoid fluid.

3. Low-Grade Synovial Inflammation

Although OA lacks the intense, pannus-forming neutrophilic or lymphoplasmacytic infiltration seen in rheumatoid arthritis, low-grade chronic synovitis is present in the vast majority of symptomatic patients:

Breakdown fragments of cartilage matrix (fibronectin fragments, degraded type II collagen, low-molecular-weight hyaluronan) act as Damage-Associated Molecular Patterns (DAMPs) .

These DAMPs bind to pattern recognition receptors, particularly Toll-Like Receptors 2 and 4 (TLR-2, TLR-4) , on synovial macrophages and fibroblast-like synoviocytes.

Receptor activation triggers NF-κB signaling, inducing the secretion of pro-inflammatory cytokines ( Interleukin-1β [IL-1β] , Tumor Necrosis Factor-alpha [TNF-α] , and Interleukin-6 [IL-6] ), nitric oxide, and prostaglandin E2 ( PGE 2 \text{PGE}_2 PGE 2 ​ ). These mediators diffuse back across the joint space to further stimulate chondrocyte apoptosis and catabolism in a self-amplifying feed-forward loop.

Epidemiological & Biomechanical Risk Factors SYSTEMIC AND BIOMECHANICAL RISK FACTORS FOR OSTEOARTHRITIS

• Factor Category Specific Etiologic Factor Pathophysiological Mechanism
• ═════════════════════════════════════════════════════════════════════════════════════════════════════════════

Systemic / Constitutional • Advanced Age (>50-60 years) Accumulation of AGEs, chondrocyte senescence, loss of ECM

• Female Sex Estrogen withdrawal post-menopause; altered joint kinematics
• Genetics / Heredity Heritability ~40-60%; polygenic traits affecting COL2A1, GDF5
• ─────────────────────────────────────────────────────────────────────────────────────────────────────────
• Metabolic / Endocrine • Obesity (Adipokines) Adipose secretion of LEPTIN, RESISTIN, and TNF-α inducing
• cartilage catabolism; metabolic syndrome synergy
• ─────────────────────────────────────────────────────────────────────────────────────────────────────────

Biomechanical / Mechanical • Excess Weight (Mechanical) Every 1 lb of weight increases compressive load by 4 lbs

• across the tibiofemoral knee joint per step
• Prior Joint Trauma Post-traumatic OA (ACL rupture, meniscal tear, ankle fracture)
• Occupational Overuse Repetitive squatting, heavy lifting (>25 kg), kneeling
• Joint Malalignment Genu varum (medial load) vs Genu valgum (lateral load);
• cam/pincer femoroacetabular impingement (FAI)
• ═════════════════════════════════════════════════════════════════════════════════════════════════════════════

Note

THE BIOMECHANICS OF WEIGHT LOSS IN OSTEOARTHRITIS During standard ground-level walking, ground reaction forces and quadriceps muscle contractions multiply the compressive force across the knee joint to 3 to 5 times total body weight . Consequently, a weight loss of just 10 pounds (4.5 kg) relieves an astonishing 30 to 50 pounds of joint compressive load with every single step taken. Furthermore, visceral adipose tissue actively synthesizes pro-inflammatory adipokines (leptin, resistin) that cross the synovial barrier and stimulate chondrocyte MMP-13 production. Weight reduction therefore confers a powerful dual benefit: profound mechanical unloading combined with systemic anti-inflammatory hormonal suppression.

Clinical Manifestations & Physical Examination

The onset of osteoarthritis is typically insidious, evolving over months to years. Clinicians must recognize cardinal symptoms, physical examination findings, and key discriminators that differentiate OA from inflammatory and systemic arthritides.

1. Cardinal Symptoms

Mechanical Joint Pain : The hallmark of OA is deep, dull, aching pain localized to the affected joint that is characteristically worsened by weight-bearing, physical activity, and joint use, and relieved by rest . In early stages, pain is intermittent; in advanced end-stage disease, pain becomes persistent, occurring at rest and waking the patient at night.

Brief Morning Stiffness : Joint stiffness upon awakening characteristically lasts less than 30 minutes (typically 5 to 15 minutes). This represents a vital clinical discriminator: morning stiffness persisting for >60 minutes strongly points toward an inflammatory systemic arthropathy (such as Rheumatoid Arthritis, Psoriatic Arthritis, or Polymyalgia Rheumatica).

The "Gel Phenomenon" : Transient joint stiffness that develops following periods of daytime rest or immobility (e.g., stiffness upon standing after sitting in a car or chair for an hour). The gel phenomenon in OA resolves rapidly within a few minutes of gentle joint movement.

2. Physical Examination Findings

Bony Crepitus : A palpable (and sometimes audible) rough, grinding, crunching sensation felt throughout passive or active range of motion, caused by the friction of denuded, roughened cartilaginous surfaces and eburnated bone rubbing together.

Joint Line Tenderness : Well-localized tenderness elicited along the anatomical margins of the joint (e.g., medial or lateral tibiofemoral joint line).

Bony Enlargement vs. Synovial Proliferation : Palpable hard, unyielding, non-tender bony enlargements caused by marginal osteophytes. This contrasts sharply with the soft, spongy, "boggy", warm synovial hypertrophy characteristic of rheumatoid arthritis.

Cool, Non-Inflammatory Effusions : Joint effusions, when present, are typically mild to moderate in volume and "cool" (lacking significant erythema or warmth). Arthrocentesis reveals clear, straw-colored fluid with high viscosity, a white blood cell count <2,000/mcL , and <25% polymorphonuclear neutrophils (Class I / non-inflammatory synovial fluid).

Restricted Range of Motion & Muscle Atrophy : Progressive loss of joint excursion due to osteophytic impingement, capsular fibrosis, and joint surface incongruity. Periarticular muscle disuse atrophy is prominent (e.g., marked quadriceps wasting in advanced knee OA). CLINICAL DIFFERENTIATION: OSTEOARTHRITIS VS. RHEUMATOID ARTHRITIS

• Feature Osteoarthritis (OA) Rheumatoid Arthritis (RA)
• ═════════════════════════════════════════════════════════════════════════════════════════════════════════════
• Pathophysiology Biomechanically driven cartilage loss, Autoimmune chronic inflammatory synovitis with
• subchondral sclerosis, and osteophytes pannus formation and bone erosions

• Pattern of Involvement Asymmetric, oligoarticular or monoarticular; Symmetrical, polyarticular (>4 joints);
• weight-bearing joints (knees, hips) small joints of hands, wrists, and feet

• Morning Stiffness Brief, < 30 minutes; transient gel Prolonged, > 60 minutes (often lasting
• phenomenon after inactivity several hours or all morning)

• Pain Characteristics Worsened by activity / weight-bearing; Improves with activity; worsened by rest
• relieved by rest and prolonged immobility

• Hand Joint Predilection DIP, PIP, and 1st CMC (thumb base); MCP, PIP, and Wrist joints;
• STRICTLY SPARES MCP JOINTS STRICTLY SPARES DIP JOINTS

• Palpation / Effusions Hard, bony enlargement (Heberden/ Soft, warm, "boggy" synovial hypertrophy;
• Bouchard nodes); cool effusions hot, erythematous inflammatory effusions

Systemic Symptoms Absent (no fever, fatigue, weight loss) Prominent (malaise, fatigue, rheumatoid nodules)

• Laboratory Markers Normal ESR and CRP; negative RF and Elevated ESR and CRP; positive RF and
• anti-CCP; WBC < 2,000 in synovial fluid anti-CCP; WBC 2,000 - 50,000 in synovial fluid

• Radiographic Hallmarks Asymmetric joint space narrowing, Symmetric joint space narrowing, periarticular
• subchondral sclerosis, osteophytes, osteopenia, marginal bone erosions WITHOUT
• subchondral cysts (geodes) osteophyte formation
• ═════════════════════════════════════════════════════════════════════════════════════════════════════════════
• Anatomical Subtypes & Clinical Phenotypes
• 1. Hand Osteoarthritis

Hand OA exhibits a striking predilection for specific digit joints, with characteristic physical manifestations:

Heberden Nodes : Hard, palpable, bony enlargements located on the dorsolateral aspects of the Distal Interphalangeal (DIP) joints, representing marginal osteophytes.

Bouchard Nodes : Bony prominences located at the Proximal Interphalangeal (PIP) joints.

1st Carpometacarpal (CMC / Trapeziometacarpal) Joint OA : Involvement of the base of the thumb causes localized tenderness, functional weakness in grip and pinch strength, and a prominent "squared" appearance of the hand base. The Grind Test (axial compression and circumduction/rotation of the thumb metacarpal against the trapezium) reproduces sharp localized pain and crepitation.

CRITICAL EXAM PEARL: Sparing of the Metacarpophalangeal (MCP) Joints : Osteoarthritis spares the MCP joints and wrist joints . Involvement of MCP joints or wrists with swelling, tenderness, and warmth is the classic presentation of Rheumatoid Arthritis. (Exception: Isolated 2nd and 3rd MCP joint narrowing with "hook-like" osteophytes is pathognomonic for Hemochromatosis / Calcium Pyrophosphate Deposition disease).

Erosive Hand OA : An aggressive, highly inflammatory subset of hand OA occurring predominantly in postmenopausal females. Presents with abrupt, painful, erythematous flares of DIP and PIP joints. Radiographs reveal central subchondral bone erosions paired with marginal bone proliferation, producing the classic "gull-wing" or "sawtooth" contour .

2. Knee Osteoarthritis

The knee joint comprises three distinct functional compartments: the medial tibiofemoral, lateral tibiofemoral, and patellofemoral compartments:

Medial Compartment : Most commonly affected by OA due to the physiological adduction moment during gait, which concentrates 60% to 70% of ground reaction forces across the medial plateau. Progressive medial cartilage loss produces an asymmetric narrowing that tilts the lower extremity into Genu Varum (bow-legged deformity) .

Lateral Compartment : Less frequently isolated; progressive lateral joint space loss results in Genu Valgum (knock-knee deformity) .

Patellofemoral Compartment : Characterized by anterior knee pain that is sharply exacerbated by stair climbing, descending stairs, squatting, or prolonged sitting with flexed knees ("theater sign"). Physical exam reveals crepitus beneath the patella and a positive patellar grind (Clarke) test .

3. Hip Osteoarthritis

Pain Localization : The true intra-articular hip joint is innervated primarily by the femoral, obturator, and sciatic nerves. Consequently, hip OA pain classically manifests as deep groin pain radiating into the anterior thigh, buttock, or down to the ipsilateral knee .

The Knee Pain Distractor : Many patients with advanced hip OA present complaining primarily of medial knee pain (referred via the anterior branch of the obturator nerve). Primary care physicians must examine the hip in any older adult presenting with unexplained knee pain.

Physical Exam Pearls : The earliest physical finding of hip OA is limitation and pain during internal rotation with the hip flexed to 90 degrees (normal internal rotation is approximately 35° to 45°; restriction to <15-20° strongly suggests OA). The FABER (Patrick) test (Flexion, ABduction, External Rotation) reproduces deep groin pain. Advanced disease produces an antalgic Trendelenburg gait (the patient shifts the torso over the affected hip during the stance phase to decrease abductor muscle contraction force and reduce joint compressive load).

Trochanteric vs. Intra-articular Pain : Pain localized strictly over the lateral aspect of the hip (greater trochanteric prominence) that is aggravated by direct pressure (lying on that side in bed) is Greater Trochanteric Pain Syndrome (gluteal tendinopathy / trochanteric bursitis) , NOT intra-articular hip osteoarthritis.

Radiographic Hallmarks & Kellgren-Lawrence Grading

When osteoarthritis is clinically suspected, plain radiography represents the initial diagnostic imaging modality of choice. Routine magnetic resonance imaging (MRI) is not indicated for uncomplicated OA, as MRI is excessively sensitive, reveals incidental meniscal tears that do not require surgical intervention, and does not alter non-surgical management.

Important

MANDATORY WEIGHT-BEARING RADIOGRAPHIC PROTOCOL Radiographs of the lower extremity joints MUST be performed in the standing, weight-bearing position . Non-weight-bearing (supine) radiographs fail to demonstrate physiological joint space narrowing and will significantly underestimate disease severity. Standard knee series must include: 1) Standing AP view, 2) Standing lateral view, 3) 45-degree flexion posteroanterior (Rosenberg) view (detects early posterior joint space narrowing), and 4) Merchant or sunrise axial view (evaluates the patellofemoral joint). Hip evaluation requires a standing AP pelvis and frog-leg lateral view.

The Four Cardinal Radiographic Signs of Osteoarthritis

Asymmetric Joint Space Narrowing : Loss of articular hyaline cartilage thickness localized to the primary load-bearing compartment (e.g., medial compartment of the knee, superior pole of the acetabulum). This contrasts with the uniform, symmetric joint space narrowing seen across inflammatory joint diseases.

Subchondral Bone Sclerosis : Dense, ivory-white radiodense band of bone thickening immediately adjacent to the denuded joint line (eburnation).

Marginal Osteophytes : Bony projections or spurs arising at articular margins.

Subchondral Cysts (Geodes) : Well-circumscribed, round or oval radiolucencies with sclerotic margins located in the subchondral bone. THE KELLGREN-LAWRENCE (KL) RADIOGRAPHIC GRADING SYSTEM

• Grade Classification Radiographic Criteria Clinical Correlate
• ═════════════════════════════════════════════════════════════════════════════════════════════════════════════
• Grade 0 None No radiographic features of osteoarthritis Normal joint
• ─────────────────────────────────────────────────────────────────────────────────────────────────────────
• Grade 1 Doubtful Minute, doubtful osteophytic lipping; Minimal or asymptomatic;
• possible joint space narrowing rarely clinically diagnosed
• ────────────────────────────────────────────────────────────────────────────────════════════════════════
• Grade 2 Mild Definite marginal osteophytes; Mild, intermittent symptoms;
• possible or unimpaired joint space narrowing definite structural OA
• ─────────────────────────────────────────────────────────────────────────────────────────────────────────
• Grade 3 Moderate Moderate, multiple osteophytes; definite joint space Moderate to severe mechanical pain;
• narrowing; some subchondral sclerosis; possible cysts functional limitations
• ─────────────────────────────────────────────────────────────────────────────────────────────────────────
• Grade 4 Severe Large osteophytes; marked/severe joint space Severe, intractable pain; rest/night
• narrowing (bone-on-bone); severe sclerosis; deformity pain; candidate for arthroplasty
• ═════════════════════════════════════════════════════════════════════════════════════════════════════════════

Clinical-Radiographic Discordance : Radiographic severity correlates imperfectly with clinical symptoms. Approximately 30% to 40% of patients with severe KL Grade 4 radiographic changes experience minimal or manageable pain, whereas patients with mild KL Grade 1-2 changes may suffer from severe, debilitating pain. Clinical management must treat the patient's pain and functional impairment, not the X-ray alone.

American College of Rheumatology (ACR 2019) Treatment Guidelines

The American College of Rheumatology (ACR) and Arthritis Foundation published comprehensive, evidence-based guidelines classifying therapeutic modalities for knee, hip, and hand OA based on high-quality randomized controlled trials. ACR 2019 OSTEOARTHRITIS TREATMENT RECOMMENDATIONS

• Recommendation Tier Therapeutic Modality Joint Sites & Clinical Directives
• ═════════════════════════════════════════════════════════════════════════════════════════════════════════════
• STRONGLY RECOMMENDED • Land-based physical exercise / PT Knee, Hip, Hand (quadriceps/core strengthening)
• Weight loss (>= 5% to 10% reduction) Knee, Hip (reduces mechanical load & adipokines)
• Topical NSAIDs (Diclofenac 1% gel) KNEE OA: FIRST-LINE PHARMACOTHERAPY
• Oral NSAIDs (lowest effective dose) Knee, Hip, Hand (co-prescribe PPI if GI risk)
• Tai Chi Knee, Hip (balance, proprioception, pain relief)
• Walking cane / assistive devices Knee, Hip (contralateral hand to unload joint)
• First CMC joint splints / orthoses Hand OA (stabilizes trapeziometacarpal joint)
• ─────────────────────────────────────────────────────────────────────────────────────────────────────────
• CONDITIONALLY RECOMMENDED • Intra-articular Corticosteroids Knee, Hip (short-term 4-8 week flare relief)
• Duloxetine (SNRI 30 - 60 mg daily) Knee, Hip (ideal for multi-joint / centralized pain)
• Topical Capsaicin Knee OA only (depletes substance P)
• Chondroitin Sulfate HAND OA ONLY (strongly against for knee/hip)
• Radiofrequency ablation / genicular Knee OA (refractory to meds, nonsurgical candidates)
• Balance / gait training exercises Knee, Hip
• ─────────────────────────────────────────────────────────────────────────────────────────────────────────
• STRONGLY RECOMMENDED • Hyaluronic Acid (HA) Injections Knee, Hip (marginal benefit, high cost, pseudosepsis)
• AGAINST (DO NOT USE) • Glucosamine & Chondroitin Knee, Hip (no proven structural/clinical benefit)
• Opioid Analgesics (routine use) Knee, Hip, Hand (dependence, falls, hyperalgesia)
• Stem Cell / PRP Injections Knee, Hip (lack of standardization / proven efficacy)
• Oral Hydroxychloroquine / Biologics Hand, Knee, Hip (ineffective for OA)
• ═════════════════════════════════════════════════════════════════════════════════════════════════════════════
• 1. Strongly Recommended Non-Pharmacologic Foundations

Structured Exercise Programs : Exercise is the cornerstone of conservative therapy. Land-based physical therapy focusing on progressive quadriceps strengthening, hip abductor (gluteus medius) strengthening, and low-impact aerobic conditioning (walking, stationary cycling, aquatic therapy) significantly reduces pain and improves physical function with effect sizes comparable to oral NSAIDs. Tai Chi combines slow, controlled weight-shifting with mental focus, providing proven improvements in balance, postural stability, and pain reduction.

Weight Loss : For overweight or obese individuals with knee or hip OA, a weight loss of >=5% of baseline body weight produces measurable reductions in joint pain and functional improvement; a loss of >=10% body weight slows articular cartilage loss on MRI and provides profound, clinically transformative relief.

Biomechanical Assistive Devices : A single-point cane should be held in the hand contralateral to the affected lower extremity (advancing the cane simultaneously with the affected leg). This biomechanical positioning reduces abductor muscle contraction across the diseased hip or knee, unloading the joint by up to 50% to 60%. For unicompartmental medial knee OA, a valgus unloader knee brace applies a corrective lateral force during ambulation, decreasing medial compartment joint stress.

2. Pharmacotherapy: Nuances, Safety & Risk Mitigation

Topical NSAIDs (Diclofenac 1% Gel / Patch / Solution) :

FIRST-LINE PHARMACOTHERAPY FOR KNEE OA : The 2019 ACR guidelines strongly recommend topical NSAIDs as initial pharmacologic therapy for knee OA, ahead of oral NSAIDs.

Topical diclofenac delivers local anti-inflammatory drug concentrations to periarticular tissues and cartilage equivalent to oral formulations, but systemic plasma absorption is <5% to 10% of oral dosing.

Yields equivalent analgesic efficacy to oral NSAIDs with dramatically lower incidences of gastrointestinal ulceration, renal toxicity, and cardiovascular thrombotic events.

Particularly mandatory in patients aged >=65 years , those with a history of peptic ulcer disease, mild-to-moderate chronic kidney disease, hypertension, or cardiovascular disease.

Oral NSAIDs :

Indicated for knee, hip, and hand OA when topical therapy is ineffective, impractical (e.g., deep hip joints cannot be reached by topical preparations), or when multiple joints are involved.

Prescribe at the lowest effective dose for the shortest possible duration , or use on an intermittent, PRN basis.

Gastrointestinal Risk Mitigation : In patients with elevated GI bleeding risk (age >=65, history of peptic ulcer disease, concomitant use of aspirin, anticoagulants, or systemic corticosteroids), co-prescribe a Proton Pump Inhibitor (PPI) (e.g., omeprazole 20 mg daily) or use a selective COX-2 inhibitor ( celecoxib 100-200 mg daily). Note: Co-administration of low-dose aspirin eliminates celecoxib's GI safety advantage, necessitating a PPI.

Cardiovascular & Renal Monitoring : All oral NSAIDs (selective and non-selective) inhibit renal prostaglandins ( PGE 2 \text{PGE}_2 PGE 2 ​ , PGI 2 \text{PGI}_2 PGI 2 ​ ), causing sodium retention, blunting antihypertensive efficacy, elevating blood pressure, and increasing risks of acute kidney injury and heart failure exacerbations. Avoid in patients with severe CKD (eGFR <30 mL/min/1.73 m²) or severe heart failure.

Acetaminophen (Paracetamol) :

Meta-analyses demonstrate that acetaminophen has a very small, clinically negligible effect size in OA pain reduction. The ACR 2019 guidelines downgraded acetaminophen to conditionally recommended solely as an adjunctive short-term option for patients who cannot tolerate or have contraindications to NSAIDs.

Maximum daily dose must not exceed 3,000 mg/day (or 2,000 mg/day in older adults or those with mild liver disease) to avoid hepatotoxicity.

Duloxetine (Cymbalta) :

Serotonin-Norepinephrine Reuptake Inhibitor (SNRI) dosed at 30 to 60 mg orally once daily.

Conditionally recommended for knee, hip, and multi-joint OA, particularly when complicated by centralized pain amplification, depression, or neuropathic pain components.

3. Interventional Therapies: The Evidence

Intra-articular Corticosteroid Injections :

Formulation: Triamcinolone acetonide (40 mg) or methylprednisolone acetate (40 mg) combined with 1-2 mL of local anesthetic (1% lidocaine or 0.5% bupivacaine).

Clinical Role: Conditionally recommended for acute inflammatory flares with effusion refractory to topical/oral therapies.

Duration of Efficacy: Provides rapid, significant pain relief that peaks at 1 to 2 weeks, but benefits typically wane after 4 to 8 weeks .

Critical Caution: Large randomized trials (e.g., McAlindon et al., JAMA 2017) demonstrated that repeated intra-articular steroid injections every 3 months over 2 years resulted in greater articular cartilage volume loss on MRI without sustained clinical improvement compared to saline. Clinical consensus mandates limiting injections to no more than 3 to 4 times per year in a given joint.

Hyaluronic Acid (HA) Viscosupplementation: STRONGLY RECOMMENDED AGAINST :

Despite widespread marketing, rigorous systematic reviews and the ACR guidelines conclude that intra-articular HA provides minimal to no clinically meaningful pain relief compared to intra-articular placebo (saline) injections.

Poses significant financial cost and carries a risk of acute post-injection inflammatory flares ( "pseudosepsis" —a severe sterile inflammatory reaction with synovial WBC counts >50,000/mcL mimicking septic arthritis).

Opioid Analgesics: STRONGLY RECOMMENDED AGAINST :

Routine use of systemic opioids (tramadol, codeine, oxycodone, fentanyl) is strongly discouraged. Opioids do not improve physical function, carry catastrophic risks of addiction, fatal overdose, sedation, cognitive decline, falls, hip fractures, and opioid-induced hyperalgesia (OIH).

4. Indications for Total Joint Arthroplasty (TJA)

Referral to an orthopedic surgeon for Total Knee Arthroplasty (TKA) or Total Hip Arthroplasty (THA) is indicated when patients fulfill both clinical and radiographic criteria:

Severe, persistent, disabling joint pain that significantly impairs activities of daily living (bathing, dressing, ambulating, climbing stairs), causes sleep deprivation, or destroys quality of life;

Failure of comprehensive non-surgical management (adequate trials of exercise/PT, weight reduction, assistive devices, and optimized pharmacotherapies);

Objective radiographic evidence of advanced joint destruction (Kellgren-Lawrence Grade 3 or 4 joint space collapse, severe sclerosis, bone-on-bone contact).

Loading diagram... American College of Rheumatology Stepped-Care Management Algorithm for Knee & Hip Osteoarthritis