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OSTEOARTHRITIS Two Major Forms of Musculoskeletal Pain Articular Degenerative: Osteoarthritis (OA) Inflammatory: Rheumatoid Arthritis (RA), etc., Crystal-induced: Gout, CPPD Other Nonarticular Fibromyalgia Soft tissue trauma Tendonitis, Bursitis, etc. Arthritis Care: An Increasing Burden on Healthcare Resources Prevalence 49.8 (19.2) Millions of Cases in US (% Population)* 50 40 28 (10.2) 30 20 10 15.8 (6.1) 2.1 (0.8) 0.3 (0.12) 0.6 (0.23) 0 *Data for 1993/94 †National Osteoporosis Foundation. www.nof.org. Dec 6, 2000. The Arthritis Foundation Fact Book for the Media. Atlanta, Georgia. Arthritis Foundation; 1994:1–4. Arthritis 43 Million people in the US have some form of arthritis 2020 it is expected that 103 million people will be effected For approximately 3 million people in the US, the primary cause of limitation of movement is arthritis Extent of Musculoskeletal Diseases in United States 37.9 million people affected by arthritis – 21 million with clinical signs and symptoms of OA – 2.1 million with RA Data from 1990 Lawrence et al. Arthritis Rheum. 1998;41:778–799. 315 million physician visits/yr 8 million hospital admissions/yr 17 million people with activity limitation 1.5 billion days of restricted activity/yr Data from 1990–1992 Yelin, Callahan. Arthritis Rheum. 1995;38:1351–1362. 5 Economic Impact of Musculoskeletal Conditions in the United States Direct Costs 12% 12% 5% 20% 46% 1% 4% Direct medical costs Indirect costs (lost wages) Total costs Physician Hospital Other provider Drugs Nursing home Administrative Other $ 72.3 billion* $ 77.1 billion $149.4 billion (2.5% of GNP) *In 1992 dollars Data from Yelin, Callahan. Arthritis Rheum. 1995;38:1351–1362. 6 Osteoarthritis: AKA Degenerative Arthritis Osteoarthrosis Old Age Arthritis Degenerative Joint Disease Wear and Tear Arthritis DJD Osteoarthritis Definition Slowly progressive deterioration of a joint in which localized loss of cartilage occurs in association with subchondral sclerosis, osteophytosis, cyst formation, and synovial thickening SOCIOECONOMIC IMPACT OF OA Most common reason for physician visits in people >55 years of age Lost and limited work days Impaired leisure activities Co-morbidity: Heart disease, depression, etc. Cost = Billions Normal vs OA Joint Normal knee Osteoarthritic knee Thickened capsule Capsule Cartilage Synovium Cyst formation Sclerosis in subchondral bone Fibrillated cartilage Synovial hypertrophy Bone Osteophyte formation 11 Presentation Symptoms Pain: worse during the day—with activity or after activity Stiffness: Minimal in the morning (<30 min); gelling after inactivity Range of motion: decreased Signs Crepitus Swelling—variable effusions Restricted movement Bony enlargement Joint instability Location & Prevalence of OA 80 Men Prevalence of OA (%) 60 DIP 40 Knee 20 Hip 0 20 40 60 80 80 Women 60 DIP 40 Knee 20 Hip 0 20 40 60 Age (years) 80 Articular Cartilage Integrity depends on a balance between degradation and synthesis of extra-cellular matrix constituents Homeostasis Degradation Synthesis Pathogenesis of OA Biomechanical Matrix synthesis IGF-1 TGF-b Chondrocytes Matrix degradation Cytokines Enzymes N.oxide Genetic Loss of matrix integrity Metabolic OA IGF = insulin-like growth factor; TGF = transforming growth factor 15 Articular Cartilage A specialized connective tissue “organ” with a highly ordered anatomic structure that is avascular and aneural A sparse chondrocyte population is embedded in extra-cellular matrix composed predominantly of water, proteoglycans, and type II collagen The mechanical properties of articular cartilage are attributable to the extra-cellular matrix Normal Hyaline Cartilage Cartilage Ultra-structure Collagen fiber alignment assists distribution of forces Chondrocyte morphology varies within the tissue Cartilage Structure Proteoglycans attach to hyaluronic acid via link protein to form an “aggregate” or aggrecan Aggrecan interactions dampen compressive loads Type II Collagen encapsulates aggrecan and distributes forces, providing tensile strength and resisting shear Cartilage Structure Osteoarthritis Biochemistry Proteoglycan changes Decreased () total proteoglycan (PG) content hyaluronic acid (HA) content aggregate size and aggregation of proteoglycans Collagen Changes Ultrastructural changes in collagen Increased water content Chondrocyte response division to form “clusters” cellular hypertrophy Osteoarthritis Cytokines can promote degradation and inhibit synthesis of extra-cellular matrix constituents OA Degradation Synthesis OA: Cartilage Changes Osteoarthritic Cartilage Radiographic Findings Bony sclerosis Joint space narrowing Marginal osteophytes Subchondral cysts Malalignment Osteoarthritis of hands Osteoarthritis of Hands: X-rays Osteoarthritis: Synovial Cyst Osteoarthritis of the Knees Osteoarthritis of the Knee Subchondral bone Femoral condyle Patella OA of the Hip Pain often is located deep in the groin and radiates to the thigh Check ROM Osteoarthritis Cervical Spine Narrowed Neural Foramina Osteoarthritis Lumbar Spine Diffuse Idiopathic Skeletal Hyperostosis (DISH) EPIDEMIOLOGY OF OA Most common form of chronic arthritis 1:5 affected worldwide, increases with age >50% require medical therapy for pain and disability Risk Factors Age Female sex Trauma Obesity (micro-trauma) Genetic or hereditary links Neuromuscular dysfunction Metabolic disorders WEIGHT AND OA Degree of Obesity (Range of BMI) Males RR(95% CI) Females Normal (>20 to 25) 1.00 1.00 Overweight (>25 to 30) 1.69(1.03-2.80) 1.89(1.24-2.87) Obese (>30 to 35) 4.78(2.77-8.27) 3.87(2.63-5.68) Very Obese(>35) 4.45(1.77-11.18) 7.37(5.1510.53) Am J Epidemiol 1988;128:179 Goals of Arthritis Therapy Relieve pain/inflammation Minimize risks of therapy Retard disease progression Provide patient education Prevent work disability Enhance quality of life and functional independence 43 Drug Therapy Options in Osteoarthritis Analgesics NSAIDs (Rx, OTC), COX-2 Inhibitors Topical agents Intra-articular glucocorticoids Intra-articular hyaluronan Investigational agents 44 American Pain Society Treatment of Chronic Pain in OA Plus, as needed: • Mild pain • Little or no inflammation • Acetaminophen Continued pain? Yes • Moderate to severe pain/inflammation • COX-2–specific inhibitor Continued pain? Conduct GI risk-factor analysis • Nonpharmacologi c interventions • Glucosamine • Tramadol • Adjunctives • Intra-articular hyaluronic acid • Surgical intervention • High risk • Nonselective NSAID plus PPI or misoprostol • Not high risk • Nonselective NSAID Continued pain? American Pain Society, 2002. Yes • Hyaluronic acid injection for knee pain • Glucocorticoid intraarticular injection for other joint pain ACR Osteoarthritis Guidelines ACR Subcommittee on OA Guidelines. Arthritis Rheum 2000; 43: 1905-1915 ACR Osteoarthritis Guidelines Nonpharmacologic Measures Cornerstone of Therapy ACR Subcommittee on OA Guidelines. Arthritis Rheum 2000; 43: 1905-1915 Nonpharmacologic Modalities Patient education Personalized social support through telephone contact Aerobic exercise program Range-of-motion exercises Assistive devices for ambulation Appropriate footwear Bracing Joint protection and energy conservation ACR Subcommittee on OA Guidelines. Self-management programs Weight loss (if overweight) Physical therapy Muscle-strengthening exercises Patellar taping Lateral-wedge insoles Occupational therapy Assistive devices for Arthritis Rheum activities 2000; 43: 1905-1915 of daily living Physical Therapy WOMAC 6 Minute Walk Deyle, et al., Ann. Int. Med. 2000: 132; 173-81 ACR Osteoarthritis Guidelines Nonpharmacologic Measures Acetaminophen for the relief of mild-to-moderate joint pain ACR Subcommittee on OA Guidelines. Arthritis Rheum 2000; 43: 1905-1915 Acetaminophen Symptomatic relief comparable to ibuprofen Provides analgesia Avoids adverse effects of NSAIDs, which are especially worrisome in the elderly Minimal risk of toxicity when chronic therapy is kept equal to or below 4 gm per day COX-3 & Acetaminophen ACR Osteoarthritis Guidelines Nonpharmacologic Measures Acetaminophen for the relief of mild-to-moderate joint pain Topical Agents* (methylsalicylate or capsacian) *for those who do not wish to take systemic therapy COX-2 Specific Agents or (celecoxib, valdecoxib or rofecoxib) Intraarticular injections (glucocorticoids or hyaluronan) ACR Subcommittee on OA Guidelines. Arthritis Rheum 2000; 43: 1905-1915 Capsaicin Derived from capsicum, i.e., chili peppers Topical application Mediated through Substance P receptors Major effect is analgesia Additional analgesics include tramadol, narcotics Corticosteroid Injections Reserved for patients with an effusion or local inflammation Triamcinolone, hexacetonide, or betamethasone Potential chondroprotective effects Limited to 3-4 injections per year Pond-Nuki dog model: corticosteroids reversed early fibrillation assist rehab Potential deleterious effect on ligaments, tendon, NSAIDs Effects on chondrocytes, i.e., PG synthesis In vitro: decreased by indomethacin and sodium salicylate increased by ibuprofen, sulindac, and benoxaprofen Ø from naproxen and diclofenac Effects on cartilage Degradation reduced by tiaprofenic acid and possibly piroxicam Progression of X-Ray s in knee OA by indomethacin • suppression of matrix synthesis and possibly COX-3 Versus COX-2 & COX-1 Pincus. Curr. Rheum. Reports. 2001; 3: 524-34 Considerations for Treatment Selection COX-2 vs. NSAID? Evaluation of risk factors for UGI complications Age > 65 years Comorbid medical conditions Oral glucocorticoids History of peptic ulcer disease History of UGI bleeding Anticoagulants Smoking? Alcohol consumption? ACR Subcommittee on OA Guidelines. Arthritis Rheum 2000; 43: 1905-1915 COX-2 Inhibitors Features Selectively inhibit the COX isoform upregulated with inflammation, Inhibits production of PGE2 and IL-6 Reduce side effects of NSAIDs including GI toxicity & platelet inhibition Still has Renal effects, CV effects Ulcer Complication/Symptomatic Ulcer Rate Non-Aspirin Users 4 Celecoxib Long-term Arthritis Safety Study Annualized Incidence (%) P = 0.02 2.91 3 Celecoxib 400 mg BID P = 0.04 Conventional NSAIDs 2 1.40 1.27 1 0.44 0 Complications Complications and Symptomatic Ulcers Silverstein, et al. JAMA. 2000;284:1247–1255. Rates of Complicated Confirmed Events VIGOR Trial 57% reduction Annual Incidence (%) 2.0 1.6 * 1.4 1.2 0.8 0.6 0.4 0 Rofecoxib 50 mg QD *P 0.05 Bombardier, et al. N Engl J Med. 2000;343:1520–1528. Naproxen 500 mg BID RR for Hospital Admission for GI Bleeds 4 3,5 Nsaid Arthrotec Vioxx 3 2,5 2 1,5 1 0,5 Celebrex 0 Mamdani,et.al.BMJ 2002;325:624-7 Controls N=100,000 NSAID 5391 Arthrotec 5087 Vioxx 14,583 Celebrex 18908 Population based Canadian % Patients Hospitalized GI Safety Time from Index Date (Days) Mamdani M. BMJ 02 Recurrent Ulcer Bleeding in High Risk Patients with Prior PUD 30 20 GI bleeding CV 15 HTN 25 10 edema 5 Celecoxib v. Diclofenac/omeprazole 287 pts.(144c+143d/p) Healing Endoscopic PUD C: 4.9%(95%CI 3.1-6.7) D+P: 6.4%(4.3-8.4) Renal fail 0 cel d+PPI Chan,et.al.NEJM2002;347:210410 Relationship Between Selective COX-2 Inhibitors and Acute Myocardial Infarction Solomon, et. al. Arth.&Rheum. 48;2003:S697 Retrospective analysis of two state sponsored pharmaceutical benefit programs Comparison of patients on rofecoxib, celecoxib, NSAIDs, or none 54,475 patients included 941 on rofecoxib, age 82; 2140 on celecoxib, age 81 Matched for age, HTN, gender, AMI hx., duration of rx. Relationship Between Selective COX-2 Inhibitors and Acute Myocardial Infarction Solomon, et. al. Arth.&Rheum. 48;2003:S697 Rofecoxib vs. Celebrex: OR 1.24 (1.05-1.46) Rofecoxib vs. no NSAID: OR 1.14 (1.00-1.31) Celecoxib vs. no NSAID: OR 0.93 (0.84-1.02) Rofecoxib >25mg vs. Celecoxib >200mg: OR 1.70 (1.07-2.71) Rofecoxib <25mg vs. Celecoxib <200mg: OR 1.21 (1.01-1.44) Relationship Between Selective COX2 Inhibitors and Acute Myocardial Infarction Solomon, et. al. Arth.&Rheum. 48;2003:S697 Rofecoxib vs. Celecoxib: 1-30 days OR: 1.39 (1.10-1.74) 31-90 days OR: 1.37 (1.09-1.71) >90 days OR: 0.96 (0.73-1.26) Rofecoxib vs. Naproxyn: OR: 1.17 (0.90-1.52) vs. other NSAID: 1.17 (0.99-1.38) Celecoxib vs. Naproxyn: OR: 0.95 (0.74-1.21) vs. other NSAID: 0.95 (0.82-1.09) Considerations for Treatment Selection Evaluation of risk factors for reversible renal failure in patients with intrinsic renal disease (Scr > 2.0 mg/dL) age > 65 years hypertension congestive heart failure use of diuretics use of angiotensin-converting enzyme ACR Subcommittee on OA Guidelines. Arthritis Rheum 2000; 43: 1905-1915 inhibitors 6-Week Elderly HTN*/OA† Trials: Celecoxib vs Rofecoxib Incidence of Clinically Meaningful BP Elevation Trial 1P1 = 0.03 Trial 22 P < 0.01 5 16. 5 14. 9 % of Patients 15 12 11.2 9 6.9 6 NS NS 3 2.3 2 3 1 0 0 SBP > 20 mm Hg and > 140 mm Hg Trial 22 4 % of Patients 18 Trial 11 SBP > 20 mm Hg and > 140 mm Hg *HTN = hypertension; †OA = osteoarthritis 1. Whelton, et al. Am J Ther. 2001;8:85-95. 2. Data on file. Searle, Skokie, IL. 1.5 2.2 1.3 Celecoxib 200 mg QD (n = 411) Celecoxib 200 mg QD (n = 549) Rofecoxib 25 mg QD (n = 399) Rofecoxib 25 mg QD (n = 543) DBP > 15 mm Hg and > 90 mm Hg DBP > 15 mm Hg and > 90 mm Hg Annual Use of Non-narcotic Analgesics and NSAIDs in the United States* Non-narcotic analgesics: 22.2 million prescriptions1 Total sales of OTC analgesics: $2.5 billion2 NSAIDs: 71.4 million prescriptions1 *Data from 1997 1IMS; 2IRI InfoScan 70 Arthroscopic Surgery Moseley, et al. New Eng. J. Med. 2002; 347: 81-8 THERAPEUTIC INTERVENTIONS Symptom Modifying Physiotherapy Analgesia NSAIDs Surgery Intra-articular injections Structure Modifying MMP Inhibitors Specific: None have made it thru Phase III Non specific: The tetracyclines are in testing Growth Factor: IGFI Dietary Vitamin C Glucosamine Other Dietary Interventions MSM: Unable to find any controlled trials showing benefit. However, many individuals note significant relief of pain and swelling in hands with OA. SAMe: Meta-analysis in 2002 found efficacy equal to NSAIDs (Soeken, et. al.) Recent Developments Glucosamine & Chondroitin Sulfate • Dose: • No FDA oversight • Brand to brand and intrabrand consistency are lacking Building blocks of Glucosaminoglycans, namely aggrecan • Glucosamine 1500mg/day Chondroitin 1200mg/day Decrease synovial fluid IL-1b and collagenase Clinical Evidence Glucosamine • Reginster, et al. Lancet. 2001; 357(9252):251-6 • 3 yr, d-b, p-c; studied joint space narrowing and WOMAC Chondroitin • Verbruggen, et al. Osteoarthritis & Cartilage. 1998; 6 Suppl A:378. • 3year study in erosive OA of the hand: X-ray progression Glucosamine-S & Symptom Relief Drovanti A, Bignamini AA, Rovati AL. Therapeutic activity of oral glucosamine sulfate in osteoarthrosis: a placebo-controlled double-blind investigation. Clin Ther 1980;3:260-272.