Defining Arthritis





Arthritis is an umbrella term for over
100 types of rheumatic diseases


Rheumatoid Arthritis

Ankylosing Spondylitis
Juvenile Rheumatoid Arthritis
Osteogenesis Imperfecta
Lyme Disease
Carpel Tunnel
Psioriatic Arthritis

Two Most Common Types


Rheumatoid Arthritis


Definisi  Merupakan suatu penyakit ditandai dengan hilangnya keseimbangan normal proses sintesis dan degradasi makromolekuler yang dibutuhkan dalam menjaga fungsi dan kemampuan biomekanikal rawan sendi artikuler.  Merupakan peny sendi degeneratif yang berkaitan dengan kerusakan kartilago sendi. .

000 Americans .Osteoarthritis    Typically affects people over the age of 50 A biologic process which effects cartilage with subsequent inflammatory component Characteristically the major component of the clinical presentation is pain and decreased function    >75% of people over the age of 75 have x-ray evidence of disease > 75% of people over the age of 85 are symptomatic Probably affects 16-20.000.

Osteoarthritis Normal Joint Joint with Osteoarthritis .

Risk Factors


Abnormal components of the joint as an organ
Abnormal range of motion
Congenital anomalies

Overuse syndromes

Etiology of Osteoarthritis

Disease of the synovial joints
Primary changes of OA begin in the cartilage
 Most pronounced in load bearing areas of articular
 Fibrocartilaginous repair is inferior to original
hyaline cartilage
 Other tissues affected include: subchondral bone,
synovium, meniscus, ligaments, muscle

Etiology of Osteoarthritis

Articular cartilage is composed of:


Provide compressive stiffness and ability to withstand


Provides tensile strength and resistance to shear

Etiology of osteoarthritis  Articular cartilage (1-2 mm thick)  Provides a smooth bearing surface   With synovial fluid as a lubricant. the coefficient of friction for cartilage on cartilage is 15X lower than rubbing 2 ice cubes together Prevents the concentration of forces when bones are loaded .

Etiology of Osteoarthritis    Growth of cartilage and bone at the joint margins leads to osteophytes which can restrict movement Chronic synovitis and thickening of the joint capsule further restrict movement Periarticular muscle wasting is common and plays a major role in sx and disability .


Conceptual Model of OA Biochemical changes/ cells and tissue Structural changes Pain and other signs and symptoms Functional limitation Reduced quality of life Surgical replacement .

Classification of OA  Primary (idiopathic) unidentified causes  Secondary precipitating factors 16 .

Joints affected by OA      Knees (41%) Hands (30%) Hips (19%) Spine (cervical and lumbar regions) Toes (first metatarsophalangeal joint) 17 .

Clinical signs of OA       Crepitus Restricted joint movement Joint instability Bony swelling Soft tissue swelling Joint deformity     Joint tenderness Increased joint warmth Muscle atrophy or weakness Limp while walking 18 .

Sources of OA joint pain       Subchondral bone Nerve endings in periosteum Stretching of ligaments Distention of joint capsule Inflammation of synovium Periarticular muscle spasm 19 .

Pain drawings Mark the area on your body where you feel the described sensations Use the appropriate symbol Mark the areas of radiation Include all affected areas Numbness ==== Pins and needles °°° ° ° ° Burning xxxxxxxx Stabbing /////// .

Rating scales Visual analogue scale  Worst possible pain No pain  Pain intensity 0 1 2 3 4 5 No pain Mild Discomforting Distressing Horrible Excruciating       .

Clinical Approach to Knee Pain Valgus Test (MCL) Varus Test (LCL) McMurray Maneuver (menisci) Lachman Test (ACL) Duck Waddle (stability) .

Diagnosis of OA  Symptoms Pain  Decreased function  Due to boney change  Due to soft-tissue change or swelling  Due to alteration of the normal structures   Crepitance or “crunching within the joint” .

Diagnosis of OA  Signs  On physical exam Asymmetry of findings usually of large joints  Heberdens/Bouchard’s nodes (may be symmetrical)   Classic hand involvement: DIP/PIP nodular disease Some boney swelling  Some swelling and pain out of proportion to inflammatory findings  .

Typical OA Hand: Know It When You See It     Hard boney enlargements Heberden’s nodes at the DIP joints Bouchard’s nodes at the PIP joints Often have “squared” first CMC joint due to osteophytes at that joint .

1981 sensitivity 95%.Diagnosis of Knee OA Classic Clinical Criteria    established by ACR. specificity 69% knee pain plus at least 3 of 6 characteristics: • • • • • • > 50 yo Morning stiffness < 30 min Crepitus Bony tenderness Bony enlargement No palpable warmth 5 .

4.  WBC<2000/mm3 Clear color High Viscosity No OA X-rays 1. 3.Diagnosis of Knee OA Classification Tree  Clinical symptoms  Synovial fluid 1. 3. 2. Osteophytes Loss of joint space Subchondral sclerosis Subchondral cysts  Confirmed by arthroscopy (gold standard) 6 Sensitivity 94 %. 2. Specificity 88 % .

Diagnosis of Knee OA .


how to predict which patient falls into which category Increased sclerotic change in subchondral bone  When significantly progressive might reflect eburnation .Diagnosis of OA  By imaging  X-ray   Presence of osteophytes (biologic evidence of an attempt to repair?) Progressive joint space narrowing which is a surrogate measure of cartilage thinning   Now known not to be linear and some patients are rapid progressors while others are slow progressors or somewhere in between.


OA Hip: .

bilateral. joint space narrowing (arrows) at the hips that is worse on the left side .OA Hip: 1997.

.Osteoarthritis: • Narrow joint space • Lipping – osteophyte • Dislocation • Osteoporosis.

Radiographic Features of the Knee in OA      Joint space narrowing Marginal osteophytes Subchondral cysts Boney sclerosis Malalignment Joint space narrowing .

Osteoarthritis: Ankylosis  varus deformity of the knee and collapse of the joint space with destruction of the medial cartilage and the subchondral cortex (open arrowheads). .

. The osteophytes are best seen in this view.Osteoarthritis:  Lateral view of the left knee shows sclerosis with marked osteophyte formation (arrows).

Osteoarthritis:  Subchondral cysts (solid arrowhead) .

OA Fingers: .

Diagnosis of OA  Imaging  MRI Newer technique  Able to provide a 3 D image of the joint as an organ     Can approximate the volume of cartilage May be able to identify early change in cartilage metabolism Can approximate early bone change (bone “edema”?) .

Laboratory findings in OA   THERE ARE NO DIAGNOSTIC LAB TESTS FOR OSTEOARTHRITIS OA is not a systemic disease. therefore:   ESR. CBC. Chem 7. CPPD. or septic arthritis if diagnosis is in doubt  . and UA all WNL Synovial fluid Mild leukocytosis (<2000 WBC/microliter)  Can be used to exclude gout.

Management: Algorithm Lifestyle Modifications NSAIDs PRN Steroid Injections Acetaminophen PRN Celecoxib Opioids PRN Hyaluronan Injections Surgical Referral .

biking 7 Ambulatory assist devices   Nutrition referral Cane Walker Insoles Unloader knee braces .g. swimming.Management: Lifestyle  Weight loss   Exercise Program        PT referral Quadriceps strengthening ROM exercises Low impact activities e.

4 per 10 lb increase in body weight 44 .Weight reduction  Increased odds ratio for knee OA = 1.

Thermal modalities  Heat Relaxes muscles Stimulates blood flow  Cold Eases muscle spasms Blocks pain signals 45 .



Management: Lifestyle Varus (bowlegged) vs Valgus (knock-kneed) G2 Unloader Brace .

Exercise  Range of motion  Muscle strengthening  Aerobics 49 .

arthritis.Patient education   1-800-283-7800 Education can improve arthritis symptoms 15% to 30% Can last up to 2 years following intervention 50 .

Management: Medical       Glucosamine/Chondroitin Acetaminophen NSAIDs Cox-2 inhibitors Opioids Intraarticular injections   Glucocorticoids Hyaluronans .

structure and integrity  MSM + Glucosamine more effective than Glucosamine alone Clinical Drug Investigation. .24:353-363.163:1515-22 Chondroitin sulfate  Clinical effectiveness documented in 9 double-blind clinical trials  Controversies remain over quality control issues and mechanism of action MSM  Sulfur critically important to cartilage formation. best clinical documentation. 2004.Natural Products for Osteoarthritis Glucosamine sulfate  Most useful. 2003. and cost effective  Long-term studies now document significant clinical benefit  Meta-analysis shows structural and symptomatic efficacy of glucosamine and chondroitin in knee osteoarthritis Arch Intern Med.

placebo-controlled. Feb 23. N=1583 Symptomatic mild or moderate-severe knee OA Infrequent mild side effects e. NEJM. bloating For mild OA. 24 wks. 2006       Multicenter. double blind. combination showed benefit 8 Patient satisfaction .Management: Medical  Glucosamine/Chondroitin     1500 mg/1200 mg daily ($40-50/month) Glucosamine: building block for glycosaminoglycans Chondroitin: glycosaminoglycan in articular cartilage GAIT study. not better than placebo For moderate-severe OA.g. Reumatol 2001. proteoglycanase. al. etc. 1: 12-17. (Supplement A). 14-21. fosfolipase A2. .CHONDROITIN SULFATE ACTION MECHANISMS3-4 STIMULATES:  proteoglycans  HA EFFECT: -anti-inflammatory activity -Membrane stabilising action INHIBITS:  cartilage degradative enzymes (collagenase. Esp. Osteoarthritis Cart (1998) 6. 28. Rev.elastase. N-acetylglucosaminidase.)  cartilage damaging substances (free radicals)  apoptosis  NO  Stromelysin (MMP-3)  NF-kB (3) Ronca F et. (4) Blanco FJ.

Management: Medical  Acetaminophen      Indication: mild-moderate pain 1000 mg Q6h PRN Better than placebo but less efficacious than NSAIDs 9 Caution in advanced hepatic disease NSAIDs     Indication: moderate-severe pain. failed acetaminophen GI/renal/hepatic toxicity. use anti-ulcer agents concurrently Agents have highly variable efficacy and toxicity . fluid retention If risk of GIB.



g. 400 BID  Increased risk at higher doses 11 CLASS Trial: 8.Management: Medical  Cox-2 inhibitors       Indication: mod-severe pain. symptomatic ulcers. fluid retention Increased risk of CV events?   APC Trial: 700 pts each assigned to placebo.000 pts compared Celecoxib vs Ibuprofen  Similar risk to Ibuprofen 12 . GIB Celecoxib 200 mg daily GI/renal toxicity. risk of GIB OA pain relief similar to NSAIDs Fewer GI events e. failed NSAID. 200 BID.

promotes synthesis of pro-inflammatory prostaglandins . cytokine.physiologic production of PG in gastric mucosa. endothelium.induced by mitogen. platelet. kidney • Cyclooxygenase-2 (COX 2): inducible . endotoxin .Cyclooxygenase (COX) Two isoenzymes • Cyclooxygenase-1 (COX 1): constitutive .

Cox-2 What the drug companies wanted us to believe. Arachidonic acid COX-1 “Constitutive” Good Prostaglandins  GI cytoprotection  Platelet activity  Renal function COX-2 “Inducible” Bad Prostaglandins  Inflammation  Pain  Fever .Cox-1 vs.

Arachidonic acid COX-1 “Constitutive” Prostaglandins COX-2 “Inducible” Prostaglandins Pathological  GI cytoprotection  Platelet activity  Renal function  Inflammation  Pain  Fever Physiological  Renal function  Vascular  Tissue repair .Cox-1 vs. Cox-2 The reality.

constipation .Management: Medical  Opioid Analgesics      Indication:  Moderate-severe pain  Acute exacerbations  NSAIDs/Cox-2 inhibitors failed or contraindicated Oxycodone synergistic w/ NSAIDs 13 Tramadol/acetaminophen vs codeine/acetaminophen  Similar pain relief 14 Avoid long-term use Caution in elderly  Confusion. sedation.

opioids can be used Tylenol + codeine (T-3)  Tramadol  63 .Opioids  For moderately severe to severe pain.

Capsaicin topical cream   Capsaicin derived from pepper plants Induces depletion of substance P involved in transmitting pain 64 .

5 inch needle Approach accuracy:       Lateral mid-patellar 93% 18 Patient supine Leg straight Manipulate patella Angle needle slightly posteriorly Inject after drop in resistance or fluid aspirated .Management: Medical Intraarticular Injections  Technique   22 gauge 1.

Management: Surgical When to Refer  Knee pain or functional status has failed to improve with non-operative management Types of Procedures      Arthroscopic Irrigation Arthroscopic Debridement High Tibial Osteotomy Partial Knee Arthroplasty Total Knee Arthroplasty .

Management: Surgical High Tibial Osteotomy  Indication:   Unicompartmental arthritis Genu varus or valgus  Realign mechanical axis  Age < 60yo  < 15 degrees deformity19 .

Management: Surgical Partial Knee Arthroplasty  Indication:  Unicompartmental arthritis  Ligaments spared  Increased ROM  Faster recovery  Prosthesis 10-yr survival: 84% 20 .

Arthroplasty .

Management: Surgical Total Knee Arthroplasty  Indication:        Diffuse arthritis Severe pain Functional impairment Pain relief > functional gain ACL sacrificed PCL also may be sacrificed Prosthesis 10-yr survival: 90% .


Management option Symptomatic slow-acting drugs of OA  Symptomatic slow-acting drugs of OA (SYSADOA)      glucosamine chondroitin hyaluronic acid Supported by increasing evidence. although further research is still required Given that these agents appear to be well tolerated and do show some benefit their use should be considered13 .

Management option 10 Surgery     Refer for orthopaedic evaluation if patient is disabled by OA or in pain unrelieved by medical management Joint replacement can be very effective Newer techniques such as metal-on-metal resurfacing are less invasive Patients should be made aware of the risks and benefits of surgery .

Thank you .

Human Cell Membrane .

Fatty Acid Metabolism Omega 6 Fatty Acids Omega 3 Fatty Acids Most salad oils Evening primrose oil LA ALA d6d d6d GLA Meat SDA el Mother's milk DGLA Flax seed oil Black currant oil el d5d AA EPA cyc cyc lip cyc PGE1 PGE2 LEUK PGE3 Fish .

Cell Membrane Phospholipids Phospholipase A2 Arachidonic Acid Cyclooxygenase COX -1 .inducible Prostaglandin H2 Thromboxane A2 TXA2 synthase isomerase PGI2 synthase Prostacyclin (PGI2) reductase Prostaglandin D2 Prostaglandin F2α Prostaglandin E2 .constitutively expressed COX -2 .

Vasoconstrictor . Prostaglandin H2 Thromboxane A2 Prostacyclin - Platelet Aggregation .Vasodilation .Vasoconstriction - Platelet Aggregation . 12-HPETE .Amplifies platelet response to other agonists.promotes inflammation and allergic signs/symptoms Isoprostanes . .Metabolic Pathways of Arachadonic Acid Membrane Phospholipids Non-Enzymatic Lipid Peroxidation Catalyzed by Free Radicals ARACHIDONIC ACID 12-Lipoxygenase COX 12-HETE.Plasma levels 1-2 orders of magnitude > COX -derived metabolites.

Thromboxane A2 vs. Prostacyclin ARACHIDONIC ACID COX -1 Platelet TXA2 Vasoconstriction Platelet Aggregation COX -2 Endothelial PGI2 (Prostacyclin) Vasodilation Anti-Platelet Aggregation .

Why do Cox-2 inhibitors increase risk for heart disease? #1. Because they adversely effect the ratio of thromboxane to prostacyclin Aspirin COX-1 COX-2 inhibitors Prostacyclin Thromboxane Thromboxane Decreased CV events COX-2 Prostacyclin Increased CV events .


Anti-Inflammatories .