About The Author Dr Manoj R.

kandoi is the founder president of Institute of Arthritis Care & Prevention an NGO involved in the field of patient education regarding arthritis. Besides providing literature to patient & conducting symposiums, the institute is also engaged in creating patients Self Help Group at every district level. The institute also conducts a certificate course for healthcare professionals & provide fellowship to experts in the field of arthritis. The author has many publications to his credit in various journals. He has also written a book The Basics Of Arthritis for healthcare professionals. The author can be contacted at: Dr manoj R. kandoi C-202/203 Navare Arcade Shiv Mandir Road, Opposite Dena Bank Shiv mandir Road, Opposite Dena bank Shivaji Chawk, Ambarnath(E) Dist: Thane Pin:421501 State: Maharashtra Ph: (0251)2602404 Country: India Membership Application forms of the IACR for patients & healthcare professionals can be obtained from. Institute of Arthritis Care & Prevention C/o Ashirwad Hospital Almas mension, SVP Road, New Colony, Ambarnath(W) Pin:421501 Dist: Thane State: Maharashtra Country: India Ph: (0251) 2681457 Fax: (0251)2680020 Mobile ;9822031683 Email: drkandoi@yahoo.co.in Preface: Studies have shown that people who are well informed & participate actively in their own care experience less pain & make fewer visits to the doctor than do other people with arthritis. Unfortunately in India & many third world countries we do not have patient education & arthritis self management programs as well as support groups. This is an attempt to give a brief account of various arthritis, their prevention & self management methods which can serve as useful guide to the patients of arthritis. It would be gratifying if the sufferers of the disease knew most of what is given in the book. Acknowledgement\ I am thankful to Dr (Mrs) Sangita Kandoi for her immense help in proofreading & for her invaluable suggestions. The help rendered by Nisha Jaiswal is probably unrivalled. Thanks also to vidya, praveen, rizwana and parvati for their continous support throughout the making of the book. The author is grateful to his family for the constant inspiration they offered. The author alone is responsible for the shortcoming in this piece of work. He welcomes suggestions for improvement from the readers.

Osteoarthritis
Introduction: Osteoarthritis is a noninflammatory disorder of movable joints characterized by deterioration of articular cartilage & formation of new bone at the joint surfaces & margins. Osteoarthritis consists of "Morphologic, biochemical, molecular and biomechanical changes of both cells and matrix leading to softening fibrillation, ulceration and loss of articular cartilage, sclerosis and eburnation of subchondral bone, osteophytes and subchondral cyst. From keuttner KE, Golbberg V, eds. Osteoarthritic disorders. Rosemont IL: American Academy of Orthopaedic Surgeons 1995: 21 -25. Classification of degenerative joint disease: A. Primary a. Peripheral Joint b. Spine c. Subsets: Primary generalized osteoarthritis Erosive (inflammatory): hands DISH syndrome (Diffuse Idiopathic Skeletal hyperostosis) Chandromalacia B. Secondary: This may develop in following disease processes: Acutetrauma Hyperparathyroidism Chronic trauma Overuse of intraarticular Steroid Alcaptonuria Injection Wilsons disease Neurological disease including Hemochromatosis Diabetes Acromegaly Syringomyelia Hemophilia Frost bite Epidemiology: Frequency increases with age Men under 45 years are more commonly affected than female"whereas prevalence is greater in women after age 55 years. Risk factors for OA: Age -Repetitive stress e.g. vocational Female sex -Obesity Race -Congenital/developmental defects Genetic factors -Prior inflammatory joint disease Major joint trauma -Metabolic / endocrine disorders Pathology: Early degeneration or distruption of the articular cartilage surface in the for of flaking or fibrillation most commonly on the weight bearing surface of the joint. This gradually proceeds to complete loss of articular cartilage & eburnation of bone which has a ivory like sclerotic surface. Cyst formation occur in the sub articular bone usually on the

weight bearing surface due to micro fracture that degenerate. New bone formation usually found at the bone of the articular cartilage & surrounding the cyst creating on area of sclerosis. Osteophyte form of out growth usually of ossified cartilage. Because of the vascularisation in the subchondral bone, proliferation of adjacent cartilage and enchondral ossification occur. These out growth extend from the free articular space along the path of least resistance. In advanced stage fragmentation of osteochondral surface occurs leading to loose body formation. In long standing case destruction and distortion of capsular ligaments can lead to deformity and malalignment. Microscopic stages of osteoarthritis: Early: Surface irregularities or fibrillation with small clefts not extending beyond the superficial zone. Slight hyper cellularity, minimum loss of mucopolysacharides not extending beyond the transitional zone or upper middle zone. Moderately advanced: More extensive loss of surface Clefts extend into the middle zone and occasionally into calcified zone. Loss of mucopolysaccharides extend into middle zone Hyper cellularity in clusters of cells or chondrocyte clones. Advanced: Thickness of cartilage reduced Clefts may extend down to subchondral bone Muopolysaccharides markely diminished through out entire thickness of articular catilage In some area there may be complete loss of articular cartilage with exposure of thick, ebumated subchondral bone. Causes of loss of mobility in an arthritic joint (kenwright & duthie, 1971): 1. Loss of bone & articular cartilage symmetry leading to incongruity. 2. Atrophy, spasm or contracture of muscles with the appearance of intrafibrillary fibrosis within the muscle, in overlying fascia & at the musculo tendinous junction. 3. Capsular contracture 4. Mechanical blockage by loosebodies, osteophytes & cartilaginous or bone debris. Causes of instability in arthritic joint: a. Muscle disorganization & in co-ordination especially in response to pain. b. Joint surface incongruity & roughness. c. Loose bodies d. Meniscal degeneration and/or looseness with or without frank fear. e. Trapping of intra-articular synovial folds e.g. the infrapatellar fold.

Causes of joint pain in patients with OA Source -Mechanism Synovium -Inflammation Subchondral bone -Increased intraosseous pressure microfractures Osteophyte -Stretching of periosteal nerve endings Ligaments -Stretch Capsule -Inflammation, stretch Muscle -Spasm Cockin and duthie (1971) hypothesis for hip joint osteoarthritis: 1. Low velocity repetitive movements with longitudinal and compressive forces produced by muscle activity of a static or dynamic type and by gravitational load of body weight. 2. Change in articular geometry by reduction in surface area, symmetry and stability of joint surface. 3. There is decrease in the resilience of cartilage from loss of matrix proteoglycons and water carried by the release of cathepsins into the matrix of cartilage. 4. Lubrication of hip joint is severly disturbed by the alteration in joint congruity and alteration of viscosity of the fluid due to the joint effusion. Clinical manifestation: OA affects limited number of joints. Pain is the first-feature increasing in frequency subsequently. Cold aggrevates the pain while warmth reduces it. Stiffness of joints occurs but lasts for less than 10 minutes. Physical examination reveals asymmetrical tenderness over the joint. Crepitus is found in older patients. Joint enlargement is due to spur formation. Chronic synovitis or effusion is seen. Boggy synovitis if present is not as severe as with rheumatoid arthritis, usually effusion is minimal Increased effusion is common after slight twisting or giving away episode Later subluxation results due to periarticular Instability. . Commonest joints involved: Hands: DIP joints involvement: Heberden nodes PIP joints involvement: Bouchard's node MCP joints involvement CME joints involvement Feet: MTP joints invl()vemcnt Temporo mandibular joint Knees Spine: L3 -L4 more common Mid cervical mid thoracic Other joint: Primary OA almost never affects mcp, wrist, elbow, shoulder, ankle. Involvement of these joints is usually secondary.

Investigation: X-ray: The diagnosis of otteoarthritis is mainly radiological I. Narrowing of joint space which may involve one or more compartments e.g. medial compartment involvement in knee: II. Subchondral cysts III. Subchondral sclerosis -dense bone under the articular surface IV. Osteophyte formation V. Loose bodies VI. Deformity of the joint CT scan and MRI are particularly useful in OA and lumbar spine and Lumbar canal stenosis.

Kellgren and Lawrence classification based on x-rays: 1. Formation of osteophytes on the joint margins 2. Periarticular ossicles, particularly in relation to the DIP and PIP joints of hands & feet 3. Narrowing of the joint cartilage associated with sclerosis of subchondral bone. 4. Small pseudocystic areas with sclerotic margins situated in the same area. 5. Altered shapes of bone ends, particularly of the head of femur e.g. (coxa magna). Other investigations: These are done primarily to detect an underlying cause. These consist of following: 1. Serological tests and ESR to rule out RA 2. Synovial fluid analysis aids in ruling out inflammation 3. Serum uric acid to rule out gout 4. Arthroscopy to rule out miniscal injuries or loose bodies. 5. Ochronosis, hyper parathyroidism haemochromatosis can be detected by laboratory findings. Causes of secondary osteoarthritis of knee 1. Obesity, valgus and varus deformities 2. Trauma, intra-articular fractures 3. RA, infection, TB etc 4. Haemophilia 5. Charcot's joint 6. Hyperparathyroidism 7. Overuse of intra-articular steroid therapy

Causes of secondary OA of the hip: Avascular necrosis: Idiopathic Post traumatic e.g. fracture of femoral neck Alcoholism Post partum osteonecrosis Chronic liver failure Patient on steroids Patient on dialysis Sickle cell anaemia Coxa vara Congenital dislocation of hips Old septic arthritis of the hip Malunited fracture Fracture of acetabulum. Figure 2.3: Secondary OA of HIP Osteoarthritic Hip treatment protocol Suspected arthritis -Laboratory tests -X-rays -Joint aspiration

- History of trauma infection systemic disease - Clinical examination

Degenerative Conservative

Effective

Not Effective

Septic - Debridement and antibiotics - Arthrodesis - Resection arthroplasty - Staged joint replacement

Inflammatory Treat underlying disease and local conservative therapy

Observe continue treatment

Response + ve Continue

Poor Response

Disease progression Total Joint Replacement

Old patient Destroyed Joint Total joint replacement

young patient partial joint surface involvement Osteotomy

Causes of secondary arthritis in the wrist joint: 1. Kienbock's disease (osteonecrosis of the lunate) 2. Trauma 3. Non union of the scaphoid 4. Gout 5. COPD disease 6. Carpal instability from bony or ligament injury Differential diagnosis of osteoarthritis: Rheumatoid arthritis Gouty arthritis Calciumpyro phosphate arthropathy Osteonecrosis Neuropathic joints Important terminologies: Heberdens node: 'These are the bony enlargement which can be felt about the DIP joints of the hands. Bouchards node: These bony enlargement are present at PI P joint. Mucinous Cyst: These cyst containing degenerative myxomatous fibrous tissue arises from the joint capsules in the distal or PIP joints.
OSTEOARTHRITIC HAND

DID of extensive arthritis of multiple DIP joints Primary osteoarthritis Psoriatic arthritis Multicentric reticulohistiocytosis

DID of 2nd and 3rd MC joint arthritis Erosive arthritis: RA or psoriasis Degeneration with hook like osteophytes: Hemochromatosis and acromegaly

Difference between inflammatory and noninflammatory arthritis: Features Morning Stiffness Spontaneous Exacerbations Night Pains Constitutional Symptoms Exacerbated by use of joint Improvement with use of joint Elevated acute phase reactants (ESR, CRP etc) Inflammatory Arthritis + + + + + + Non inflammatory Arthritis + -

Treatment: Principles of treatment I. Prevention of occurence of the disease II. To provide symptomatic relief and retard further progression of patient present early. III. To rehabilitate in case of advanced arthritis Recommendations for the medical management of osteoarthritis of the HIP and knee American college of rheumatology subcommittee on osteoarthritis guidelines: Nonpharmacologic therapy: Patient education Self-management programmes (e.g. arthritis foundation self-management program) Weight loss (if overweight) Aerobic exercise programs Physical therapy range of motion exercise Muscle strengthening exercises Assistive devices for ambulation Patellar taping Appropriate footwear Lateral wedged insoles (for genu varum) bracing Occupational therapy Joint protection and energy conservation Assistive devices for activities of daily living Pharmacologic therapy: Oral: Acitaminophen Cox-2 specific inhibitor Non-selective NSAID plus misoprostol or a protein pump inhibites Nonactylated salicylate Other pure analgesic tramadol Opioids Intraarticular Glucocorticoids Hyaluronan Topical: Capsaicin Methylsalicylate Risk factors for upper gastrointestinal adverse events (ACR-2000) Age > = 65 Poor general condition Oral glucocorticoids

History of peptic ulcer disease History of upper gastrointestinal bleeding Anticoagulants

ACR -2000 recommendations (Brief excerpts) Proper use of a cane (in the hand contralateral to the affected knee) reduces loading forces on the joint and is associated with a decrease in pain and improvement of function Patient may benefit from wedged insoles to correct abnormal biomechanics due to varus deformity of the knee Medial taping of the patella is another useful maneuver in symptomatic patellofemoral compartment involvement The daily dose of acetaminophen should not exceed 4 grams Capsaicin cream is a useful adjunct as a symptomatic treatment. It should be applied to-the symptomatic joints 4 times daily. In acute effusion intraarticular glucocorticoid preparation e.g. up to 40mg triamcinolone hexaacetonide is an effective short term method of decreasing pain and increasing quadriceps strength. Joints should be aspirated / injected using asceptic technique and the fluid should be sent for a cell count. Surgical treatment: These include 1. Osteotomy: The symptomatic relief obtained due to a. Release of intraosseous tension near articular ends b. Realignment of mechanical forces c. Alternation in ligament biomechanics d. Neovascularisation during healing of osteotomies e.g. high tibia osteotomy for medial compartment OA knee. 2. Joint debridement: In this procedure degenerated cartilage is smoothened, osteophyte and the hypertrophied synovium excised. The results are unpredictable. 3. Arthroscopic procedure :These are done for removal of loose bodies, degenerated meniscal tears and also for shaving of fibrillated cartilage using power driven shavers. 4. Joint replacement: Usually reserved for advanced cases with severe functional disabilities. The replaced joints last for 10-15 years. Most commonly done for hips and knees. Indications for tibial osteotomy (Jackson et al. 1969): 1. Osteoarthritis with severe pain unrelieved by conservative treatment 2. Degenerative changes localized to the medial or lateral compartment 3. Flexion range of 900 with FFD < 20 4. Absent, mild to moderate collateral ligament instability

Contraindication for HTO:

OSTEOTOMY

HIGH TIBIAL

1. Tibial subchondral bone loss 2. Flexion contracture of more than 15 3. Lateral subluxation of the tibia on femur of more than 1 cm 4. Less than 90 range of motion. 5. Peripheral vascular disease 6. Systematic inflammatory arthropathies 7. Ligament instability (lateral thrust of knee on weight bearing). Mechanism of pain relief in HTO 1. Redistribution of loading, especially where the lateral joint surface in relatively normal on arthroscopy 2. Reducing tension on the lateral collateral ligament 3. Reducing the medial impingement of the degenerate medial meniscus on the capsule 4. Reducing capsular stretching and tearing by correcting varus and flexion deformities 5. Altering of blood supply, especially reducing venous stasis. Complications associated with HTO 1. Undercorrection / overcorrection 2. Intraarticular extension 3. Patella -baja (low riding patella) 4. Avascular necrosis of tibial plateau 5. Peroneal nerve injury 6. Compartment syndrome 7. Popliteal vessel injury 8. Delayed union / nonunion 9. Infection Indications for tota1 joint replacement for osteoarthritis of the hip or knee: 1. Extreme pain not responding medication 2. Loss of joint function 3. Consistent disturbance with sleep due to night pain 4. Inability to walk for more than one block due to pain 5. Cannot stand still for> 20 -30 minutes due to pain. Vissco supplementation: Proposed role of intraarticular sodium hyaluronate injection: Indications: A. Patients with significantly symptomatic OA, non responders of pharmacologic and nonpharmacologic treatments. B. Patients intolerant of pharmacologic therapies C. Patients not requiring TKR or previous history of failed knee surgeries Mechanism postulated: 1. It contributes to joint stability

a. Offers anti-inflammatory and anti-nociceptive properties or stimulation of hyaluronic acid synthesis by the vissco supplementation. b. Functions physiologically to aid preservation of cartilage structure c. Backbone of joint cartilage d. Gives the cartilage its elasticity and compressibility 2. It prevents arthritis pain a. Dampens the response of the pain fibers in the joint membrane by coating the pain receptors. b. Provides lubricating and cushioning properties c. Offers potential of providing disease modifying effect d. Sustained effect after treatment discontinuation e. TKR may be delayed with the use of hyaluronic acid Dosage: The recommended injection schedule is one injection per week for five weeks.

Proposed role of glucosamine sulphate in OA: 1. Glucosamine stimulates the biosynthesis of glycosaminogylans and hyaluronic acid the backbone needed for the formation of proteoglycans found in the structural matrix of joints. This hyalyronic acid supresses the anticatabolic effect of interleukin-1 in chondrocytes cell cultures and has documented therapeutic efficiency in the treatment and prevention of osteoarthritis. 2. Glucosamine spurs the chondrocytes to produce more collagen. 3. Glucosamine inhibits several enzymes collagnase and phospholipase A2 which breakdown the proteoglycan molecule and thus normalize cartilage metabolism, by preventing the cartilage from breaking. 4. Glucosamine helps bind water in the cartilage matrix. 5. Glucosamine is the main ingredient of the synovial fluid that lubricates and provides nutrients to the joint structures. 6. Glucosamine sulphate promotes incorporation of sulfur into the cartilage. Proposed role of chondroitin sulphate in OA: 1. It plays an important structural role in articular cartilage, notable for its role in binding with collagen fibrics. 2. It competitively inhibits many of the degradative enzymes that break down the cartilage matrix and synovial fluid in OA. 3. It prevents fibrin thrombi in synovial or subchondral microvasculature. 4. It may maximize blood circulation to the tissues including subchondral bone and synovium due to its antiatherosclerotic effect. Theorized synergistic effect of glucosamine sulphate and chondroitin sulphate combined together: 1. Stimulate the metabolism of chondrocytes and synoviocytes. 2. Inhibits degradative enzymes and 3. Reduce fibrin thrombi in periarticular microvasculature

Experimental treatment opinion: I. Fresh osteochondral grafts. II. Chondrocyte transplantation: Chondrocytes obtained from the articular cartilage of the patients knee is cultured and placed in the defect. A periosteal flap is then sutured over the defect with the cell present. This method is being tried for medial femoral condyle defect. III. Soft tissue grafts: Periosteal or perichondral grafts are seen over defect e.g. small pieces of rib perichodrium is transplanted in to a metacorpophalargeal joint. IV. Mosaic graft: Here osteochondral autograft plug is taken from the peripheral area of anteromideal or anterolateral femoral condyle and is inserted over the defect. V. Artificial Matrix: Collagen bone matrix and polylactic acid are used to try to achieve a matrix upon which cartilage can grew. Suggested Treatment Algorithm: Osteoarthritis

Preventive measures (weight reduction) Physical therapy (exercise. heat therapy) Patient education No response Medication

Mild OA Simple analgesic Paracetamol l000mg 4 times / day

Moderate / Severe OA

Conventional NSAIDS + Misoprostol Proton pump inhibitor or H2 recepter inhibitor

Selective COx2 inhibitors (celecoxib, Nabumetoile Rofecoxib

No response Topical Agents (capsaicin) / paracetamol / Tramadol

No response Oral glucosamine / chondroitin supplementation No response

Intraarticular injection [steroid / hyaluronic acid (viscosupplimentation)

Not responding Surgical intervention [Arthroscopy. realignment osteotomy, arthrodesis.arthroplasty] Subsets of osteoarthritis: Erosive osteoarthritis: This hereditory condition mainly involve DIP or PIP joint. It presents with severe inflammatory episodes leading to joint deformities and sometime ankylosis. Cyst may be painful and tender. Postmonopausal woman are more frequently invloved. X-rays feature include severe bony erosions and subchondral bony sclerosis. Nodular osteoarthritis of the fingers: More common in women Swelling at DIP or PIP joint with progressive development unsightly nodes involving one or several joint is the presenting complaints. X-rays: It shows typical feature of osteoarthritis. In addition erosion and apposition of articulating phalanges can occur, sometimes leading to subluxation. This apposition, together with osteophyte is responsible for the nodular appearance of the affected joint. There is often a familiar element, the patient's mother, grandmother, or a maternal aunt having had the same problem. The genetic penetrance is variable and the progression of the lesions is therefore not inevitable and usually normal functions of the finger is retained. There is no direct relationship between nodular osteoarthritis of the fingers and crippling osteoarthrosis of the large joints. Although the painful flare ups are very unpleasant, they prove transitory. Immobilization and if required intraarticular steroids may be used during acute flare ups. Classification of osteoarthrosis of hand: Type I: Confines to DIP joint with haberden' s nodes formation. More common in elderly but may occur in younger age groups with family history. Type II: Generalized osteoarthritis invloving multiple joints in the hand and thumb. Commonly DIP joint and thumb metacarpophalangeal joint affected. Type III: Erosive arthritis involving DIP and PIP joints

Comparison between rheumatoid and osteoarthritic hand Joint involvement Wrist involvement Swelling Rheumatoid PIP and MCP Usual Soft, boggy and periarticular ++ Osteoarthrosis DIP more common -Hard -Bony osteophyte felt -

Tenderness

DISH (Diffuse idiopathic skeletal hyperostosis): It is associated with excessive amount of osteophyte formation. The spine shows calcification on the anterior longitudinal ligament and peripheral disc margins with disc space bight maintained. Calcification may be seen in patellar, iliolumbar, sacrotuborous ligament. Generally pain is absent, stiffness being the main presenting complaint. Marginal osteophyte may be seen in all of the peripheral joints. Stiffness in the joint: Limitation of movements can be a. In all directions -Due to arthritis b. Not in all directions -Due to synovitis and/or spasm of muscle c. Fixed movement in -Due to fixed deformity one or more directions Types of joint stiffness: Extrarticular 1. Biological factors like Scar adhesion, sinus or contracted tissue can be seen 2. Joint line is usually non tender 3. Whatever range of motion possible is using painless 4. On X-Rays joint surface and space appear normal. 5. Dealing with extra articular contracted tissue improves the movements dramatically 6. Manipulation under anaesthesia does not improve range. Intraarticular 1. No obvious scar adhesion, sinus or contracted tissue can be seen. 2. Joint line tender 3. Possible movements are usually painful 4. Joint space is reduced, joint margin fluffy, osteoporosis is usually present. Evidence Of underlying pathology may be present. 5. Dealing with extrarticular contracted tissue does not improve the movement. 6. It may help.

Knee Joint Stiffness: Clinical examination

Mechanical block

No evident mechanical block

. Flexion contracture Exercises

Extension contracture Physical therapy If no relief

Pain absent Exercises

Pain causing Rom

? Internal derangement Arthroscopy

?Inflammatory investigation Medication physical therapy

Effective

Ineffective Recent Onset Long Duration

Continue Serial Casting Manipulation Quadricepsplasty no relief

Effective Resume Exercise

Not Effective

Artholysis Effective include release of Exercise posterior capsule and hamstring