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

- History of trauma infection -Laboratory tests

systemic disease -X-rays

- Clinical examination -Joint aspiration

Degenerative Septic Inflammatory

- Debridement and

Conservative antibiotics Treat underlying

- Arthrodesis disease and local

- Resection conservative therapy

arthroplasty

Effective Not Effective - Staged joint

replacement

Observe continue

treatment Response + ve Poor Response

Continue Disease progression

Old patient young patient

Destroyed partial joint Total Joint Replacement

Joint surface involvement

Total joint Osteotomy

replacement

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:

Heberden’s node: 'These are the bony enlargement which can

be felt about the DIP joints of the hands.

Bouchard’s 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

Difference between inflammatory and noninflammatory arthritis:

Features Inflammatory Arthritis Non inflammatory Arthritis

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)

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

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: HIGH TIBIAL

OSTEOTOMY 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 Moderate / Severe OA

Simple analgesic

Paracetamol l000mg

4 times / day Conventional Selective COx2

NSAIDS inhibitors

+ Misoprostol (celecoxib,

Proton pump inhibitor Nabumetoile

or H2 recepter inhibitor Rofecoxib

No response No response

Topical Agents Oral glucosamine / chondroitin

(capsaicin) / paracetamol / supplementation

Tramadol

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

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 Intraarticular

1. Biological factors like Scar adhesion, sinus 1. No obvious scar adhesion, sinus or

or contracted tissue can be seen contracted tissue can be seen.

2. Joint line is usually non tender 2. Joint line tender

3. Whatever range of motion possible is using 3. Possible movements are usually painful

painless 4. Joint space is reduced, joint margin fluffy,

4. On X-Rays joint surface and space appear osteoporosis is usually present. Evidence

normal. Of underlying pathology may be present.

5. Dealing with extra articular contracted tissue 5. Dealing with extrarticular contracted tissue

improves the movements dramatically does not improve the movement.

6. Manipulation under anaesthesia does not 6. It may help.

improve range.

Rheumatoid Osteoarthrosis

Joint involvement PIP and MCP DIP more common

Wrist involvement Usual -

Swelling Soft, boggy and -Hard

periarticular -Bony osteophyte

felt

Tenderness ++ -

Knee Joint Stiffness:

Clinical examination

Mechanical block No evident mechanical block

.

Flexion Extension Pain absent Pain causing Rom

contracture contracture

Exercises

Exercises Physical therapy

? Internal ?Inflammatory

If no relief derangement investigation

Effective Ineffective Arthroscopy Medication

Recent Long physical

Onset Duration therapy

Continue Serial Casting

Manipulation Quadricepsplasty

Effective Not Effective no relief

Resume Artholysis Effective

Exercise include

release of Exercise

posterior capsule

and hamstring