osteoarthritis
DESCRIPTION
doctor's guideTRANSCRIPT
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: [email protected]
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