This document discusses arthritis and related diseases. It defines arthritis as inflammation of a joint and describes its main causes and types. Rheumatoid arthritis is discussed in detail, including its pathology, clinical features, diagnostic criteria, and treatments. Ankylosing spondylitis and osteoarthritis are also summarized. The document provides overviews of the classifications, presentations, investigations, and management approaches for different forms of arthritis.

1. Arthritis and Related
Diseases
Dr. Sanjib Kumar Das, PhDDr. Sanjib Kumar Das, PhD

2. DEFINITIONS
• Arthritis is an inflammation of a joint.
• It is characterized by pain, swelling and limitation of joint
movement.
• Cause may be purely a local pathology such as pyogenic
arthritis or a more generalized illness such as rheumatoid
arthritis.
• Arthralgia is a term used for pain in a joint, without any
associated signs of inflammation.

3. CLASSIFICATION
• Arthritis can be divided into two types:
(i) Monoarthritis
(ii) Polyarthritis
Monoarthritis
• Pyogenic arthritis
• Tubercular arthritis
• Haemophilic arthritis
• Secondary osteoarthritis
• Gout – sometimes
Polyarthritis
• Rheumatoid arthritis
• Rheumatic fever
• Juvenile chronic polyarthritis
• Primary osteoarthritis
• Seronegative spondarthritis

4. Rheumatoid Arthritis is a chronic inflammatory joint disease . It is
symmetrical, destructive, deforming polyarthritis affecting small and large
synovial joints with association of systemic disturbances, variety of extra
articular features and presence of rheumatoid factors.

5. New Diagnostic Criteria for Rheumatoid Arthritis (1987)
By American Rheumatism Association
5. Rheumatoid nodule
6. Rheumatoid factor - positive
7. Radiological changes – erosion or periarticular osteopenia
1. Morning stiffness (> 1 hour)
2. Arthritis of three or more joint areas
3. Arthritis of hand joints
4. Symmetrical swellings/arthritis
Duration
should be 6
weeks or
more
If four or more of these are present, it is Rheumatoid Arthritis

6. PATHOLOGY
• Initially the synovium becomes oedematous, filled with fibrin
exudates and cellular infiltrates. There is an increase in synovial
fluid.
• As the inflammation persists, the synovium gets hypertrophied
and surrounds the periphery of the articular cartilage to form a
pannus.
• The articular cartilage loses its smooth shiny appearance.

7. • The pannus extends over the cartilage from the periphery and
burrows into the subchondral bone.
• With further progress of the disease, the cartilage becomes worn
off and the bone surfaces become raw.
• The joints gets deformed, initially because of severe muscle
spasm associated with pain, but later due to fibrosis of the
capsule and other soft tissue structures.
• In some cases, adhesions develop between apposing layers of
pannus, leading to fibrous ankylosis, and later bony ankylosis.
PATHOLOGY

8. CLINICAL FEATURES
• It occurs between the age of 20 to 50 years.
• Women are affected about 3 times more commonly than men.
• Following presentations are seen:
Joints affected in Rheumatoid arthritis
Common • MCP joints of hand
• PIP joints of fingers
• Wrists, knees, elbows, ankles
Less common • Hip joint
• Temporo-mandibular joint
Uncommon • Atlanto-axial joint
• Facet joints of cervical spine

9. ON EXAMINATION
• One finds swollen boggy joints as a result of intra-articular effusion,
synovial hypertrophy and oedema of the periarticular structures. The
joints may be deformed.
Deformities in Rheumatoid arthritis
Hand • Ulnar drift of the hand
• Boutonniere deformity
• Swan neck deformity
Elbow • Flexion deformity
Knee • Flexion deformity
Ankle • Equinus deformity
Foot • Hallux valgus, Hammer toe, etc.

10. Extra-articular manifestations of Rheumatoid arthritis
Vasculitis • Digital arteritis
• Raynaud's phenomenon
• Fever, skin lesions, chronic leg ulcers
• Peripheral neuritis (mononeuritis multiplex)
• Necrotising arteritis involving coronary, mesentric or renal vessels
Rheumatoid
nodules
• Commonest site - olecranon
• Other sites - dorsal surface of forearm, tendoachilles
Serositis • Lung and pleura - pleurisy, parenchymatous nodules, Caplan's syndrome, Honey
comb lung
• Heart - cardiomyopathy, pericarditis
• Eye - iridocyclitis
• Nervous system - peripheral neuritis, carpal tunnel syndrome
Others • Anaemia
• Felty's syndrome
• Sjogren's syndrome
• Amyloidosis

11. INVESTIGATIONS
1) Radiological examination: This consists of X-
rays of both hands and of the affected joints.
• Reduced joint space
• Irregular subchondral erosions of affected
joints.
• Subchondral cysts formation
• Juxta-articular rarefaction
• Soft tissue shadow at the level of the joint
because of joint effusion or synovial
hypertrophy
• Deformities of the hand and fingers
Fig: X-rays of both hands, AP view, showing
juxta-articular rarefaction

12. 2) Blood: It shows the following changes:
• Elevated ESR
• Low haemoglobin value
• Rheumatoid factor (RF): Positive
3) Synovial fluid examination and Synovial biopsy: Arthroscopically or
by open methods.
INVESTIGATIONS
• All patients with positive rheumatoid factor do not have RA.
• Conversely, all patients with RA do not have a positive rheumatoid factor.

13. DIFFERENTIAL DIAGNOSIS
a) Systemic lupus erythematosus (SLE):
• In SLE, the joint involvement is not symmetrical; nor are ankylosis
and erosions common.
• Absence of anti-nuclear antibody factor (ANF) is in favour of
rheumatoid arthritis, although its presence does not confirm SLE. It
is present in 25 per cent cases of RA.
b) Osteoarthritis:
• This occurs in older patients.
• There is complete lack of the systemic features of RA such as fever,
weight loss, fatigue, etc.
• Distal inter-phalangeal (DIP) joints are often involved.
• Duration of morning stiffness, joint swelling, ESR etc., are less
compared to RA.

14. c) Psoriatic arthropathy:
• Characteristic skin and nail lesions may be present.
• Distal inter-phalangeal joints are usually involved.
• Rheumatoid factor is negative.
DIFFERENTIAL DIAGNOSIS

15. Principles of treatment
a) Induction of remission and its maintenance:
• To be brought under control by drugs.
b) Preservation of joint functions and prevention of deformities:
• Physical therapy, Occupational therapy, Rehabilitation -
Orthosis/ splintage.
c) Repair of joint damage:
• Require surgical intervention.

16. METHODS OF TREATMENT
• Medical treatment: These consist of anti rheumatic
drugs:
(i) Non-steroidal anti-inflammatory drugs (NSAIDs)
(ii) Disease modifying anti-rheumatic drugs (DMARDs)
(iii) Steroids.

17. Non-Operative Methods
A) Physiotherapy: This consists of:
(i) Splintage of the joints in proper position during the acute
phase
(ii) Heat therapy – wax bath, hot water fomentation for
symptomatic relief
(iii) Joint mobilisation exercises to maintain joint functions
(iv) Muscle building exercises to gain strength.

18. B) Occupational therapy:
• To help the patient cope with his occupational requirements
in the most comfortable way or by modifying them.
C) Rehabilitation:
• To improve the functions of the patient with the help of
devices like braces, walking aids etc.
Non-Operative Methods

19. • Surgical treatment of rheumatoid arthritis can be divided into:
(i) Preventive surgery: This is done to prevent damage to the joint
and nearby tendons by the inflamed, hypertrophied synovium. It
consists of synovectomy of the wrist, knee and MP joints.
(ii) Palliative surgery: This is done in situations where general
condition of the patient does not permit corrective surgery, but
some relief can be provided by limited surgical procedures such
as bone block operations, tendon lengthening etc.
Operative Methods

20. iii) Reconstructive surgery: It includes tendon transfers,
interposition arthroplasties and total joint replacement. With
improvement in surgical techniques and better design of artificial
joints, it is now possible to replace any joint of the body.
iv) Salvage surgery
Non-Operative Methods

21. • Soft tissue release
• Tendon repair
• Osteotomy
• Excision Arthroplasty
• Joint replacement
• Arthrodesis
Operative Methods

23. ANKYLOSING SPONDYLITIS
(Marie strumpell disease)
ETIOLOGY
• A strong association has been found between a genetic
marker—HLA-B27 and this disease.
• HLA-B27 is less than 1 per cent in general population.
• It is present in more than 85 per cent of patients with AS.
This is a sero-negative, progressive inflammatory disease presenting
with pain and stiffness of the spine leading to bony ankylosis of the
sacroiliac and spinal joints.

24. PATHOLOGY
Sacro-iliac joints are usually the first to get involved
Followed by the spine from the lumbar region upwards.
The hip, manubrio-sternal joints are also involved frequently
Initially Synovitis occurs
Followed by cartilage destruction and bony erosion.
Ultimately leads to fibrous, followed by Bony Ankylosis.
Ossification also occurs in the anterior longitudinal ligament and other ligaments of the spine.
After bony fusion occurs, the pain may subside, leaving the spine permanently stiff
(burnt out disease)

25. CLINICAL FEATURES
• This is a disease of young adults, more common in males (M:F=10:1).
• Classic presentation: The patient is a young adult 15-30 years old male,
presenting with a gradual onset of pain and stiffness of the lower back.
• Initially, the stiffness may be noticed only after a period of rest, and improves with
movement.
• Pain tends to be worst at night or early morning, awakening the patient from
sleep.
• He gets better only after he walks about or does some exercises.
• There may be pain in the heel, pubic symphysis, manubrium sterni and costo-
sternal joints.
• In later stages, kyphotic deformity of spine and deformity of the hips may be
prominent features.

26. CLINICAL FEATURES
• Unusual presentations: Patient may
occasionally present with
involvement of peripheral joints
such as the shoulders and knees.
• Smaller joints are rarely involved.
• Sometimes, a patient with
ankylosing spondylitis may present
with chronic inflammatory bowel
disease.
X-rays showing changes in AS.
X-ray of the pelvis, AP view, showing bilateral
SI joint
and hip involvement.
X-ray of the lumbar spine, Lateral
view, showing calcification of the ligaments.

27. ON EXAMINATION
• Stiff spine: There may be a loss of lumbar lordosis. Lumbar spine flexion
may be limited.
• Tests for detecting sacro-iliac involvement:
• Tenderness, localised to the posterior superior iliac spine or deep in the
gluteal region.
• Sacro-iliac compression: Direct side to side compression of the pelvis may
cause pain at the sacro-iliac joints.
• Gaenslen's test: The hip and the knee joints of the
opposite side are flexed to fix the pelvis, and the
hip joint of the side under test is hyperextended
over the edge of the table. This will exert a
rotational strain over the sacro-iliac joint and give
rise to pain

28. • Straight leg raising test: The patient is
asked to lift the leg up with the knee
extended. This will cause pain at the
affected SI joint.
• Pump-handle test: With the patient lying
supine, the examiner flexes his hip and
knee completely, and forces the affected
knee across the chest, so as to bring it
close to the opposite shoulder. This will
cause pain on the affected side.
ON EXAMINATION

29. • Tests for cervical spine involvement: In advanced stages, the cervical
spine gets completely stiff. The Fle'che test may detect an early
involvement of the cervical spine.
• Fle'che test: The patient stands with his heel and back against the wall
and tries to touch the wall with the back of his head without raising the
chin. Inability to touch the head to the wall suggests cervical spine
involvement.
• Thoracic spine involvement: Maximum chest expansion, from full
expiration to full inspiration is measured at the level of the nipples. A
chest expansion less than 5 cm indicates involvement of the costo-
vertebral joints.
ON EXAMINATION

30. EXTRA-ARTICULAR MANIFESTATIONS
• Ocular: About 25 % patients develop acute iritis , many suffers from recurrent
episodes, resulting in scarring and depigmentation of iris.
• Cardiovascular: Long standing illness develops manifestations in the form of
aortic incompetence, cardiomegaly, conduction defects, pericarditis etc.
• Neurological: Spontaneous dislocation and subluxation of the atlanto-axial joint
or fractures of the Cx spine with trivial trauma, presents with signs and symptoms
of spinal cord compression.
• Pulmonary: Involvement of costo-vertebral joints leads painless restriction of
thoracic cage, detected by diminished chest expansion, or PFT. Bilateral apical
lobe fibrosis with cavitation may occur, which simulates TB on X-ray.
• Systemic: Osteoporosis occurs commonly and occasionally, may develop
amyloidosis.

31. INVESTIGATIONS
Following changes may be seen on X-ray of the pelvis:
• Haziness of the SI joints
• Irregular subchondral erosions in SI joints
• Sclerosis of the articulating surfaces of SI joints
• Bony ankylosis of the SI joints
• Calcification of the SI ligament and sacro-tuberous ligaments
• Evidence of enthesopathy – calcification at the attachment of
the muscles, tendons and ligaments, particularly around the
pelvis.

32. X-ray of the lumbar spine may show the following:
• Squaring of vertebrae: The normal anterior concavity of the vertebral body is
lost because of calcification of the anterior longitudinal ligament.
• Loss of the lumbar lordosis.
• Bridging ‘osteophytes’ (syndesmophytes)
• Bamboo spine appearance.
Other investigations are the following:
• ESR: elevated
• Hb: mild anaemia
• HLA-B27: positive
INVESTIGATIONS

33. TREATMENT
Conservative methods:
(i)Drugs—NSAIDs are given for pain relief; Indomethacin is effective in
most cases; long acting preparations are preferred;
(ii) Physiotherapy -posture guidance, electrotherapy (heat therapy), mobility
maintenance exercises
(iii) Radiotherapy – in resistant cases
(iv) Yoga
Operative methods:
• Correction of kyphotic deformities of the spine by spinal osteotomy
• Joint replacement in hip or knee joint ankylosis.

35. OSTEOARTHRITIS
• Osteoarthritis (OA) is a degenerative joint disease. Two types of OA are recognized:
• Primary OA: This occurs in a joint at old age, mainly in the weight bearing joints
(knee and hip).
• The trapezio-metacarpal joint of the thumb and the distal IP joints of the fingers are
also affected.
• Secondary OA: There is an underlying primary disease of the joint which leads to
degeneration of the joint, often many years later.
• Predisposing factors are: (i) congenital maldevelopment of a joint (ii) irregularity of
the joint surfaces from previous trauma (iii) previous disease producing a damaged
articular surface (iv) internal derangement of the knee, such as a loose body (v) mal-
alignment (bow legs etc.) (vi) obesity and excessive weight.

36. 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 hip (CDH)
• Old septic arthritis of the hip
• Malunited fractures
• Fractures of the acetabulum

37. PATHOLOGY
• The degeneration primarily affects the articular cartilage by increase in
water content and depletion of the proteoglycans from the cartilage
matrix.
• Repeated weight bearing on it leads to its fibrillation.
• The cartilage gets abraded by the grinding mechanism at points of
contact between the apposing articular surfaces, until eventually the
underlying bone is exposed.
• With further ‘rubbing’, the subchondral bone becomes hard and glossy
(eburnated).

38. • The bone at the margins of the joint hypertrophies to form a rim of projecting
spurs known as osteophytes.
• A similar mechanism results in the formation of subchondral cysts and sclerosis.
• The loose flakes of cartilage incite synovial inflammation and thickening of the
capsule, leading to deformity and stiffness of the joint.
• Often one compartment of a joint is affected more than the other. eg, in the knee
joint, the medial compartment is affected more than the lateral, leading to a varus
deformity (genu varum).
PATHOLOGY

39. ON EXAMINATION
Following findings may be present:
• Tenderness on the joint line
• Crepitus on moving the joint
• Terminal limitation of joint movement
• Irregular and enlarged-looking joint due to formation of peripheral
osteophytes
• Effusion – rare and transient
• Deformity – varus of the knee, flexion-adduction-ER of the hip
• Subluxation detected on ligament testing
• Wasting of quadriceps femoris muscle

40. The following are some of the radiological features:
• Narrowing of joint space, often limited to a part of the joint
e.g., may be limited to medial compartment of tibio-femoral
joint of the knee.
• Subchondral sclerosis – dense bone under the articular surface
• Subchondral cysts
• Osteophyte formation
• Loose bodies
• Deformity of the joint
RADIOLOGICAL -INVESTIGATIONS

41. These consist of the following:
• Serological tests and ESR to rule out Rheumatoid arthritis
• Serum uric acid to rule out Gout
• Arthroscopy, if a loose body or frayed meniscus is suspected
OTHER -INVESTIGATIONS

42. KELLGREN AND LAWRENCE SYSTEM FOR
CLASSIFICATION OF OSTEOARTHRITIS OF KNEE
• The Kellgren and Lawrence system is a common method of classifying the
severity of knee OA using five grades. This classification was proposed by
Kellgren et al. in 1957 and later accepted by WHO in 1961.
CLASSIFICATION
• Grade 0: No radiographic features of OA are present
• Grade 1: Doubtful joint space narrowing (JSN) and possible osteophytic lippings
• Grade 2: Definite osteophytes and possible JSN on anteroposterior weight-
bearing radiograph
• Grade 3: Multiple osteophytes, definite JSN, sclerosis, possible bony deformity
• Grade 4: Large osteophytes, marked JSN, severe sclerosis and definite bony
deformity

43.  Drugs: Analgesics are used mainly to suppress pain.
 Chondroprotective agents: Glucosamine and Chondroitin sulphate
repairs damaged cartilage.
 Viscosuplementation: Sodium Hylarunon injected in the joint 3-5
times at weekly interval. Improves cartilage functions, and is
chondroprotective.
 Local application of counter-irritants and liniments provides
dramatic relief.
METHODS OF TREATMENT

44.  Supportive therapy: It consists of the following:
• Weight reduction, in an obese patient.
• Avoidance of stress and strain to the affected joint in day-to-day
activities. For example, a patient with OA of the knee is advised to
avoid standing or running whenever possible.
• Sitting cross legged and squatting to be avoided.
• Local heat relieves pain and stiffness.
• Exercises for building up the muscles controlling the joint help in
providing stability to the joint.
METHODS OF TREATMENT

45. Surgical treatment:
• Osteotomy: A high tibial osteotomy for OA of the knee with genu varum and
inter-trochanteric osteotomy for OA of the hip have been shown to be useful for
pain relief.
• Joint replacement: An artificial joint serves for about 10-15 years.
• Joint debridement: Affected joint opened, degenerated cartilage smoothened,
osteophytes and the hypertrophied synovium excised.
• Arthroscopic procedures: Arthroscopic removal of loose bodies, degenerated
meniscal tears, fibrillated cartilage is excised.
METHODS OF TREATMENT

47. Gout
• Disturbed purine metabolism leading to excessive accumulation of uric
acid in the blood — an inherited disorder; or impaired excretion of uric
acid by the kidneys.
• The result is accumulation of sodium biurate crystals in some soft tissues.
• Tissues of predilection are cartilage, tendon, bursa.
• Patient, usually beyond 40 years of age, presents as
(i) Arthritis – MP joint of the big toe being a favourite site, onset is acute,
pain is severe
(ii) Bursitis – commonly of the olecranon bursa
(iii) Formation deposit of uric acid salt in the soft tissue
• Confirmation of diagnosis – urate crystals in the aspirate from a joint or
bursa, high serum uric acid levels
• Treatment – NSAIDs, uricosuric drugs, uric acid inhibitors.
• Cryotherapy (crushed ice pack), other non thermal modalities to reduce
inflammation and pain.

48. Pseudogout
• Calcium pyrophosphate (CPP) crystal
deposition
• Symptoms like those of gout
• Meniscus calcification may be seen on X-rays
of the knee
• Treatment – NSAIDs (Rx same as gout).

49. Psoriatic arthropathy
• Presentation is like rheumatoid arthritis – a
polyarthritis, distal IP joints of hands involved
(unlike rheumatoid arthritis, where these are spared)
• The autoimmune disease has classic skin lesions (dry,
itchy, and scaly) help in diagnosis
• Treatment is by steroids.

50. Alkaptonuric arthritis (Ochronosis)
• An inherited defect in enzyme system involved in metabolism of phenylalanine and
tyrosine.
• As a result homogentisic acid is excreted in patient's urine.
• As a long term result, it accumulates in the cartilage and other connecting tissues.
• Joint symptoms occur after 40 years of age.
• Spine and shoulder joint are commonly affected.
• X-ray – disc space calcification, peri-articular calcification in large joints.
• There may be evidence of pigment deposit in the sclera.
• Homogentisic acid is present in the urine, and results in the colour of the urine turning
dark brown on standing (due to oxidation of homogentisic acid on exposure to air)
• Treatment same as that for osteoarthritis.

51. Haemophilic Arthritis
• Occurs due to a number of bleeding disorders
• Occurs in males
• Joints affected commonly are knee, elbow and ankle
• May present as acute or chronic haemarthrosis. There are other manifestations
of bleeding disorders
• X-ray – non-specific signs including bone resorption, cyst formation,
osteoporosis, widening of intercondylar notch in the knee.
• Treatment – rest during acute stage along with factor VIII supplementation or
other deficient factor replacement.
• In the chronic stage, physical therapy, bracing and others are required.
• Deformities may be corrected by conservative or operative methods.

52. Neuropathic Arthropathy (Charcot's joint)
• These are changes seen in a neuropathic joint, where repeated
strain on a joint due to loss of sensations leads to severe
degeneration
• Clinically, the joint manifests as painless effusion, deformity or
instability
• The X-ray changes are those of severe osteoarthritis but without
much clinical findings like pain, muscle spasm etc.
• Bracing is usually advised for some joints.
• Fusion of the joint may be required.

53. THANK YOU
Dr. Sanjib Kumar Das
MPT (Musculoskeletal),
Fellow Doctoral, NITIE- Ergonomics and Human Factors,
AIPT, Amity University, Noida
Mail: sanjib_bpt@yahoo.co.in
Contact: +91 8169951520