Rheumatoid Arthritis

- a major subclassification within the category of diffuse connective tissue

disease. (O’Sullivan p.1057).
- a connective tissue disease characterized by chronic inflammatory changes in
the synovial membrane and other structures, by migratory swelling and stiffness
of the joints in it’s early stage, and by a variable degree of deformity, ankylosis,
and invalidism in its late stage. (Brashear p.140)

Related Anatomy (Tortora 10th Edition pg. 245-250)

Joints
Site where 2 or more bones come together, whether or not there is movement between
them.

Classification according to tissues lies between the bones:

I. Fibrous Joints
The bones are held together by fibrous connective tissue. Very little movement is
possible between the bones. The degree of movement depends on the length of the collagen fibers
uniting the bones.

Ex: Sutures of the vault of the skull and inferior tibiofibular joints.

Types of Fibrous Joints:

• Sutures- a fibrous joint composed of a thin layer of dense connective tissue that unites
only bones of the skull.
• Syndesmoses- a fibrous joint in which, compared to suture, there is a greater distance
between the articulating bones and more fibrous connective tissue.
• Dentoalveolar- or Gomphoses, a fibrous joint in which cone shaped peg fits into the
socket.

II. Cartilaginous Joints

Lack a synovial cavity allows little or no movement. The articulating bones are tightly
connected by hyaline cartilage.

Types of Cartilaginous Joints:

• Synchondroses- are a cartilaginous joint in which the connecting material is hyaline
cartilage.
• Symphyses- are a cartilaginous joint in which the end of the articulating bone are covered
with hyaline cartilage connects the bones.

III. Synovial Joints

The unique characteristics of synovial joint is the presence of synovial cavity between
articulating bones it allows a joint to be freely move.

Classification according to the arrangement of the articular surfaces and type of joint
movement:

• Plane Joints
- the apposed articular surfaces are flat or almost flat
 - permits the bone to slide upon each other
- Ex. SC joint and AC joint
• Hinge Joints
- resembles the hinge in a door
- allows flexion and extension
- Ex. elbow, knee and ankle joints

• Pivot joints
- have a central body pivot surrounded by a ligamentous ring
- rotation only movement possible
- Ex. atlanto-axial joint and radioulnar joint

• Ellipsoid Joints
- there is an elliptical convex articular surface that fits into an elliptical concave
articular surface.
- allows flexion, extension, abduction, adduction but not rotation
- Ex. wrist joint

• Condyloid Joints
- have to distinct convex surfaces that articulates with 2 concave surfaces
- allows flexion, extension, abduction, adduction and small amount of rotation
- Ex. MCP joint

• Saddle Joints
- the articular surfaces are reciprocally concavoconvex and resembles a saddle on a
horse back.
- allows flexion, extension, abduction, adduction and rotation
- Ex. CMC joint of the thumb

• Ball and Socket Joints

- a ball-shaped head of one bone fits into a socket like concavity of another
- allows flexion, extension, abduction, adduction, lateral rotation, medial rotation and
circumduction.

 Stability of a joint depends on 3 main factors (De Lisa pg. 722)

- the shape, size, and the arrangement of the articular surfaces
- the ligaments surrounds the joint
- muscle tone

The 1987 Revised Criteria For the Classification of RA (O’Sullivan p.1058. table 26.1)

Criterion Definition
1. Morning Stiffness 1. morning stiffness in and around the
joints, lasting at least one hour before
maximal improvement
2. Arthritis of 3 or more joint areas. 2. at least 3 joint areas simultaneously have had
soft tissue swelling or fluid (not bony
overgrowth alone) observed by a physician.
The 14 possible areas are right or left PIP,
 MCP, wrist, elbow, knee, ankle and MTP
joints.
3. Arthritis of hand joints 3. at least one area swollen (as defined above)
in a wrist, MCP, or PIP joints.
4. Symmetric Arthritis 4. Simultaneous involvement of the same areas
(as defined in 2) of both sides of the body
(bilateral involvement of PIPs, MCPs, or MTPs
is acceptable without absolute symmetry.)
5. Rheumatoid Nodules 5. Subcutaneous nodules, over bony
prominences, or extensor surfaces, or in
juxtarticular regions, observed by a physician.
6. Serum Rheumatoid Factor (RF) 6. Demonstration of abnormal amounts of
serum rheumatoid factor by any method for
which the result has been positive in <5% of
normal control subjects.
7. Radiographic changes 7. Radiographic changes typical of RA on
posteroanterior hand and wrist radiographs,
which must include erosions or unequivocal
bony decalcification localized in or mosr
marked adjacent to the involved joints (OA
changes alone do not qualify)

**For classification purposes, a patient shall be said to have RA if s/he has satisfied at least 4 of
these 7 criteria.
**Criteria 1 through 4 must have been present for at least 6 weeks.

Important determinants in classifying arthritis (De Lisa pg.722)

• Inflammatory or non-inflammatory
• Symmetrical or asymmetrical
• Accompanied by systemic and extrarticular manifestation

Clinical features that suggest inflammatory disease (De Lisa pg. 722)
• Acute painful onset
• Fever
• Erythema of the skin over the joint/s involved
• Warmth of the joint/s
• Tenderness (usually parallels the degree of inflammation)

Inflammation arthritis falls into 4 different groups

• Inflammatory connective tissue diseases (Ex. RA, JRA, SLE, DM-PM mixed
connective tissue diseases)
• Inflammatory crystal-induced disease (Ex. gout and pseudogout)
• Inflammation induced by infectious agents (Ex. bacterial, viral, TB and fungal
arthritis)
• Seronegative spondyloarthropathies
- Ankylosing spondylitis
- Psoriatic arthritis
- Reiter’s disease
- Inflammatory bowel diseases
 EPIDEMIOLOGY
» Affects women 2x to 4x more often than men at all ages. (O’Sullivan p.1058)
» 80% of cases begin in persons bet. 25 and 50 years of age; highest incidence is about 35 &
40 years of age. (Brashear p141)

ETIOLOGY (O’Sullivan p.1058-1059)

» UNKNOWN.
» Some theory believe that RA is an autoimmune disorder based on the fact that individuals
with RA produce antibodies to their own immunoglobulins. But it is not clear wheater this
antibody production is a primary event or results as a response to a specific antigen from an
external stimulus.
» Current theory and research of on the cellular basis of autoimmunity suggest that abberant
functioning of cell mediated immunity and defective T lymphocytes may trigger the
autoimmune response that underlie RA.
» Other bacterial organism such as streptococcus, clostridia, diptheroidsand mycoplasmas,
but no connection have been definitely proven.
» Rheumatoid Factor (RF)- they are found in the sera of approx. 70% of all RA patients.
- it is an antibodies specific to IgG
- RA occurs in the absence of RF in substantial number of
ndividuals.

PATHOLOGY (O’sullivan p.1059)

1. Long standing RA- char. By grossly edematous appearance of the synovium c slender
villous or hair-like projections into the joint cavity.
2. (+) distinctive vascular changes: venous distention, capillary obstruction, neutrophilic
infiltration of the arterial walls and areas of thrombotic hemorrhage.
3. synovial proliferation of vascular granulation known as Pannus, dissolves collagen as it
extends over the joint cartilage.
4. if RA continues the Pannus will result in fibrosis or Bony ankylosis of the joint.
5. Chronic inflammation can weaken the joint and it’s supporting ligaments and may lead
to tendon rupture and fraying tendon sheaths may caused imbalanced muscle pull on
these pathologically altered joint, resulting in musculoskeletal deformities seen in RA.

PATHOPHYSIOLOGY (O’sullivan p.1059)

Key features: synovial joints (susceptible to persistent inflammation)
↓
Rapid changes in the cellular content and vol of synovial fluid ff alterations in blood flow
↓
Low pressure to joint space and the lack of limiting membrane bet jt space and synovial blood
vessels
↓
Hig mol subs (macgroglobulins & fibrinogens) can pass through the synovial capillary during
perion of inflammation and are not easily cleared
↓
Antigen-antibody complexes may be sequestered bt the joint cavity and may facilitate process of
phagocytosis and further devlt of pannus
↓
 In established synovitis, poly morphonuclear (PMN) leukocyte are chemotactically drawn in to
the joint cavity and may contribute to unflammatory destruction of synovium (unknown exact
mechanism)
↓
PMN leukocyte releases lysozomal enzymes can directly injure synovial tissue.

VARIANTS OF RA (Brashear. P.147-148)

1. Juvenile RA (JRA) / Still’s dse

an uncommon crippling dse. Of childhood, the systemic form of which is
associated c fever and enlargement of lymph nodes and spleen
sometimes continues into adult life
Manifestation: Morbiliform rash & severe systemic manifestation.
Prognosis: usually favorable c ¾ of patients
Complication: Iridocyclitis and may lead to blindness
(-) RF

2. Felty’s Syndrome
 A severe arthritis associated c leucopenia, splenomegaly, subcutaneous
nodules, and high titers of RF in serum.

3. Reiter’s Syndrome
 An ill-defined disease occurring chiefly in adult male
 Triad: Polyarthritis, nongonorheal urethritis, conjunctivitis.
 May be an allergic response to Chlamydia, Shigella or other infectious
organism.
 >75% have HLA-B27 phenotype suggesting a genetic-based susceptibility.

4. Psoriatic Arthritis
 A polyarthritis resembling but probably distinct from RA, which is associated
with psoriasis
 Features: involvement of DIP, sometimes associated c marked destruction of
bone (arthritis mutilans), (-) subcutaneous nodules, (-) RF in the serum.
 Spondylitis may be associated with this.

5. Palindromic Rheumatism
 Characterized by brief episodes of acute arthritis with signs of local
inflammation but without residual joint damage.
 May be an atypical or prodromal form of RA or other connective tissue
disease.

6. Intermittent Hydrarthrosis
 A recurring joint effusion characterized by absence of acute inflammatory
signs and by a relatively constant periodicity
 Most affected: Knee

7. Ankylosing Spondylitis
 A chronic arthritis usually beginning in the sacroiliac joint and lumbar spine
 and extending proximally.

8. Enteropathic Arthritis
 A peripheral polyarthritis associated c chronic bowel disease (ulcerative
colitis or Crohn’s disease)

SIGNS AND SYMPTOMS:( Brashear p. 143-144)

Insidious onset (75% of cases)
Joint pain
Stiffness (esp. in morning)
Fleeting pains in 1 or more joints.
Later Stage:
Painful joint upon motion
Pain tends to worst at bad weather, overexcercise and fatigue
Constitutional symptoms
Weakness
Fatigue’
Malaise
Low-grade fever

ROENTGENOGRAPHIC PICTURES :( Brashear p. 144-145)

Early Stage:
 Swelling of tissues on affected joints
 Distended joint capsule by increased synovial fluid
 Slight bone atrophy
 Contour of articular surface is not necessarily altered.
Later Stage:
 Cartilage space become uniformly narrowed.
 Small areas of bone absorption (punched-out areas), develop near the joint margins & the
attachments of synovial membrane and ligaments.
Advanced Stage:
 extensive bone erosions and produce cyst-like areas adjacent to the joints.
 Subluxation or dislocation (esp. in MCP & MTP)
 Articular margins shows bony spurs, ridges and prominences
 Articular surface may become ankylosed

LABORATORY FINDINGS: :( Brashear p. 145-146)

 Elevated Erythrocyte sedimentation rate (ESR)
 Slight leukocytosis
 Alpha2 fraction of gamma globulin is often increased
 Low level of serum albumin
 Serum will agglutinate or flocculate suspended particles (hemolytic streptococci, sheep
erythrocyte, latex, and bentonite sensitized c human gamma globulin.)
 The synovial fluid:
 appears cloudy, and when acetic acid is added, it’s mucin clot is friable.
 Decreased viscosity
 High white cell count (vary c severity)
 Numerous neutrophils (during acute attacks)
  Most of cells are lymphocytes (chronic stage)
 WBC is usually bet. 5000 & 20,000 cells/mm3.
 Complement levels, esp. C2 & C4, are low, oftel <1/3 of the serum values,
suggesting an active immune process in the joint.

TREATMENT :( Brashear p. 148-151)

I. General Measures
During Acute stages Brief period of bed rest
Patient’s posture in bed must be supervised
 Ankles should not be held in equinus by tight sheets, nor the knees supported
in flexion on pillows.
 Neck, low back or hips should not be kept in flexed position for a long period
of time while the patient is sitting
 A program of exercises for recumbent patient should be prescribed and carried
out regularly, with emphasis on major muscle groups in the trunk and lower
limb, particularly the extensor muscle.

II. Drug Therapy

No curative drug for RA has been found
There are preparations that are currently use for arthritis but these drugs have
serious side effects, the hazards of each must be carefully weighed against it’s
effectiveness.
The LEAST TOXIC, BEST TOLERATED, and MOST AVAILABLE drug
must be used FIRST.
The more dangerous with significant side effects should be held for reserve
for most severe cases.
Salicylates
most helpful in alleviating pain and suppressing inflammation, are the
mainstay in the primary treatment of RA.
2. Aspirin
 most commonly used drug.
 Dosage: 1 to 3 325mg (g-grain) tablets 2x to 6x a day (depending on
the severity of arthritis and patient’s tolerance)
 Complication: gastrointestinal bleeding (result from local irritation or
interference c platelet fxn)
3. Phenybutazone
 Often relieve arthritic symptoms, but it is no way curative.
 Too dangerous to be given over a long period of time.
 Dosage: initially, 600mg a day & gradually reduced to 100 to 200 mg
daily.
 Complication: rash, thrombocytopenia, or symptoms suggesting
peptic ulcer appear.
4. Indomethacin
 Anti-inflammatory drug sometimes helpful to RA.
 Dosage: 25-50mg tid
 Complication: GI bleeding or ulceration (upon prolonged treatment)
 CI: children
 5. Anti-malarial compounds
Hydroxychloroquine, often seem to exert a slow but long-lasting
suppressive effect in RA.
 Complication: retinal damage.

6. Soluble Gold Salts or Chrysotherapy

May suppress or even arrest the active rheumatoid process and so
induce lengthy remission.
Its mode of action is poorly understood.
Gold salts, are given in intramuscular injection in small doses over a
long period of time.
The usefulness of it is limited to it’s toxic effect on bone marrow,
kidneys and spleen.

7. D-Penicillamine
 May be helpful in refractory cases of RA and is used in place of gold
when toxic reaction develop to gold therapy.
 Complication: can cause disease to kidneys, bone marrow, skin and CNS.

8. Corticosteroid
 Have a limited space in systemic treatment of RA.
 They are potent anti-inflammatory agents that may produce dramatic
alleviation of symptoms and signs, reduction of fever, reversal of abnormal
laboratory findings, and psychologic improvement.
 However, they do not alter the pathologic process of RA.
 Their suppressive action is temporary.
 Complication: adrenocortical hyperfunction in cushing’s syndrome. Skeletal
demineralization, pathologic fractute, peptic ulcer, edema, from sodium and
water retention, hyperkalemia and muscle weakness, depressive psychosis,
reactivation of infection,

9. Steroids
 Should be reserved for temporary use in small doses as supplementary
treatment for patients in whose joints rheumatoid inflammation is not
adequately suppressed by other forms of treatment.

II. Local Joint Treatment

 In acute arthritis the pain is sometimes so severe that it is advisable to provide
rest for the joint by immobilizing it in a light splint or plaster cast.
 Aspiration of synovial fluid will sometimes relieved the pain of an acutely
distended joint capsule.
 Synovectomy, it is the excision of the lining of a joint . commonly used in
wrist, knee, MCP joints.
 Tenosynovectomy, excision of tendon sheath lining. Most value at wrist and
MCP.
V. PT management
1. HMP
2. Infrared Radiation
3. Whirlpool baths
 4. Diathermy
5. Paraffin wax bath for arthritic hands and feet.
6. Gentle massage – of muscles above and below affected joint after applying
heat.
7. Active Exercise of affected joints without weight bearing
– to minimize joint stiffness and muscle atrophy.

RA IN SPECIFIC REGION OF THE BODY:

1. SPINE (Brashear p. 153)
 Incidence
 Women > Men
 Bet. 25 & 45 years of age.
 Pathology
 Synovitis of facet joints (initial change)
 Vertebrae and cartilages become atrophic.
 Cervical spine subluxation of slight degree are common.
 One of the most dangerous life-threatening complications is the
subluxation of C1 to C2 vertebra.
 Later stage: spine is more likely to develop fibrous ankylosis.
 Subcutaneous nodules of RA may be present.
 Clinical Picture
 Back pain and stiffness
 Worse discomfort upon bending and lifting
 Symptoms begin from cervical region but in other patient its from lumbar.
 Sometimes pain may radiate to the front of the chest and abdomen or down the
thigh.
 Coughing and sneezing often cause sharp pain in the back
 As the disease progress muscle spasm and contracture may lead to dorsal
kyphosis.
 The stiffness may become greater but usually does not progress to bony ankylosis.
Differential Diagnosis
 Ankylosing Spondylitis, OA, tuberculosis, malignancy, IVD lesion,
vertebral epiphysitis, fracture, sprain, visceral disease with referred pain.
Treatment
Careful assessment of cervical spine stability should be made from
roentgenograms taken with the neck in flexion and extension.
When excessive instability is detected, posterior spinal fusion may be
advisable.

ANKYLOSING SPONDYLITIS (Brashear p. 153-157)

  One of group of seronegative (negative for RF)
spondyloarthropathies associated with HLA-B27 antigen. This group includes reiter’s
syndrome, psoriatic arthritis, intestinal arthroplasty and others.
 Characterized by ossification of the ligaments of the
spine and involvement also of the hips and shoulders.
 Sacroiliac joint affects early.
 10x common in men than in women.
 Begin bet. 20 & 30 years of age.
 (+) family history.
 Pathology
Progressive ossification occurs in the capsular and other intervertebral
ligaments, fusing the lower and, often in later stages, the entire spine into
the single mass.
 Costevertebral joints may become ankylosed.
 In the IVD, peripheral ossification occurs earlier than central ossification.
 Vertebral bodies become osteoporotic.
 Their contour changes little except in the dorsal spine, where they often
become wedge shape.
 They may be regular spur formation and lipping of vertebra.
 Clinical Picture
 Onset is associated with acute pain but stiffness without pain is sometimes
the first symptoms.
 Malaise and fatigability may be accompanied by weight loss.
 Pain first appears in hips, buttocks, or lumbosacral region.
 The pain, followed by stiffening, may progress very slowly from the low back
farther &farther upward until finally the entire spine becomes ankylosed.
 The hip becomes stiff, a characteristic gait develops in which the pelvis is
rotated from side to side to compensate for lack of hip motion.
Roentgenographic Picture
Earliest findings are changes in the density along the margins of the
sacroiliac joints.
 As the disease progresses small erosions and narrowing appear in the facet joints.
 Later changes: obliteration of sacroiliac and facet joint spaces, ossification of
longitudinal ligaments and the periphery of annulus fibrosus (appearance of
“bamboo spine”), and bony bridging of laminae and spinous process.
Diagnosis
High incidence in young men
Onset of symptoms start at low back & their small proximal
progression
Sedimentation rate is elevate (80% of cases)
(-) RF
(+) HLA-B27 (90% of cases)
Treatment
a. General Measure
 Ample arrest
 Well-balanced diet
 Aspirin for pain control
 Phenylbutazone
  Indomethacin
b. Local nonsurgical procedure
 Is used for the relief of pain & prevention and correction of deformity
 Bed rest for acutely painful stage
 Hyperextension exercise
 Three point brace – helps to prevent the development of kyphosis
 Breathing exercises – useful in maintaining vital capacity and lessening chest deformity.
c. Surgical procedures
 Osteotomy of the spine may be indicated to improve a severe, incapacitating
flexion deformity.
 Bilateral pelvic osteotomy for moderate improvement
 Joint replacement required for painful ankylosis of the hips.

2. TEMPOROMANDIBULAR JOINT (O’Sullivan p.1060)

 Involvement of this synovial joint results in an inability to open the mouth
fully (approx. 2 in.) c normal side-to-side gliding and protrusion.

3. SHOULDER (O’Sullivan p.1060)

 Site: GH jt., SC jt., or AC jt.
 This joints may demonstrate degeneration,pain, and los of ROM.
 Chronic inflammation of the shoulder causes the capsule and ligaments to
become distended and thinned.
 Joint surfaces may become eroded until shoulder become eventually unstable.
 Tendinitis and bursitis may complicate the management.

4. ELBOW (O’Sullivan p.1060)

 Inflammation, capsular and ligamentous distention and joint surface erosion
may lead to elbow disability and irregular or catching movements.

5. WRIST (O’Sullivan p.1060)

 Decrease power grasp because of early synovitis bet. The 8 carpal bones and
the ulna that leads to rapid development of flexion contracture.
 Chronic inflammation of the proximal row of carpal can lead to a volar
subluxation of the wrist and hand on the radius, accentuating the normal 10⁰
to 15⁰ of volar inclination of the carpus on the distal radius.
 Loss of radial ligamentous support
 Destruction of extensor carpi ulnaris
 Destruction of fibrocartilage on the distal side of ulna.
 The attenuation of these restraining structures allows the proximal carpals to
slide down the distal row of carpals in the wrist relative to the 2 bones of the
forearm, where normally there are 5⁰ to 10⁰ of ulnar deviation.
 Stenosing tenosynovitis of the first dorsal compartment of the wrist
(deQuervain’s disease) may also occur.

6. HAND JOINTS (O’Sullivan p.1060-1061)

 Metacarpophalangeal
 soft tissue swelling around the MCP joints is very common.
  The volar subluxation and ulnar drift of the MCPs frequently seen in RA are
thought to result from accentuation of the normal structural shapes of these
joints the tilt the proximal phalanges in ulnar direction.
 The anatomical placement and length of collateral ligamaents, which are most
stretched during MCP flexion, and the insertions of the intrinsics, which also
pull from the ulnar direction, also contribute to ulanr drift at MCP during hand
motion.
 Treatment: early synovectomy, may prevent or postpone the onset of severe deformities.
 PIP
Swelling of PIP joints produces a fusiform or “sausage-like” appearance in the
fingers.
 Swan Neck Deformity – PIP hypertext. & DIP Flexion.
 Boutonniere or buttonhole deformity – DIP extension c PIP flexion.
 As a result of extensor digitorum communis into the middle phalanx (known as central slip)
lengthens, and the lateral bands slide volarly to force the PIP into flexion.
 Osteophytes boby formation or outgrowths around the end of the joint
 DIP
Most often uninvolved in RA
Mallet Finger Deformity – the tendon of the extensor digitorum communis will rupture, and the
unopposed pull of the flexor digitorum profundis will pull the DIP into flexion.
Thumb
The fibers of the dorsal hood mechanism over the MCP, the joint capsule and
the collateral ligaments and the tendons of extensor pollicis longus are
particularly affected.
 Type I deformity, MCP flexion c IP hypertext. Without involvement of CMC joint,
is most commonly seen.
 Type II deformity, subluxed CMC and IP held in hypertext.
 Type III deformity, more commonly found in RA than type II.
 Mutilans Deformity (Opera-Glass Hand)
Grossly unstable thumbs and severely deformed phalanges.
The transverse folds of the skin of the thumb and fingers resemble a folded
telescope.

Involvement of tendons and nerves (Brashear p.159)

the extensor tendon may be invaded by inflamed synovium and so weakened
that tendon rupture may occurs.
 Arthritic Nodule, may form within a tendon and impair it’s strength.
 other contributing of tendon ruptures are abrasion and attrition over a prominent bony
spiculeand ischemia from compression by a hypertrophied paratenon within an
inelastic fascial tunnel.
 Ruptures in extensors of liitle, ring and middle finger and long extensor of the thumb.
 Trigger finger, chronic synovitis in the flexor tendon sheaths may produce the
symptoms.
 CTS, compression of median nerve by the swelling of inflamed synovial lining of the
flexor tendon within the carpal tunnel.
 7. HIP (O’Sullivan p.1062)
 Although patients may present c complaints of pain in the groin, often owing to
trochanteric bursitis, the hip is less commonly involved in RA than in pother
kinds of arthritis.
 Severe inflammatory destruction of the femoral head and the acetabulum may
push the acetabulum into the pelvic cavity, a condition known as Protrusio
Acetabuli.

8. KNEE (O’Sullivan p.1062)

 One of the most frequently affected joints in RA because of the relatively large
amount of synovium in it.
 Chronic synovitis results in distension of the joint capsule, attenuation of
collateral and cruciate ligaments, and destruction of joint surfaces.
 Flexion contracture may occur, because of flexed position of knee when it’s
painful.

9. ANKLES AND FEET (O’Sullivan p.1062-163)

 Chronic synovitis accentuates the natural tendency of the talus to glide medially
and plantarward, resulting in pressure on the calcaneus and leading to hindfoot
pronation.
 The spring ligament is also stretched by these occurrences, flattening the medial longitudinal
arch.
 splayed forefoot, weakened transverse arch, metatarsal spread may develop.
 Synovitis of MTP joints is extremely common.
 Metatarsalgia, the pain over metatarsal head may occur.
 Hallux valgus or bunion, a painful bursitis over the medial aspect of 1st MTP
may be present.
 Hammer Toes, when volar subluxation combines with flexion of the PIP and hypertext.
Of the DIP joints.
 Cock up or claw toes, volar subluxation of metatarsal head with flexion of PIP and DIP
joints.

IMPAIRMENTS AND COMPLICATIONS (O’Sullivan p.1065-1066)

1. Deconditioning
 Patient’s are less physically fit (cardiorespiratory status, muscular strength and
endurance, flexibility and body composition)

2. Rheumathoid Nodule
 Most common extra-articular manifestations of RA
 Most commonly found in subcutaneous or deeper connective tissues in areas
subjected to repeated mechanical pressure.
 Usually asymptomatic, although they may be tender and may cause skin breakdown or become
infected.

3. Vascular Complication
 Most from of vascular lesions of RA are silent, although the fulminant form of rheumatoid
arteritis can be life-threatening, and accompanied malnutrition, infection,congestive heart
failure,and GI bleeding.
4. Neurological manifestation
 Mild peripheral neuropathies are often seen in RA, particularly in elderly patient and
are unrelated to vasculitis.
 Most neuropathies result from carpal and tarsal tunnel syndrome.

5. Cardiopulmonary Complication
 Pericarditis

6. Ocular Manifestation
 Ocular lesions are usually associated with the dry eyes of Sjogren’s syndrome,
which is an anti-inflammatory disorder of the lacrimal and salivary glands.
 Scleritis, and the relatively more benign episcleritis can also be present and
require careful medical treatment.

CLASSIFICATION OF PROGRESSION OF RA (O’Sullivan p.1065. table 26.1)

Stage I, early
No destructive changes on radiographic examination
radiographic evidenc of osteoporosis may be present

Stage II, Moderate

Radiographic evidence of osteoporosis, with or without slight subchondral bone
destruction; slight cartilage destruction may be present.
No joint deformities, although limitation of joint mobility may be present
Adjacent muscle atrophy
Extra-articular soft tissue lesions, such as nodules and tenosynovitis may be
present.

Stage III, Severe

1. Radiographic evidence of cartilage and bone destruction, in addition to osteoporosis.
2. Joint deformity, such as subluxation, ulnar deviation, or hypertext., without fibrous por
bony ankylosis.
3. Extensive muscle atrophy.
4. Extra-articular soft tissue lesions, such as nodules and tenosynovitis may be present.

Stage IV, Terminal

1. Fibrous or bony ankylosis
2. Criteria of stage III

AMERICAN COLLEGE OF RHEUMATOLOGY REVISED CRITERIA FOR

CLASSIFICATION OF FUNCTIONAL STATUS IN RA
(O’Sullivan p.1066 table 26.2)
CLASS I Completely able to perform usual activities of daily living.
CLASS II Able to perform usual selfcare and vocational activities, but limited in
avocational activities.
CLASS III Able to perform usual self-care activities, but limited in and vocational &
avocational activities.
CLASS IV Limited in ability to perform usual self-care, vocational, and avocational
 activities.

Differential Diagnosis: (brashear p 146-147)

1. RA
 Systemic dse
 Patients are sick
 Acute inflammatory signs
 (+) cutaneous changes
 PIP are more often involved

2. OA
 Pt. are not sick
 Weight bearing joints are often involved.
 DIP are more commonly involve (heberden’s node)
 (-) subcutaneous nodules
 Osteoporosis and bony ankylosis are uncommon
 Normal ESR and serologic test.

3. Pyogenic Arthritis
 Single large joint is involved
 Early stages have high fever and leukocytosis
 Later stage: destructive changes in roentgenograms
 Aspiration of the joint may yield pus, and a positive culture confirms the diagnosis.

4. Gonococcal Arthritis
 May stimulate RA
 Frequently in acute gonorrheal arthritis the gonococcus can be demonstrated in the joint
fluid.

5. Joint Tuberculosis
 It may ne confused with RA in its early stage.
 TB is more often monarticular, is more insidious in it’s onset and is likely to show more
bone destruction roentgenographically.
 Culture of joint exudate or biopsy of the synovial membrane may be necessary to establish
the diagnosis.

6. Gout Arthritis
 Diagnosis: high blodd uric acid level is seen, esp. in the absence of an increase of the
nonpotein or urea nitrogen
 The joint quickly loses it’s tenderness bet, attacks and the great toe is often the first part of
the body to be affected.
 Chronic gout, more often confused with RA than acute gout.

7. Systemic Lupus Erythematosus

 May be difficult to distinguish from RA.
  Exact relationship of these with RA is unknown.
 Patients shows minimal joint changes, severe systemic symptoms, and the characteristic
lupus erythematosus cell phenomenon.

OSTEOARTHRITIS / DEGENERATIVE JOINT DISEASE (Brashear p161-162)

 A form of chronic arthritis found commonly in middle-aged and elderly people, affecting esp.
the weight bearing joints, and characterized by degenerative changes in articular cartilage and
bony overgrowth at joint margins.

ETIOLOGY
Cause is obscure
Includes mechanical, dystrophic and genetic factors.
 Degenerative changes in articular cartilage are more
common and more severe in advancing age.
 Occurs most commonly in weight-bearing joints and in
joint that have become incongruent.
 Mechanical Injury (single major or repeated minor
trauma), may cause intraarticular changes that act as predisposing or aggravating cause.
 Primary OA, bused to designate cases in which no
underlying cause for the joint disease is clearly apparent
 Secondary OA, which is antecedent dse. Or injury
believed to be related to the arthritis, may result from any condition that disturbs normal
joint function.; frequently seen in younger age.
 Obesity. Large risk factor.

EPIDEMIOLOGY:
 Common after 40 y/o.
 Men > women

 First osteoarthritic changes in articular cartilage which have been confirmed in humans,
is an increase inwater content. This increase suggest that the proteoglycans have been
allowed to swell with water far beyond normal, although the mechanism by which this
occurs is unknown.
 In later stage the proteoglycans are lost, which diminishes the water content of cartilage.
 As proteoglycans are lost the cartilage loses its compressive stiffness and elasticity.

PATHOGENESIS (O’ Sullivan p1068)

The major pathological changes occurs in articular cartilage, particularly the
concentration of proteoglycans whoxh diminishes according to the severity of the disease
furthermore, there are metabolic changes in the reate of enzyme production that facilitate the
destruction of cartilage/ even though the proteoglycan concentration decreases with OA, it is also
true that proteoglycan and collagen synthesis increases until the later stages of the disease. This
seeming paradox has given rise to several hypotheses concerning the pathogenesis of OA, which
have yet to be [proven. Given that proteoglycan synthesis increases with OA, it is possible that
the quality of this newly synthesized product may not be equal to meeting the biomechanical load
normally placed on an adult joint.
Classification
• Primary OA- used to designate cases in w/c no underlying cause for the joint disease is
clearly apparent.
• Secondary OA- ante decent disease/injury is believed to be related to the arthritis
- May result from any condition that disturbs normal function.
- Frequently seen in younger age range

Signs and Symptoms (Sullivan 3rd Edition pg. 430)

• Early Stage
- stiffness of 1 or more joints associated with aching pain
- slight enlargement of the affected joints which might be slightly tender about
the margins (most noticeable in the fingers and knee)
- bony enlargement of the DIP joints (herberden’s node) one of the most
common sign
• Late Stage
- LOM and disability
- Pain- during motion and even at rest
- Malalignment of joint
- Crepitation- occurs within the joint
- Loose intraarticular fragments- produce transient lockin (Knee)
 Examination at this stage reveals moderate swelling and puffiness
 Tendency of early fatigue is common
 Many of the patient are obese- disturbance of the body mechanics

Risk factors
• Older age
• Gender (M>F)
• Bone deformities
• Obesity
• Certain occupations
• Other diseases- having gout, RA, Paget’s disease of bone or septic arthritis can increase
your risk of developing osteoarthritis.

Diagnostic (Sullivan 3rd Edition pg. 434 and Kisner 5th Edition pg. 314)
• Laboratory findings:
- Normal ESR (except during acute phase increased)
- Normal hemoglobin
- Normal WBC
- Normal platelet count
- Synovial fluid retain its viscosity
• X-ray findings:
- Evident narrowed joint spaced

MANAGEMENT GUIDELINES—Osteoarthritis (Kisner 5th Edition pg. 315)

Impairments:
Pain with mechanical stress or excessive activity
Pain at rest in the advanced stages
Stiffness after inactivity
Limitation of motion
Muscle weakness
Decreased proprioception and balance
Functional limitations in ADLs and IADLs

Plan of Care
1. Educate the patient.
2. Decrease effects of stiffness.
3. Decrease pain from mechanical stress and prevent deforming forces.
4. Increase ROM.
5. Improve neuromuscular control, strength and muscle endurance.
6. Improve balance.
7. Improve physical conditioning.

Intervention
1. Teach about deforming forces and prevention.
Teach home exercise program to reinforce interventions and minimize symptoms.
2. Active ROM joint-play mobilization techniques.
3. Splinting and/or assistive equipment to minimize stress or to correct faulty biomechanics,
strengthen supporting muscles. Alternate activity with periods of rest.
4. Stretch muscle, joint or soft tissue restrictions with specific techniques.
5. Low-intensity resistance exercises and muscle repetitions.
6. Balance training activities.
7. Nonimpact or low-impact aerobic exercise.

Comparison of Osteoarthritis and Rheumatoid Arthritis

Characteristics Osteoarthritis Rheumatoid Arthritis
Age of onset Usually after age of 40 Usually begins between age 15
and 50
Progression Usually develops slowly over May develop suddenly, within
many years in weeks or months
response to mechanical stress
Manifestations Cartilage degradation, altered Inflammatory synovitis and
joint irreversible
architecture, osteophyte structural damage to cartilage
formation and bone
Joint involvement Affects a few joints (usually Usually affects many joints,
asymmetrical) usually bilateral;
typically typically
—DIP, PIP, 1st CMC of hands —MCP and PIP of hands,
—Cervical and lumbar spine wrists, elbows,
—Hips, knees, 1st MTP of shoulders
feet —Cervical spine
—MTP, talonavicular and
ankle
Joint signs and Morning stiffness (usually less Redness, warmth, swelling,
symptoms than 30 min), and prolonged
increased joint pain with morning stiffness; increased
weight-bearing and joint pain with
strenuous activity; crepitus activity
 and loss of ROM
Systemic signs and None General feeling of sickness
symptoms and fatigue, weight
loss and fever; may develop
rheumatoid
nodules, may have ocular,
respiratory,
hematological, and cardiac
symptoms

DIFFUSE IDIOPATHIC SKELETAL HYPEROSTOSIS (DISH) (Brashear p172)

 A relatively common disorder involving the spine to the lesser extent, the larger
peripheral joints.
 Roengenographically it is characterized by flowing ossification along the anterolateral
borders of the vertebral bodies.
 It differs from AS in that the disk spaces and apophyseal joints are spared, and in the
absence of intraarticular ankylosis of sacroiliac joint.
 Occurs in middle aged and older males.
 Cause is not known
 Peripheral joint symptoms and heel pain are common symptoms.

HEMOPHILIC ARTHRITIS (Brashear p172)

 Prolonged and repeated hemorrhage into joints is a common manifestation of hemophilia,
a hereditary dse. Of the blood that occurs in males is carried in females by a sex-linked
recessive gene.
 Knee is most commonly affected, but ankle, elbow, shoulder, hips and joints of the finger
are also subject to frequent intraarticular hemorrhages.
 Pathology:
 Changes in synovial membrane: increased vascularity, hyperplasia, & thickening.
 Changes in articular cartilage: extensive degeneration with fibrillation,
discoloration, thinning, and fragmentation of collagen fibers.
 Changes in subchondral bone: it becomes atrophic c broken trabeculae and blood-
filled cyst.
 Massive subperiosteal hemorrhage, resembling that of scurvy may occur near the
end of long bone.
 Laboratory findings:
 Includes prolonged partial thromboplastin and clotting times and very low levels
of factor VIII.

Treatment:
Preventing extensive hemarthrosis by early intravenous injection of the missing
clotting factor will forestall the intraarticular changes of hemophilic arthritis.
 The affected limb should be immobilized at once; to accomplish this a large
cotton pressure dressing and splint may be applied.
 Elevation and an ice pack may be helpful.
 Cautious muscle setting exercise should be started early. A cast to protect the
affected joint from friction and weight-bearing stress for several weeks is often
indicated; frequently it should be followed by brace.
 GOUTY ARTHRITIS (Brashear. P.176-177)
 Gout is a familial disorder of purine metabolism in which uric acid,
the normal end product, is involved.
 It is characterized by hyperuricemia and the deposition of sodium
urate in the tissues.
 Uratic deposits in and about the joints lead to severe forms of acute
and chronic arthritis.
 Cause is obscure
 90% of patients are MALE.
 Secondary Gout, found in diseases such as polycythemia, leukemia,
myeloma, all of which are characterized by overproduction of uric acid from an increased
turn over of nucleic acid.
 Clinical Picture:
Early stage: marked by reccuring attacks of acute monarticular pain and inflammation.
Later stage: precipitated by excessive intake of meats and other food high in protein, certain
drugs, fatigue, fasting, overindulgence in alcohol and occasionally trauma or surgery.
Rapid onset, usually rising to a peak within few hours.
Joints most often involved are those of the FOOT. Classically the 1st MTP joint,
and the hand, wrist, knee, and elbows. Seldom is hip, shoulder, or spine.
In acute attacks the joint is usually red, swollen, warm, tender and extremely
painful on motion.
Pathology:
the joint lesion consist of creamy or chalky deposits of sodium urate surrounded
by foreign body inflammatory reaction; they occur in synovium, ligaments,
articular cartilage and periarticular bone.
Laboratory Findings:
 Elevated blodd uric acid level (7 to 15 mg%)
 The hyperuricemia is essentially unchanged before, during and after acute attack
of gouty arthritis.
 Treatment:
 Although no cure for the metabolic defect of gout is known, certain drugs provide dramatic relief
of the pain and swelling of acute attacks.
 Colchicine is more useful.; may be given hourly in doses of 0.5mg until the pain subsides or until
toxic GI upsets supervene.
 Phenylbutazone, Indomethacin, Ibuprofen Or other NSAIDs are also effective.

CHONDROCALCINOSIS (PSEUDOGOUT) (Brashear. P.177-178)

Chondrocalcinosis, calcium pyrophosphate deposition disease (CPPD) or pseudogout.
A form of arthritis of unknown cause , associated with deposition of crystals of calcium
pyrophosphate within articular cartilage.
Characterized by acutely painful attacks of rapid onset, similar to those of gout and by the gradual
development of chronic articular cartilage like those of OA.
It is most frequently found in elderly patients and occasionally has been noted in patients with
hyperthyroidism.
Knee is more frequently affected next is the hip.
Serum chemistry levels, including the uric acid content are within normal limits.
Microscopic exam of synovial fluid aspirated during an acute attack shows the rod-
 shaped and rhombic crystals of Calcium pyrophosphate.

OCHRONOTIC ARTHRITIS (Brashear. P. 178-179)

 a rare hereditary dse. Assoc. with alcaptonuria, is manifested by progressive degenerative
arthritic changes that are most severe in the spine and proximal joints.
 Roentgenographic findings includes changes in severe degenerative arthritis, particularly
in the spine where calcification of IVD is common.
 Clinically the symptoms of arthritis usually appear in the fourth decade of life beginning
in the spine.
 No therapy is specific for the enzymatic defect is available, and treatment of the
associated chronic arthritis is largely asymptomatic.

ANKYLOSIS (Brashear. P.179)

 A stiffening or restriction of the normal range of motion of a joint by tissue changes
within or without the joint cavity.
 May occur with the joint in a position relatively favorable for function or in an attitude of
deformity.
 Etiology:
 Often a result of the incomplete healing or restoration of joint structures damaged
by chronic arthritis, infection, or trauma.
 Types:
1. Fibrous, partial or false – when connective tissue adhesions bet. The articular
surfaces of extraarticular tissues are not accompanied by actual bony union.
- may follow joint inflammation, intraarticular fractures,
repeated intraarticular hemorrhages, or extra articular
changes resulting from infection, trauma,
immobilization,.
2. Bony, complete, or true – when solid new bone have been formed between the
articular surfaces.
- often an en result of more severe infection or more advanced RA.

References:
Physical Rehabilitation
by Susan B. O’Sullivan
Fifth edition
Chapter 26

Handbook of orthopaedic surgery

By H. Robert Brashear Jr.
10th Edition
Chapter 5.