Joint pathology

Joints provide movement and support.Classification:Solid (nonsynovial)also known as synarthroses ; lack a joint spaceallow minimal movementCavitated (synovial):have a joint spaceallow for a wide range of motion.

Synovial joint

Boundary formed by synovial membrane.Lined by synoviocytes.Synovial fluid (SF): Pale yellow to clear, viscousRich in hyaluronic acid: acts as lubricantprovides nutrition for articular cartilage.Arthrocentesis: needle aspiration of SF

Routine studies of SF:Gross appearance: normally pale yellowWBC count and differential count : normally

Monosodium urate (MSU) : found in goutneedle shapedSpecial polarization shows negative birefringence

Calcium pyrophosphate dehydrate (CPPD) crystals: found in pseudogout.(rhomboid)Special polarization shows weakly positive birefringence

OsteoarthritisNeuropathic- Charcots jointRheumatoid arthritisGoutPseudogoutSLEAnkylosing spondylitisReiters diseasePsoriatic arthritisInfectionsTrauma

Most common type of joint disease and joint disability in the US

A degenerative joint disease and is characterized by: Progressive erosion of articular cartilage and Associated reactive changes at the margin of the joints and in the subchondral bone.

Not primarily an inflammatory disease

More common in women than men

Primarily targets weight bearing joints Hips, kneescervical and lumbosacral spine

Other joints:Distal interphalangeal joint (DIP) and proximal interphalangeal joint (PIP) of the hands

Causes: A combination of genetic and environmental factors.Primary: as a result of aging phenomenon; seen in older individuals

Secondary: develops as a result of a predisposing conditionseen in younger individualsTrauma to joint Obesity Ochronosis - (alkaptonuria: accumulation of homogentisic acid)Hemochromatosis

Pathogenesis: Exact etiology of OA osteoarthritis is unknown

Most important factor that predisposes to development of OA iseffect of abnormal load (mechanical trauma) on a weight bearing joint

Thinning of articular cartilageDevelopment of cracks

Erosion and loss of cartilage

Formation of :Loose body/joint mice Subchondral cyst

EburnationSclerosisNarrowing of joint spaceLoose bodyOsteophyte

Joint findings:Erosions and clefts in articular cartilageClefts penetrate into underlying subchondral boneFragmentation of cartilage and subchondral bone result in formation of loose bodies Bone rubs on bone polished ivory like appearance called eburnationSubchondral bone cysts (visible on X rays) develop beneath the articular surfaceReactive bone formation at the margins of joints produce osteophytes (bony spurs).

Heberdens nodes(DIP)Bouchards nodes(PIP)

Clinical findings: Pain worse with activity Morning stiffness : lasts less than half hourJoint stiffness: with limitation of movementHeberdens nodes develop in the DIP joints and Bouchards nodes in the PIP joints of the handHerbeden/Bouchards=>reactive bones(bony spurs)

Lab studies:No specific laboratory abnormality.Synovial fluid analysis : normal

Diagnosis: xray findings Presence of osteophyte at joint marginsJoint space narrowingSubchondral bone cysts

Joint-space narrowing in the knee with osteophyte formation

It is a non-inflammatory joint disease

Secondary to a neurologic disease.Joint destruction is due to insensitivity to pain Causes:Diabetes mellitus (Most common cause) (tarsometatarsal joint)Syringomyelia (shoulder, elbow, wrist joints)Tabes dorsalis (hip, knee and ankle joint)

Pathogenesis:loss of proprioception and deep sensation leads to recurrent trauma progressive destruction, and disorganization of the joint

Marked joint destruction is the hallmarks of a neuropathic joint

It is a chronic systemic, inflammatory diseaseGenetics, enviromental factor and autoimmunity contributes to the etiology. 30-50 years of age Affects the peripheral joints in a symmetric manner producing proliferative synovitis that causes: destruction of articular cartilage ankylosis (fusion) of joint joint deformity and disability

Clinical features:Symmetric bilateral involvement; warm, tender and swollen joints Small joints of hands and feetMCP and PIP joints (not DIP)Other joints include:Ankles, knees, wrists, and cervical spineNote: involvement of joints causes:Joint stiffness especially in the morning, which lasts more than an hour and improves with activity.

Subluxation and fusion of joints

Synovial hypertrophy with lymphocytic infiltration.

Extra-articular manifestations:Rheumatoid nodules VasculitisPulmonary: pleural effusion; interstitial fibrosis Bakers cyst increased articular pressure leads to outpouching of the synoviumCarpal tunnel syndrome median nerve entrapment Hematologic: anemia of chronic disease; Feltys syndrome( AI neutropenia/splenomegaly)

Bakers cyst (synovial cysts):It is usually found in the in the posterior aspect of the knee

It may be confused with popliteal artery aneurysm

Rheumatoid nodule- present on extesor surfaces

Interstitial lung fibrosis

Lab findings cont Blood work:Elevated ESRPositive rheumatoid factor (80%) Anticyclic -citrullinated peptide CCP(most specific marker)Synovial Fluid: WBC: 3,000 50,000Mostly PMNs (neutrophils)X-ray:Soft-tissue swelling Erosions at articular surfaceNarrow joint space (destruction of articular cartilage)Fusion of joints (ankylosis)Joint deformity

Definition: JRA is characterized by a chronic synovial inflammation of unknown cause

It usually occurs in young girls < 16 years of age RF is usually absent seronegative

Stills diseasePolyarticular JRAPauciartucular JRA

Stills disease: Commonly presents as an infectious disease with fever, rash,generalized lymphadenopathy neutrophilic leukocytosis andpolyarthritis

Polyarticular JRA: Clinically disabling arthritis affecting many joints Other features include: low-grade fevergrowth retardation, adenopathycervical spine involvement

Pauciarticular JRA:

Arthritis is present in a few joints

Inflammation of the anterior uveal tract uveitis May lead to visual loss and blindness

Gout is a disorder of uric acid metabolism characterized by:HyperuricemiaRecurrent attacks of joint inflammation (gouty arthritis) and tissue deposition of uric acid crystals

It can lead to joint destruction if untreated

Gender: males> females

Causes: Primary gout (Idiopathic)is due to:

Under-excretion of uric acid in urine- most commonOverproduction of uric acid- less common

Causes : Secondary gout: due to a secondary disorder.the cause of hyperuricemia is known but gout is NOT the main or dominant clinical disorder.Common causes include: nucleic acid turnover: leukemia, lymphomaDrugs: diuretics, aspirin, ethanolChronic Renal failureLead intoxication(Saturnine Gout)

Acute arthritis: clinical features The initial attack It commonly involves 1st metatarsophalangeal joint (big toe) inflammation of this 1st MTP joint is called podagra

The involved joint is red, hot and exquisitely tender

Chronic gout: It develops in uncontrolled or poorly controlled gout It is characterized by presence of tophi Tophi: deposits of MSU crystals in soft tissues:Pathognomonic lesion of gout found in the helix of the ear, fingers, toes

M/E: granulomatous reaction with foreign body type of giant cells surrounding amorphous MSU crystals

Complications: Arthritis:Asymmetric polyarthritis with erosion of cartilage and subchondral bone due to crystal deposition

Renal Disease gouty nephropathychronic medullary interstitial nephritisUrolithiasis (renal stones)Acute Renal failure MSU deposition in collecting tubules

Synovial fluid:Demonstration of MSU crystals in synovial fluid is diagnosticIntracellular, needle-shaped, negatively birefringent crystals

CBC: Absolute neutrophilic leukocytosisSerum uric acid levels:Hyperuricemia is usually but not always present.Only 5-20% patients with hyperuricemia develop gout10% patients with gout have normal uric acid levels

It is associated with deposition of CPPD crystals in joints i.e knee

It is a disease of the elderly

Pathogenesis:Normal aging process biochemical change in cartilage level of pyrophosphate pyrophosphate combines with Ca++ crystals deposited in the articular cartilage Release of CPDD crystals in the joint causes inflammatory reaction

Clinical findingsAsymptomatic (chondrocalcinosis)

Acute attack (pseudogout):Oligoarthritis resembling gout

Chronic form:Polyarthritis resembling RA

Clinical findings cont

Synovial fluid analysis:Blue staining rhomboid crystals.Positive birefringence

Xray - calcification of articular cartilage

A group of related disorders.Develop in genetically predisposed individualswhen they come in contact with certain environmental factors ( triggering agents)

Characteristics include: Lack Rheumatoid factor (RF negative)Individuals HLA-B27 positiveMale dominantInvolve sacroiliac joint ( sacroilitis) with or without peripheral arthritis

Types of spondyloarthropathy:Ankylosing spondylitis (AS)Reiters syndromeArthritis associated withulcerative colitis shigellosispsoriasis

Ankylosing spondylitis Usually occurs in young men (15-30 years) who are HLA-B27 positiveClinical findings:Initially targets the sacroiliac jointBilateral sacroilitis causing back pain & morning stiffness is the first manifestation

Eventually targets the vertebral column:Fusion of vertebrae bamboo spine causes forward curvature.May also target Aorta aortitis (aortic regurgitation); Uveal tract uveitis (blurry vision).

Reiters syndrome:

It comprises a triad of Urethritis (due to Chlamydia trachomatis)Conjunctivitis (noninfectious) and Arthritis and Achilles tendon periostitis.

Most commonly occurs in men of 20-30 yrs age who are HLA B27 positive.

Reiters syndrome Clinical:Arthritisa few weeks after an infectious episodeLow back pain sacroilitis Inflammation at the insertion of Achilles tendon is characteristic

Psoriatic arthritis:Is a seronegative spondyloarthropathyOccurs in approximately 7% of patients with psoriasisClinical:Arthritis usually affects small joints of the hands and feet

Not as severe as RA and there is less joint destruction.

Enteropathic arthritis: HLA B27 positive arthritis associated withInflammatory bowel disease, [ulcerative colitis (most common) and Crohns disease], or gastroenteritis due to Shigella, Salmonella Campylobacter, Yersinia species etc. Clinical:Migratory oligoarthritis of large joints and spine.May resemble ankylosing spondylitis.Less severe and remits spontaneously in a year or two.

These are inflammatory types of arthritis

Secondary to microbial pathogens.

These are uncommon, but they can rapidly destroy a joint to produce permanent loss of motion

Synovial fluid analysis:Color: yellowish greenWBC count: between 100,000 200,000 / mm3Neutrophils: >75% of total WBCs

Nongonococcal arthritis(accounts for more than 60%)

Gonococcal arthritis

Nongonococcal arthritis:Most commonly involves the knees.Extremely destructive joint diseaseMajority caused by Staphylococcus aureus.Other causes include: Strept(Pyogenes,Pneumoniae,Viridans)H.influenzae, E.coli.

N.Gonorrhoeae It is the most common cause of septic arthritis in sexually young peopleOccurs as part of Disseminated gonococcal infection (DGI)Other features includes skin lesions, pustular eruptions, tenosynovitis

Deficiency of C6-C9 is usually present

A 22 year old woman presented to The Emergency Department because of progressively severe unilateral wrist pain of 24 hours duration. She was triaged for surgical evaluation. No preceding injury or unusual physical activity was identified. Plain radiographs of the wrist were unremarkable. A splint was applied. Ibuprofen was prescribed at 600 mg po TID and she was discharged with a diagnosis of wrist sprain.

She got worse over the next 12-18 hour with development of fever and palm and hand pain. She returned to the E.RAt this juncture, she was triaged for medicine evaluation. Physical examinations shows a well-nourished woman, temperature 101oF. Articular examination was notable for swelling and warmth at the left wrist

. The wrist joint was exquisitely tender to palpation and to manipulation. Swelling extended over the dorsal surface of the hand. The fingers were spared. Skin findings were notable for several tender bilateral palmar violaceous pustular eruptions.Differentials:1Acute rheumatic fever 2.Reiter's syndrome 3.Post-streptococcal reactive arthritis 4.Disseminated gonococcal infection 5.Systemic Lupus Erythematosus 6.Lyme arthritis

Cervical examination:purulent cervical dischargeCervical culture: positive for N. Gonorrheae.

**Classification of joints:Solid (nonsynovial)classified according to type of tissue that bridges the ends of bones:fibrous synarthroses: ex: cranial sutures, bond between root of teeth and jaw bones.cartilaginous synarthroses: symphyses

*Diagram of a typical synovial joint*no basement membrane in the synovial liningallows quick exchange between blood and synovial fluid.

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other joints include: Distal interphalangeal joit (DIP) and proximal interphalangeal joint (PIP) of the hands.*Wear and tear arthritis*

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******* *Reasons for pain in OA:Joint effusionStretching of capsuleInflammation of synoviumPeriarticular muscle spasmCrepitus (feeling of crackling in the joint) are common

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Pathogenesis:loss of proprioception and deep sensation leads to recurrent trauma, which ultimately leads to progressive destruction, degeneration, and disorganization of the jointCauses : Tabes dorsalis is a slow degeneration of the nerve cells and nerve fibers that carry sensory information to the brain. The degenerating nerves are in the dorsal columns of the spinal cord (the portion closest to the back of the body) and carry information that help maintain a person's sense of position. ** ** Note that the lesion is polyarticular and symmetrical. The most common deformity of the thumb is flexion with hyperextension at the interphalangeal joint.

Question: How does RANK-L contribute to the destruction of the joint? Answer: RANK-L is released from activated lymphocytes in the synovium, stimulating the proliferation of osteoclasts. Osteoclasts rapidly erode the subchondral bone. *Rheumatoid arthritis. Low magnification reveals marked synovial hypertrophy with formation of villi.

Question: List two important histologic changes found in the synovial membrane in joints affected by rheumatoid arthritis. Answer: The synovium is proliferative and is infiltrated by numerous lymphocytes and plasma cells.

*WHAT IS A BAKER'S CYST?A bursa is a fluid filled sack that acts as a cushion between tendons, bones, and skin. A Baker's cyst is an abnormal swelling of a bursa located in the space behind the knee (the popliteal space). The cyst connects to the membrane covering the knee joint. HOW DOES IT OCCUR?No one really knows what causes Baker's cysts. However, the cysts can occur when the lining of the knee joint produces too much fluid, as in rheumatoid arthritis, or after an injury.WHAT ARE THE SYMPTOMS?You may have pain, swelling, or a feeling of fullness in the area behind the knee.HOW IS IT DIAGNOSED?Your doctor will examine you rknee and find a bulge in the back of your knee. You may need to have a magnetic resonance image (MRI) or an arthrogram to help the doctor determine if you have a Baker's cyst. For an arthrogram, dye is injected into your knee, and then an x-ray is taken to look at the joint capsule, the membrane surrounding the joint.HOW IS IT TREATED?The initial discomfort of a Baker's cyst may be treated by wearing an elastic bandage. Your doctor may prescribe anti-inflammatory medications, the cyst may be drained, or an operation may be performed to remove the cyst. Sometimes the cyst goes away on its own. If the cyst does not cause bothersome symptoms, it may not be treated.HOW CAN A BAKER'S CYST BE PREVENTED?There is really no way to prevent a Baker's cyst from forming.

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