Joint Disorders

Osteoarthritis

progressive degeneration of the articular cartilage that results in structural and functional failure of the synovial joints

What is the most common joint disease?

Osteoarthritis

Primary Osteoarthritis

aging

Secondary Osteoarthritis

previous trauma and systemic disorders

3 types of pathogenesis of OA

1. chondrocyte injury by biochemical factors (previous trauma, weight loss, activity level)

2. early OA

3. late OA

Early OA

chondrocyte proliferation, with secretion of inflammatory mediators

Early OA: cartilage degradation __ cartilage production

>

Late OA: cartilage degradation __ cartilage production

>>>>>>

Late OA

loss of bone matrix and chondrocytes with subchondral bone damage (more so than early)

Clincal Symptoms of OA

-deep achy pain

-morning stiffness

-loss of ROM

What OA findings are more common in females?

knees and hands

T/F? Narrowing of the spinal facet joint in OA can lead to radiculopathy

true

X-ray findings of OA that can reflext degree of joint damage:

-marginal osteophytes

-joint space narrowing

-subchondral sclerosis

-cysts

Nodal hand OA finding in women

bouchard's nodes and heberden's nodes

Rheumatoid arthritis (RA)

chronic systemic AI inflammatory disorder that affects many tissues and organs but principally attacks the joints producing a proliferative and inflammatory synovitis

What does an inflammatory synovitis cause?

destruction of the articular cartilage and cause ankylosis of the joints

Ankylosis

abnormal condition of stiffness

Epidemiology of RA

female with hereditary predisposition

80% of people with RA have what in their serum?

RF

RF

autoantibodies against Fc portion of IgG

Anti-citrullinated peptide antibodies (ACPAs)

autoantibodies that target protein or peptides that contain citrulline

Which RA autoantibody is more specific for RA ACPAs or RF?

ACPAs

What can you measure ACPAs with?

anti-CCPs

RA is a type ___ hypersensitivity (main one!)

IV (cell mediated)

Pathogenesis of Type IV hypersensitivity of RA

CD4+ cells activated by exposure of genetically susceptible host to an environmental arthritogenic antigen

Environmental arthritogenic antigen

smoking promotes citrullination of self proteins

Pannus

mass of edematous synovium and synovial stroma consisting of inflammatory cells, granulation tissue, and fibroblast like synviocytes that causes erosion

Pannus bridging with opposing bones forms?

fibrous ankylosis (eventually ossifies)

Oligoarticular

four or less joints

Bouchards is proximal/distal joints

proximal

Heberdens is proximal/distal joints

distal

HLA-DRB1

main allele for hereditary disposition for RA

Autoantibodies in RA

RF and ACPAs

CD4+ cells roles in RA

secrete inflammatory cytokines (TNF and IL-6) that creates an hypertrophied synovial pannus that causes destruction

Type II hypersensitivity in RA

plasma B cells that produce antibodies

Type III hypersensitivity in RA

antibodies are directed at self antigens and form immune complexes

Synviocytes

synovial cells

Clinical findings of RA

-start insidiously with systemic signs (from cytokines)

-stiffness

-joints are swollen, warm, and painful

T/F? 70% of RA are unilateral and asymmetric

false

How long does morning stiffness last?

>30-60 min

RA initally affects large/small joints then later effects large/small joints

small; large

Classic triad of joint finding for RA

tenderness, warmth, swelling

T/F? It is possible to see tendon rupture/inflammation in someone with RA

true

In OA the findings are often unilateral/bilateral and asymmetric/symmetric

unilateral; asymmetric (typically goes to the dominant side)

DIP is more common in RA or OA?

OA (MCP and PIP is RA)

RA X-ray finding

marginal erosions

Clinical deformities of RA

-radial deviation of the wrist and ulnar deviation of finger

-Swan-neck

-Boutonniere

Extra-articular manifestation of RA

-rheumatoid nodules (over elbow common)

-vasculitis

-pleuritis

-etc

Felty syndrome occurs in RA patients, consisting of this triad:

RA, splenomegaly, and neutropenia (severe)

People with Felty has more/less severe RA

more

What is the cause of Felty?

unknown

Juvenile Idiopathic Arthritis (JIA)

all forms of arthritis before age of 16 that persists for at least 6 weeks and occurs in the absence of other medical causes

Females ___ men with JIA

>

Genetic predisposition and environmental factors of JIA

immune dysfunction with increased amounts of activated CD4+ memory T cells within affected joints; leads to cytokine production

JIA differs from adults RA by:

-more oligoarticular

-systemic signs more common

-ANA+ and RF-

-no rheumatoid nodules

Systemic JIA AKA

still's disease

Presentation of Still's disease

-high fever

-rash

-arthritis

-enlarged liver, spleen, lymph nodes

To be diagnosed with Still's symptoms need to occur for _____ weeks

2

Oligoarticular JIA

affects <4 joints during first 6 months of disease

Stills: male ____ female

=

Oligoarticular: male ___ female

<

Usual clinical presentation of oligoarticular

female toddler who is limping without complaint

Oligoarticular affects small/large joints

large

Oligoarticular antibodies

ANA+, RF-

Need to watch for _______ for oligoarticular

uveitis

Uveitis

inflammation of the uvea

Polyarthritis

>5 joints involved in first 6 months of disease

RF+ polyarthrtitis common in:

teenage girls

RF- polyarthritis common in:

<10 yrs old

Enthesitis-related arthritis common in:

males >6 years old

Enthesitis-related arthritis antibodies

HLA-B27+

Enthesitis-related arthritis increased risk of:

anterior uveitis

Enthesitis

inflammation in the attachments of tendons, ligaments, and fascia to bone with pain on palpation

Seronegative spondyloarthropathies

inflammatory arthritis AND inflammation of ligamentous/tendinous attachments (entheses)

Seronegative spondyloarthropathies clinical features:

-SI joints

-HLA-B27+

-absence of RF

-bony proliferation leading to ankylosis

Pathogenesis of seronegative spondyloarthropathies

T-cell mediated response against microbial antigens that cross-react with MSK components

Types of Seronegative Spondyloarthropathies

-Ankylosing spondylitis (AS)

-Reactive arthritis

-Psoriatic arthritis

-Arthritis associated with inflammatory bowel disease

Reactive Arthritis syndromes

reiter and enteritis-associated arthritis

AS epidemiology

males 2-3x more affected (20-30s) and HLA-B27+ (90%)

AS clinical features

-back pain and stiffness worse with rest, improves with exercise

-destruction of articular cartilage and bony ankylosis

-SI joint bony fusion

-can also affect spine, shoulder, hips

-dactylitis and enthesitis

T/F? AS has no RF or ANA

true (seronegative)

Reactive Arthritis

noninfectious arthritis within 1 month of an infection elsewhere, organism cannot be recovered

Infections can include in reactive arthritis:

GU (chlamydia) and GI

Pathogenesis of reactive arthritis

AI reaction triggered by an infection

Reiter's syndrome triad (seen in minority of patients)

noninfectious arthritis, nongonococcal urethritis/cervicitis, and conjunctivitis

Epidemiology of Reiter

95% male and 80% HLA-B27+

People with Reiters have sterile culture by synovium has an increased _____________

WBCs

Reiter's clincial presentation

-1-4 weeks after infection

-knees primarily

-asymmetric

-oligoarticular

-15-20% go onto chronic disease (affects the spine)

Enteritis-associated arthritis caused by?

GI infections

Enteritis-associated arthritis pathogenesis

microbe has lipopolysaccharide which stimulates an immunological response

Enteritis-associated arthritis timeline

about a year

Entheses

Sites where ligaments and tendons attach to bones

What joint is primarily affected by psoriatic arthritis?

DIP (dactylitis and pencl in cup on X-ray)

T/F? Nail changes in psoriatic arthritis is very common

true

DDX of joint stiffness

polymyalgia rheumatica

Joints with psoriatic arthritis affected by?

entheses moreso

Polymyaglgia Rheumatica clinical features

-older patient

-stiff neck

-not an arthritis

-morning stiffness (increase ESR/CRP)

-associated with giant cell arteritis

-unknown AI cause

Organism get into the joint by:

hematogenous, contiguous spread, or latrogenic (direct inoculation)

Most common cause of septic arthritis

Staph A.

What others things can infect the joint, besides bacteria?

TB, lyme, and viruses