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bones and soft tissue

Infectious arthritis
hematogenous spread – involving other site
o ex: lungs – pneumonia
o bacteria can hop aboard capillaries and find their way into joint space
o seeding from neighboring sites
o direct inoculation
o contiguous spread from a soft tissue abscess or focus of osteomyelitis
Suppurative Arthritis
- bacterial infections enter joints from distant sites via hematogenous spread
 Etiological Factors
 Gonococcus – adolescents and younger adults
 Staphylococcus
 Staph aureus - main cause in older kids and adults
 Streptococcus
 Haemophilus influenzae
 Gram-negative bacilli
 Pseudomonas aeruginosa
 Most common in children under 2
 Pasteurella multocida
 Eikenella corrodens
 Fungi
 2 organisms – staph and strep
 Pyogenic bacteria – cause infection of purulent exudate created from the tissue damage
of this bacteria
 Any agent can lead to suppurative arthritis
 Pathophysiology
 Synovial membrane contamination (1st)
 Edema as a reaction to the inflammation – synovial membrane hypertrophy
 Synovial fluid (2nd)
 Synovial fluid is a nice culture medium for bacteria to proliferate
 Pathology
 Synovial membrane edema
 Synovial membrane hypertrophy
 Purulent exudate accumulation
 Cartilage destruction
 Fibrin deposition on cartilage
 Joint destruction / Erosion
Suppurative Arthritis
Classic presentation
- Sudden development of a painful and swollen joint
o Hip, knee, shoulder, elbow
o Painful, hot, red, acute, swollen
- Limited ROM
- Fever, leukocytosis
- Elevated sedimentation rate
- Nongonococcal cases – infection involves only a single joint – most commonly the knee
- Axial joints most commonly involved in drug users
Joint aspiration is diagnostic if it yields purulent fluid in which the agent can be
o Purulent effusion
 extremely high WBC count
o Inflammatory effusions
 Leukocytes
o Hemorrhagic effusions
 Coagulation defect, hemophilia A or B
Do CBC and white count
Aspiration and culture based on H and P
Single or multi joint involvement
Rapid joint destruction without treatment
o Need to rule out joint infection quick or irrev joint damage can occur
o Cellulitis, bursitis, acute osteo
 Tissue damage – dead immune cells sequestered to that area – some cells die along with
tissue debris accumulate in that joint secondary to infection
 These tissues will be compromised as well
 Fibrin depositions- found in infective – widespread joint destruction
 Total loss of cartilage involving erosion
Pre disposing conditions:
- Immune deficiency
o Parts of the complement system membrane attack complex (C5,6,7) are more
prone to gonococcal attacks
- Illness, joint trauma, chronic arthritis, IV drug use
Disseminated Gonococcal Infection
- Subacute symptoms
- Single joint
o Oligoarthritic pattern
o Knee, ankle, hip, shoulder, elbow, wrist, sternoclav
- Migratory type of joint
Bacteremia infection stage
o Migratory polyarthritis
o Tenosynovitis
o Dermatitis
Septic arthritis
Joint localization stage
o Myalgia, fever, chills, rash
o Joint fluid
 Leukocytes
 Synovial culture negative
 Blood culture positive
o Purulent exudate in urogenital region
IV Drug Use
- Axial spine
- Sacroiliac
- Sternoclav
Tuberculosis Arthritis
- Complication of adjoining osteo
- Monoarticular pain and swelling
- Systemic symptoms vary
- After hematogenous spread from visceral (usually pulmonary) site of infection
- Onset is insidious
- Gradual progressive pain – Chronic progressive
- Caseous necrosis
- Granulomas
o Langerhans giant cells on center of granuloma and on the periphery
o Response of synovial membrane leads to pannus formation
Affected synovium grows as a pannus over the articular cartilage and erodes the bone
along the joint margins
o Fibrinous hypertrophic type of growth found on synovial membrane
Chronic disease results in fibrous ankylosis and obliteration of the joint space
Hematogenous spread
o Visceral, pulmonary, osteomyelitis
Ghon complex
o Primary infection site
o Draining lymph nodes
Large, weight bearing joints
Synovial culture +
Mycobacterium stain red
Joint fluid
o PCR fastest way to check for TB
o Neutrophils
o Acid fast stain
45 yr. old man with hx of cough now having trouble walking, weight bearing joints pain
Order of which pathology occurs:
1. Confluent granulomas
2. Central caseous necrosis
3. Pannus over articular cartilage
4. Bone erosions along joint margins
5. Fibrous ankylosis and obliteration of joint space
6. Severe destruction
7. Weight bearing joints
Pott Disease
- Similar to TB
- Bone is eroded away
- Granulomas form
- Collapse of vertebral – pushing or impinging on nerve exiting
- Annulofibrosis
HLA – D27 association
Disorganized bone formation – hyperthyroid, renal dx
Anti ds – DNA + - lupus
Bamboo spine - Buzz work for ankylosing spondylitis
Joint infiltration with basophils - Associated with leukemia mild dysplastic symptoms
Seronegative Spondyloarthropathies
Unified by the following features:
1. Pathologic changes in ligamentous attachments rather than synovium
2. Involvement of the sacroiliac joints with or without other joints
3. Absence of rheumatoid factor
4. HLA B27
Manifestations are immune mediated and are triggered by a T-cell response against an
identified antigen that may cross react with native molecules of the musculoskeletal system
1. Ankylosing Spondylitis
2. Reactive arthritis
3. Psoriatic arthritis
4. Ulcerative colitis
5. Chron Disease
Ankylosing Spondylitis
- Destruction of articular cartilage and bony ankylosis
- Chronic inflammatory joint disease
- Sacroiliac and apophyseal joints (between tuberosities and processes)
o Prominent region of tendon and ligament insertions
- 20s-30s
- Lower back pain and spinal immobility
- H:A-B27 positive
- Enthesis – site
o Point of tendon, ligament or muscle insertion into bone
- Enthesis – inflammation at site
o Erosion, osteitis, ossification
o Mononuclear cell infiltrate
- Sacroiliac infiltration
o CD4 and CD8
o Macrophages and High TNF-a
- No specific lab test
1. Chronis synovitis
2. Destruction of articular cartilage
3. Bony ankylosis
4. Tendinoligamentous inflammation and ossification
5. Bony outgrowths – severe spinal immobility
a. Syndesmophytes – osseous excrescence attached to a ligament
i. Bone on a ligament bro
ii. Bamboo spine
Clinical Features
- Chronic progressive, low back pain, peripheral joint pain
- Complications: spine fracture, uveitis, aortitis
Reactive Arthritis
- Triad of: arthritis, non-gonococcal urethritis or cervicitis, and conjunctivitis
- Men in their 20s 30s
- HLA -B27
- Autoimmune reaction caused by prior infection of the genitourinary system
(Chlamydia) or GI (shigella, Salmonella, Yersinia, Campylobacter)
- Arthritic symptoms develop within several weeks of initial bout of urethritis or diarrhea
- Joint stiffness and low back pain
- Ankles, knees, feet in an asymmetric pattern
- Sausage fingers – synovitis of a digital tendon sheath
- Calcaneal spurs DNA bony outgrowths – ossification of tendoligamentous insertion sites
- Severe cases look just like ankylosing spondylitis – sacroiliac involvement
- Extraarticular involvement:
o Balanitis,
o Cardiac conduction probs, aortic regurgitation
o Keratoderma blennorrhagia – skin lesions on palms and soles
o Plaques/ erosion of tongue
o conjunctivitis
Immunologic responses against lipopolysaccharide components
Macrophage infiltration of fibrocartilage
Self-limited 3-12 months
50% of patients get recurrent arthritis, tendonitis, fasciitis, lower back pain
25 you man had a UTI 7 weeks ago and resolved now his right ankle and knee hurt
o Low fever, fatigue, superficial oral ulcers
o Anemia, synovial fluid in knee
o Chlamydia infection
- Degenerative bone disease
- Degeneration of cartilage
- Structural and functional failure of synovial joints
- Collagen 2 is degraded by matrix metalloproteases
- Degradations exceeds synthesis
- Environmental factors – age and biomechanical stress
3 phases:
1. Chondrocyte injury
a. Genetic
b. Biochemical factors
2. Early OA
a. Chondrocytes proliferation
b. Secrete inflammatory mediators
i. Collagens, proteoglycans, and proteases
ii. Remodel the cartilaginous matrix
iii. Initiate inflammatory changes
c. Remodeling of cartilage matrix
d. Secondary inflammatory changes in the synovium and subchondral bone
3. Late OA
a. Repetitive injury and chronic inflammation
b. Chondrocyte drop out
c. Marked loss of cartilage
d. Extensive subchondral bone changes
- Fissures and clefts at articular surface
- Loss of articular cartilage
- Full thickness portions of the cartilage are sloughed
- Joint mice
o Dislodged pieces of cartilage and subchondral bone tumble into the joint,
forming loose bodies
o Pieces of cartilage and subchondral bone break off
- Exposed subchondral plate becomes new articular surface
- There are some chondrocytes there trying to make new cartilage but not enough
- Bone eburnation – loss of articular cartilage
- Fracture gaps – force synovial fluid into the subchondral space causing micro fissures
- Synovial fluid leaks in forming subchondral cysts
- Fibrous-walled cysts develop  fibrous tissue deposition  bony outgrowths occur
Collagen 2 is cleaved causing fissures and clefts
Granular soft articular surface
Chondrocytes die and full thickness portions of cartilage are sloughed
Dislodged pieces of cartilage and subchondral bone tumble into the joint – JOINT MICE
Exposed subchondral bone becomes new articular surface
Friction with the opposing bone smooths the surface – ENUBRIATION
Sclerosis of the underlying bone
Small fractures through the articulating bone
Fracture gaps allow synovial fluid into the subchondral regions
o Forming fibrous walled cysts
Osteophytes develop at the margins of the articular surface
Deep achy pain that worsens with use, morning stiffness, ~20 mins
Crepitus, limited ROM
Asymmetrical, single joint or few
Hips, knees, lumbar, cervical, proximal and distal IPJ, first mets
Heberden nodes – prominent osteophytes at the DIPJ
 Impingement on Spinal Foramina by Osteophytes
 Results in cervical and lumbar nerve root compression
 Radicular pain
 Muscle spasms
 Muscle atrophy
 Neurologic deficits – immediate and through investigation
 Osteo – subchondral space, thin and fibrillated cartilage can be wiped out completely
 Rheumatoid – immune complex mediated – can have fibrous ankylosis, eroding cartilage
pannus formation, and inflamm involving the joint and soft tissue surrounding the joint
Rheumatoid Arthritis
 Chronic inflammatory disorder of autoimmune origin that may affect mani tissues and
organs but primarily attacks the joints
 Non suppurative proliferative and inflammatory synovitis
 Progresses to destruction of the articular cartilage and ankylosis of the joints
 Extra articular lesions may involve the heart, skin, vessels, and lungs
o May resemble other auto immune things like lupus or scleroderma
CANNOT tell diff btw endogenous and exogenous antigens
Enzymatic modification – proteins that have largely in their makeup
an enzyme modified __ and turns it into citrulline – citrulline combines with another
macromolecule to form antigen
This is what the body attacks
T and b cells respond to self-antigens
Fibroblast chondrocyte proliferation – synovial cells are proliferated release collagenase etc all
contribute to formation of pannus leading to bony and cart destruction – what you have Is
fibrosis and eventually ankylosis
- CD4+ Helper T cells may initiate autoimmune response in RA by reacting with an
arthritogenic agent
- Microbial or self antigen
- T cells produce cytokines that stimulate with inflammatory cells to effect tissue injury
o TH1 releases IFN-y to activate macrophages and resident synovial cells
o TH17 releases IL-17 to recruit neutrophils and monocytes
o TNF and IL-1 from macrophages stimulate protease release that destroy hyaline
The synovium of RA contains germinal centers with secondary follicles and plasma cells
that produce autoantibodies against self-antigens
Autoantibodies are specific for citrullinated peptides
o arginine peptides are post-translationally converted to citrulline
in RA, antigen-antibody complexes containing citrullinated fibrinogen, type 2 collagen,
enolase, and vimentin deposit in the joints
antibodies against these peptides are diagnostic markers
 Morphology
 Joints
 Symmetric arthritis
 Small joints of the hand and feet
 Synovium
 (Bulbous villi)
 Edematous
 Thickened
 Hyperplastic
 Dense inflammatory infiltrates
 Lymphoid follicles
 Increased vascularity
 Fibrinopurulent exudate on the synovial and joint surfaces
Rheumatoid cutaneous nodules
- most common cutaneous lesions
- Areas of skin subjected to pressure
- forearm, elbow, occiput, lumbosacral
Blood Vessels
- Severe erosive disease, rheumatoid nodules, and high titers of rheumatoid factor are at
risk for developing vasculitis
- Acute necrotizing vasculitis
o Small and large arteries
- Obliterating endarteritis
o Affects segments of small arteries such as vasa vasorum, digital arteries
o Results in peripheral neuropathy, ulcers, and gangrene
- Leukocytoclastic vasculitis
o Produces purpura, cutaneous ulcers, and nail bed infection
- Uveitis and keratoconjunctivitis
 Diagnosis of RA
 (1) characteristic radiographic finding
 (2) sterile, turbid synovial fluid
 (3) combination of rheumatoid factor and anti-CCP antibody (80% of patients)
Manifests as a symmetric arthritis of small joints of the hand and feet
Synovium becomes edematous, thickened, and hyperplastic
Smooth contour turns into bulbous villi (A,B)
Histo changes  Pannus formation
1. Synovial hyperplasia and proliferation
2. Dense inflammatory infiltrate of CD4+ helper T cells, plasma cells, dendritic cells and
3. Increased vascularity due to angiogenesis
4. Fibrinopurulent exudate on the synovial and joint surfaces
5. Osteoclastic activity in underlying bone
a. Allowing the synovium to penetrate into the bone and cause periarticular
erosions and cysts
i. Periarticular erosions and subchondral cysts
WTF is a pannus?
- Mass of edematous synovium, inflammatory cells, granulation tissue, and fibroblasts
that grow over the articular cartilage and cause erosion
- After cartilage has been destroyed, pannus bridges the opposing bones to form a fibrous
- Eventually ossifies and results in fusion of the bones  bony ankylosis
Osteoarthritis (degenerative joint disease), the most common disease of joints, is a degenerative process of articular
cartilage in which matrix breakdown exceeds synthesis. Inflammation is minimal and typically secondary. Local production of
inflammatory cytokines may contribute to the progression of joint degeneration.
Rheumatoid arthritis (RA) is a chronic autoimmune inflammatory disease that affects mainly small joints, but can be
systemic. RA is caused by a cellular and humoral immune response against self-antigens, particularly citrul- linated proteins.
TNF plays a central role and antagonists against TNF are of clinical benefit.
Seronegative spondyloarthropathies are a heterogeneous group of likely autoimmune arthritides that prefer- entially involve
the sacroiliac and vertebral joints and are associated with HLA-B27.
Suppurative arthritis describes direct infection of a joint space by bacterial organisms.
 Tumors and Tumor-Like Lesions Involving Joints and Tendons
 Reactive(?)
 Secondary Trauma or Degenerative Processes
 Neoplastic
 Cytogenetic Studies
 Reveal consistent Chromosomal Aberrations
 Benign neoplasms
Tenosynovial Giant Cell Tumor
- Several neoplasms that develop in the synovial lining of joints, tendon sheaths, and
- 20s-40s
- Both types
o are heavily infiltrated by macrophages
o May contain hemosiderin or foamy lipid
o Scattered multinucleated giant cells
o Patchy fibrosis
Diffuse type
o Pigmented villonodular synovitis
o Involved large joints
o Normally smooth synovium is converted into a tangled mat by red-brown
folds, finger-like projections and nodules
o Spread along the surface and infiltrate the sub synovial tissue
o Knee involved 80%
o Symptoms: pain, locking, recurrent swelling, ROM limits
o Palpable mass
o Most common mesenchymal neoplasm of the hand
o Surgical excision
o Recurrence is common
Localized Type
o Giant cell tumor of the tendon sheath
o Occurs at discrete nodules attached to a tendon sheath
o Common in hand
o Well circumscribed
o Polygonal, moderately sized, resemble synoviocytes
o Solitary, slow growing, painless
o Tendon sheaths along wrists and fingers
PVNS – diffuse
o Involves the synovium
o One or more joints diffusely
o 20s-40s
o Synovial Hypertrophy
 Nodules
 Fronds
o Finger-like projections
o Microscopic
 Multinucleated giant cells
 Foamy macrophages
o Clinical
 Monoarticular Arthritis
 ROM Limitation
 Aggressive
 Surgery
 Significant recurrence rate
GCTTS – localized
o Discrete nodule on a tendon sheath
o Wrist, Fingers
o Arise in the 20s – 40s
o Solitary, Slow-growing
o Painless mass
o Cortical erosion
o Often recurs locally
o Surgery
o Localized
o Well circumscribed (walnut shaped)
o Microscopic
o Tumor cells
o Polyhedral
o Histiocytes
o Multinucleated Giant Cells
o Resemble synoviocytes
Synovial Sarcoma
- Arise near joints, especially the knee
- Lump painful or tender, slow-growing
- Deep seated mass present for several years
- Cell of origin unclear
- Lower extremity
- Lack synovium
- Inconsistent with origin from synoiocytes
- 20s-40s
- Chromosomal translocation
o X and 18
o Fusion genes
- Morphology
o Monophasic or biphasic
o Spindle shaped
o Uniform spindle cells with scant cytoplasm and dense chromatin in short tightly
packed fascicles
o May calcify
o Biphasic type
 gland link structures composed of cuboidal to columnar epithelium
 positive for epithelial markers (keratin) – differ from other sarcomas
o Monophasic type
 Misdiagnosed as fibro or adeno
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