Joint Diseases Flashcards
Joint Classification
Solid
- Bony (synostosis - two bones come into contact, sutures in the skull)
- Fibrous (Syndesmosis - fibrous tissue connects two bones, Fibia attaches to the distal end of tibia)
- Cartilangous (Symphysis - cartilage connecting two bones, Discs of cartilage)
Caviated Spaces
- synovial (cavitated joint, Knee)
Normal Synovial Joint Structure
- ends of bone = articular cartilage (touch, glide smoothly, move with one another)
- around bone and cartilage is a space = a capsule - capsule lined by cells called the synovium - cells produce fluid to lubricate the joint to move freely and painlessly, it nourishes the cartilage
- muscles, tendons, and spaces - help cushion the joint
Histology of Normal Synovium
- synovium lining cells are 1-2 cell layers thick
- fibrous connective tissue, fat cells, blood cells - no significant number of inflammation or inflammatory cells
- A and B cells (one responsible for producing fluid, the other is more phagocytic in nature)
- adipocyte - fat cells
Normal Joint Physiology and Function
- cartilage is firm but pliable and changes shape under increasing loads causing it to come into increasing contact, therefore distributing the load
- Cartilage is elastic and extracellular membrane allows for the retention of water
- when force is administered, cartilage fluid is compressed, and extracellular water is extruded
- removal of the force allows for the extracellular matrix to draw the fluid back inward and the cartilage returns to original shape
- cartilage is avascular and receives all nourishment from synovium fluid - even under force, synovium fluid can still flow to the cartilage
- cartilage and subchondral bone are constantly undergoing remodeling to optimize load
The functioning of joints depends on the following:
1.) Maintenance of stability during use
2.) freedom of opposed articular surfaces to move painlessly over one another with a normal range of motion
3.) Correct distribution of load across joint tissues to avoid damage
- joint function governed by the shape of articulating joint surfaces, the integrity of supporting tissue, and biological cellular control of the mechanical properties of the tissue
- disturbance of any of these -> joint disease
Joint Disease Classification
- Arthritis (inflammation/degenerative, most common)
- Infectious (septic arthritis - due to microorganism)
- Tumours (least common)
Classification of Arthritis
Non-inflammatory
- Osteoarthritis
Inflammatory
- Infectious
- Non-infectious
1. Rheumatoid Arthritis,
2. seronegative arthropathies,
3. crystal-induced arthritis
Osteoarthritis
Epidemiology
- degenerative joint disease
- most common in NA
- 10% of individuals >60
- incidence increases with age
Clinical Presentation
- insidious development (gradual)
- pain, stiffness, decreased mobility
- worse with movement
- single or few large, weight baring joints (hips, knees, ankles)
- asymmetrical
- pain eased with rest
Radiographic Features
- loss of joint space
- osteophyte formation
- increased density of bone immediately beneath 1.) articular cartilage (subchondral bone sclerosis and 2.) subchondral cyst formation
Osteoarthritis Pathological Features
Gross features
- articular surface and bone are misshapen with the formation of peripherally located bone spurs (osteophytes)
- articular cartilage is not smooth, pearly-blue, or shiny - it will present areas of thinning, roughening (fibrillation), red-brown discolouration, areas with complete loss of cartilage -> eburnation (exposure of bone that then becomes smoothly polished marble)
- cross-sectioning causes subchondral bone sclerosis, and subchondral cysts are visible
- regenerative process at the periphery exceeds loss - joint larger than normal joint
- will eventually need a replacement prosthesis
Microscopic Features
- duplication and irregularity of the tidemark (the line where cartilage undergoes endochondral ossification)
- chondrocyte clones (large clusters of chondrocytes trying to replace lost articular cartilage)
- synovial cell hypertrophy/hyperplasia ( villous change of the synovium and nil to minimal chronic inflammation
- inflammation is negligible
- will not see WBCs in synovium fluid, see broken pieces of cartilage, no culture bacteria
- multiple cracks, deep fissures
- complete loss of Hyaline cartilage with thickening of subchondral bone and replacement of fibrocartilage
Osteoarthritis Stages
Early Degenerative changes
- Surface fibrillation of articular cartilage - fissures can extend down
□ Irregularity between bones begins
- Early disruption of matrix-molecular framework (increased water content and decreased proteoglycans) - cells not functioning properly
- Superficial fissures
- Roughened articular surfaces and minimal narrowing of joint space
- Narrowing of upper portion of joint space with early degeneration of articular cartilage - center area is where the problems first occur
- Sclerosis - thickening of subchondral bone early sign of degeneration
Advanced Degenerative Changes - Joint and Articular Changes - continued
- Release of fibrillated cartilage into joint space
- Fissure penetration to subchondral bone
- Enzymatic degradation and thinning of articular cartilage
- Loss of cartilage and narrowing of joint space
- Marked narrowing of joint space with local loss of articular cartilage, osteophyte formation, and bone remodeling
- Pronounced sclerosis of subchondral bone
End-stage Degenerative Changes
- Exposed articular surface of subchondral bone
- Loss of articular cartilage (bone-on-bone articular surface)
□ Eburnation - bone becomes smooth and polished
- Subchondral cysts
□ Cracks in subchondral bone, synovial fluid leaks in to form the cysts
□ One way valves that eventually cause expansions
- Capsular fibrosis
- Articular cartilage lost and joint space narrowing. Bone shows remodelling osteophyte and subchondral cysts
- Fibral cartilage (fibrous and rich) made instead of hyaline cartilage
- Dose does not make as much or as effective cartilage
Pathophysiology
1.) Loss of proteoglycans from the extracellular matrix (use special stains to see, if indicative of abnormal biochemical functioning of chondrocytes
2.) Chondrocyte Clones develop (enlarged chondrocytes in attempt to replace lost and damaged cartilage)
3.) Superficial cracks develop (fibrillation), deep cracks become fissures, and cracks can be vertical/horizontal and result of breaking off into the joint space (joint mice, loose bodies). Chondrocytes loose bodies are viable due to nutrition still available, and hyaline cartilage is replaced by fibrocartilage
4.) articular cartilage loss exceeds replacement -> exposure of underlying bone (subchondral), bone remodels become thickened (sclerotic) in an attempt to handle transmitted forces becoming eburnated
5.) subchondral bone cracks (microfracture) and allows synovium fluid to enter the creates forming subchondral cysts
6.) Osteophyte formation results of loss of articular cartilage and retransmission of forces; mesenchymal cells forms masses of bone and cartilage - bone spurs - in the fingers they are called Heberden and Bouchard’s nodes
osteoarthritis - Pathogenesis
- Not simply a disease of wear and tear, but occurs
Multifactorial
- Cartilage dysfunction - as we age
- Subchondral bone stress
- Synovium - IL-1, TNF-alpha - inflammatory factors
- Microvascular disease - not a huge change in blood vessels
The end stage of multiple processes
- Fracture, congenital abnormality, metabolic, etc.…
Primary Osteoarthritis
- When we do not know what caused it
- not due to increasing age, but has correlations
Secondary Osteoarthritis
- When we do know what caused it
- congenital hip dysplasia, fracture, infection, avascular necrosis, metabolic diseases
OA results:
- any condition that affects the articular surfaces of the joint, bones of the joint, tissues supporting the joint (ligaments, capsule, tendons)
Rheumatoid Arthritis
- A chronic, non-suppurative, systemic, unknown etiology, inflammatory disease with pathological changes most frequently affecting small joints (PIP, MCP, wrist, elbow, ankle, knee) in a symmetrical fashion, resulting in joint destruction, deformity, and loss of function
- No neutrophils involved, not infectious
- Changes that occur outside the joints - systemic
Rheumatoid Arthritis - Clinical Findings
- RA most common of inflammatory arthritis
- primarily attacks synovium lining of peripheral joints
- results in the secondary destruction of the articular cartilage
- characterized by bouts of remission and excerbation
- W:M = 3:1
- Extra-articular features - arthritis, neuropathy, pericarditis, pleuritis, lymphadenopathy, and rheumatoid nodules
- complain of malaise, pain, and stiffness of joints, worsening in the morning and improving throughout the day
- involves multiple joints, symmetrically, bilaterally
- small joints of hands and feet, most common
- joints are swollen, painful, hot, red
- synovium fluid indicates neutrophils and no bacterial culturing
RA Radiographic and Pathologic Features
Radiographic
- periarticular loss of bone (osteopenia)
- bone erosion
- narrowing of joint space
- subluxations
- dislocations
- soft tissue swelling
Pathological Features
Gross features
- joint destruction with little reparative activity - osteophytes and new bone formation are not prominent
- synovium is hyperplastic, thickened, and extends of articular cartilage (pannus)
- Thick synovium with finger-like projections - villi
- Focal fibrin deposition
- Iron deposition gives a brown colour
- eburnation
Microscopic Features
- synovium lining cells increase in number (hyperplasia) and in size (hypertrophy)
- synovium expanded by edema, increased number of blood vessels (angiogenesis), and chronic inflammatory genesis (lymphocytes and plasma cells - not neutrophils) they form lymphoid follicles with germinal centers
- expansion cause synovium to form fingerlike projections (papilla/villi) that extend to the joint spaces and over the articular cartilage (pannus)
RA - Pathophysiology
- pannus destroys underlying cartilage by several mechanisms:
1.) pannus physically covers there cartilage nearby, preventing it from receiving adequate nutrition from the synovium fluid
2.) Pannus releases enzymes that directly destroy cartilage
3.) Pannus releases inflammatory mediators that activate osteoclasts which destroy bone and cartilage - resulting in the destruction of articular cartilage and loss of bone with joint subluxation and instability - pannus completely extends across joint -> joint becomes fused and unable to move (ankylosis - fusion) - looks like a sharpened pencil, loss at ends
- destroys in waves - articular cartilage cannot get nutrients or get rid of waste due to the pannus blocking synovium fluid
