Patho: Joints Flashcards
What is a joint?
Joint is a union b/w two or more bones and construction varies with function of joint
What are the two types of joints?
Synovial: Freely moveable, produce synovial fluid which provides lubrication
Synarthosis: Little or no movement
Elaborate on synarthroses joints
Provide structural integrity and allow minimal movements
Lack a joint space
synarthroses joints Two types, depend on tissue 1: Explain: Examples:
2: a: example b: example
Fibrous Synarthroses aka syndesmosis
•Bones connected by fibrous tissue w/out cartilage
oCranial sutures, tibiofibular syndesmosis
Cartilaginous Synarthroses
• Symphyses: Joined by fibrocartilaginous tissue and firm ligaments
o Vertebral bodies
• Synchondrosis: Articular cartilage without synovium
o 1st rib and sternum
Elaborate on synovial joints
aka
explain
AKA Cavitated joints with dense fibrous capsules that are reinforced by ligaments & muscles
Types of Synovial joints based on the movement
Uniaxial Joints
•Movement around one axis
•Hinge joint @ elbow
Biaxial joints
•Movement around two axis
•Wrist/joint
Polyaxial joints
•Movement in any axis
•Ball and socket
Plane joint
•Articular surfaces glide over one another
•Patella
What is synovium made up of?
Composed of:
Synovial fluid is:
Synovial tissue is responsible for:
Composed of 1-4 layers of cells (usually only 2: outer layer or subintima, and inner layer or intima composed of a sheet of cells). Abuts cartilage on all sides.
Synovial fluid is in cavity.
Synovial tissue is responsible for making the fluid and has cells that can articulate cartilage in a good and bad way (can destroy in when it makes hydrolases)
Synoviocytes
type A
Type B
Expansion of type B cells is a hallmark of:
Type A: Macrophage like synoviocytes
o Macrophages with lysosomal enzymes – degrade things (cartilage) and recognize foreign bodies
o If released, can cleave away cartilage
Type B: Fibroblast-like synoviocytes
o Synthesize hyaluronic acid and proteins into synovial fluid important for the movement of the two bones. Gives viscosity and elasticity via proteins (glycoproteins)
o Expansion of these cells is a hallmark of rheumatoid arthritis
• When activated, can destroy cartilage
The synovium lacks what?
Lacks basement membrane: This is important because Capillaries very close to cells including fibroblasts, allowing plasma to be freely filtered into synovialcytes. Then synovialcytes can shuttle plasma and proteins it makes into synovial fluid. Quick exchange bw blood and synovial fluid.
What does the synovium and synovial fluid control? Synovium: Mediaties: Diffusion: Ingest: Lubrication
Synocial
appearance:
acts as a:
-
Synovium: Mediates nutrient exchange bw blood and joint fluid
•Diffusion in and out of the joint
•Ingestion of debris
•Secretion of hyaluronate, immunoglobulin, and lysosomal enzymes into the space
•Lubrication of joints by secreting glycoproteins
Synovial:
•Clear, viscous, filtrate of plasma containing hyaluronic acid
•Acts as lubricant and nourishes chrondrocytes of articular cartilage.
•Even glucose gets in – articular cartilage in osteomyelitis/osteonecrosis is fine because it receives nutrients it needs from synovial fluid
Explain what makes up hyaline cartilage (articular cartilage) and the function of each product
1: 2: 3: 4: Important-
Connective tissue of type II collagen providing tensile strength (bone is type I collagen)
Water is in collagen providing limited amount of friction
Proteoglycans provide elasticity
Chondrocytes synthesize the matrix (type II collagen) and secrete degradative enzymes in inactive form (become activated based on environment – acidic) and enrich matrix with enzyme inhibitors (keep things in check)
-Important – make everything and provide enzymes to break things down and release inhibitors to stop enzymes. In balance to replace cartilage as needed
The cartilage receives its blood and intervation from what?
Elastic shock absorber
lacks blood supply but receives things from nearby bones and synovial fluid, no lymphatic drainage or nerve innervation.
However, pain receptors present in nearby blood vessels and joint capsule, but not exactly in cartilage.
Diseases that destroy articular cartilage do so by
activating catabolic enzymes of destruction and decrease production of inhibitor.»_space; destruction, < inhibitors
What are the zones of cartilage?
Tangential or gliding zone: Closest to articular surface (synovial fluid)
•Chondrocytes
•Type II collagen
Transitional zone
•Chondrocytes
•Hyaline cartilage present
Radial zone
•Collagen fibers
Calcified zone
•Calcified matrix
at bone end plate
what is the Tidemark?
location:
what happeneds here?
Separates radial (collagen) from calcified zone (calcified matrix)
Cartilage cells regenerate her and migrate upward
Chondroblasts → chondrocytes
degenerative arthritis
degenerative arthritis
Explain what degenerative arthritis is
o Progressive destruction (erosion) of hyaline (articular) cartilage
o AKA Osteoarthritis
What are the types of degenerative arthritis? (two major types:
1:
a:
b:
2:
a:
b:
o Idiopathic (primary) OA Localized OA: Hands, feet, knee, hip, and spine Generalized OA: Involve 3 or more joint sites
oSecondary OA
Trauma: Seen with athletes with > injuries: Football players
Congenital or developmental
Location of degenerative arthritis?
Older adults:
Younger adults:
Older adults: Weight bearing joints and fingers
Younger adults: Joints subjected to trauma
What is the pathogenesis of primary osteoarthritis? Joints: Age: - - Gender - - Why?
- on xray:
Usually oligoarticular (> one joint)
Increases with age
4% of 18-24 year olds
85% of 75-79 year olds
Gender:
< 45 years old: Mainly men
>55 years old: More common in females
Why? Unsure. Conflicting research.
Some studies in animals show estrogen is protective of bones and joints. Estorgen stimulates chondrocytes, Increased replacement. Limited studies in humans. But, when estrogen levels are high (follicular stage), more tears in ACL. Opposite of animals.
Familial clustering: Hereditary predisposition. If parents have knee replacement in 50’s due to OA, you are more likely to have it yourself.
Progressive degradation of articular cartilage
• Joint space narrows as cartilage decreases→ Subchondral bone thickening bc osteocytes sense increased in pressure which send cytokines to osteoblasts → nonfunctioning, painful joint
•On x-ray, subchondral bone will be bright bc under increased pressure/friction
What are the two principal mechanisms of pathogenesis for OA? 1: ex: MOA: 1: Ex: MOA:
1: Damage to normal articular cartilage by physical forces (single event of macrotrauma or repeat microtrauma)
i. e.: Obesity with increased weight causes architectural changes and damage
MOA: Chondrocytes react to injury by releasing degradative enzymes and elaborating inadequate repair. When chondrocytes really damaged, they replace more damaging enzymes and not the inhibitors. Now you get articular breakdown and cracking of cartilage.
2: Defective cartilage (genetic predisposition based on type of collagen you make) initially fails under normal joint loading, leading to OA. (type II collagen gene defect)
- More prone to cracking allows fluid to get into cartilage.
What occurs with death of chondrocytes? 1: 2: 3: 4: 5: 6: 7: 8:
1: Tear/crack (injury/overuse/bad collagen) in articular cartilage allows influx of synovial fluid
2: Further loss and degeneration of cartilage due to fluid influx
3: Cartilage gradually worn away-Chondrocytes may release enzymes which will further breakdown cartilage
4: Due to the trauma the bone forms a hematoma with new vessels grow in from epiphysis and fibrocartilage deposited through the tidemark, forming a fibrocartilage Plug
5:Fibrocartilage plug is not mechanically sufficient and can be worn away
6: Exposure to the sybcondral bone plate which become thickened (due to increase pressure causing osteoblast formation)
7: if there is crack in that bone the synovial fluid leaks into the marrow space producing the sybchondral cyst
8: Focal regrowth of articular surface leads to formation of ostophytes.
All this will cause surrounding area to be under mechanical forces causing > osteocytes → > osteoblasts → excess growth (spurs or osteophytes)
What is the pathogenesis of primary osteoarthritis- Three phases of chondrocyte activity?
1:
2:
3:
Three phases of chondrocyte activity
Chondrocyte injury: Related to age, genetics, and biochemical factors
•Occurs with cracking, fluid that moves in, chondrocytes damaged, release enzymes for degradation than inhibitors = break down
Early OA: Chondrocytes proliferate and secrete inflammatory mediators, collagens, proteoglycans, and proteases- clean the area and heal it but if the source is still there you still get break down.
•Act to remodel cartilaginous matrix & initiate 2nd inflammatory changes
Late OA: Repetitive injury and chronic inflammation lead to chrondrocyte die out, marked loss of cartilage and extensive subchondral bone changes
• Huge areas of bone show now
- no more condrocytes to make cartilage.
Patho: what happened when you get damage?
You get damage in joint, either chondrocyte, immune cells, synovial cells, fibroblasts → all make cytokines IL-1beta and TNF-alpha
causes Chondrocytes to make MMP (matrix maltaloproteinases) → destroy matrix protein and haluronic acid.
Condrocytes also produce ADAMTS-4 degrades aggrecan (a proteoglycan) within cartilage
• Cause production of MMP, TNF → degrades type II collagen!
o Chondrocytes degrade cartilage of what they are trying to build up
o Know cytokines activate chondrocytes to produce substances that destroy cartilage.
o Due to degradation and tension, osteoblast and clast activity can affect subcondral bone
What is the multifactorial pathogenesis of primary OA Environmental and genetics: 1: 2: 3:
o Environment and genetic components
Candidate genes:
1:Prostaglandin metabolism
2:WNT signaling: Secreted signaling molecules that regulate cell to cell interactions
oWNT important bc it affects B-catenin
oWithout WNT, B-catenin phosphorolated and dies
oWith WNT, no phosphorylation, anchors the cell
3: COL2A1 gene: Type II collagen gene
•Environmental factors
1: Age: 80-90% of individuals 65+
2: Biomechanical stress: Obesity, muscle strength, joint stability, structure and alignment
what are the Systemic diseases that leads to secondary OA ?
- DM
- Trauma - Single joints: b-ball players, basketball players
- Cyrstal deposits – those with gout have > chance for OA
- Infection – osteomyelitis and osteonecrosis
- Hemarthrosis
- Hemochronatosis – iron (genetic disorder)
- Obesity - > mechanical force on joints
Chondromalacia
(OA that affects inside of patella only)
•Subcategory of osteoarthritis
•Patellar surface of femoral condyles degenerate
•Pain and stiffness of knee
Explain radiographic findings of OA
Joint spaces normally should be symmetric on each side. In OA, narrowing of joint space with loss of cartilage.
Increased thickness of subchondral bone (bright white)
•Subchondral bone cysts may appear (synovial fluid into bone after ripping through hyaline cartilage)
•Large peripheral growths of bone and cartilage (osteophytes)
Eburnation
Conversion of bone into hard ivory-like mass, occurs in subchondral area where it is more dense and becomes ivory white.
Joint mice:
dislodged pieces of cartilage and subchondral bone into the joints, map appear as if floating in joint space on imaging
Osteophytes
Bony out growths develop at margins of articular surface. Capped by fibrocartilage and hyaline cartilage that ossify.
Bone spurs do not need to have cartilage, osteophytes do need cartilage tissue
How does OA appear?
PAINFUL, with limited ROM
Joints turn into bone on bone – may eventually have fusion
Heberden Nodes:
Osteophytes at distal interphalangeal joints
