MSK Module II Flashcards
Components of a synovial joint?
-Joint capsule (fibrous joint capsule: articular layer, synovial membrane: inner layer)
-Joint space (cavity)
-Synovial fluid
-Articular cartilage
What kind of cells are found in the synovial membrane?
Type A and Type B cells
Role of Type A cells in synovial membrane?
Immune function: secrete immunoglobulins, secrete lysosomal enzymes, contain macrophages that ingest debris
Role of Type B cells in synovial membrane?
Synovial fluid production:
Secretion of
-HA (hyaluronic acid)
-Glycoaminoglycan “gel” to improve viscosity of synovial fluid
-Lubricating glycoproteins (lubricin: reduces friction in joint)
What structure is enclosed by a capsule filled with synovial fluid?
Joint space (cavity)
What is synovial fluid?
Clear, viscous fluid that contains: hyaluronic acid and lubricin, proteinases, and collagenases
What is the function of synovial fluid?
Lubrication for joint surfaces to create “frictionless” surfaces between bones
What are the thixotropic properties of synovial fluid?
Viscosity varying inversely with velocity of movement:
-Rest: resists movement of joint
-Movement: provides less resistance
What is the thin covering on the ends of most bones?
Articular cartilage
Function of articular cartilage?
Reduces friction, absorbs/disperses compressive force
How much of the articular cartilage is made up of water?
60-80%
How much of the articular cartilage is made up of proteoglycans?
10-20%
How much of the articular cartilage is made up of collagen fibers?
10-20%
How much of the articular cartilage is made up of chondrocytes (chondroblasts)?
2%
Function of chondrocytes (chondroblasts) in articular cartilage?
Produce and maintain the extra-cellular matrix, secrete components needed to maintain matrix turnover (enzymes, collagen, PGs, etc.)
Function of collagen fibers in articular cartilage?
Role in regulating fluid flow in/out of cartilage, arranged to absorb mechanical stress
What kind of collagen fibers are found in articular cartilage?
Type 2 collagen
Function of proteoglycans in articular cartilage?
Regulate fluid flow in/out of cartilage
What do proteoglycans in articular cartilage consist of?
Hyaluronic acid & proteins that anchor glycosaminoglycans (chondroitin and keratin sulfate) to hyaluronic acid
What regulates water content in articular cartilage?
PGs, proteins, collagen
Zone of cartilage that has a smooth surface, reduces friction of the joint surface, and is without blood supply?
Zone 1 (superficial zone)
Zones of cartilage that are transitional, absorb compressive forces, and are without blood supply?
Zones 2 & 3 (middle and deep layers)
Zone of cartilage that is an interface between uncalcified and calcified layers?
Tidemark
Zone of cartilage that is calcified, anchors the cartilage to bone, and has blood supply?
Zone 4 (calcified cartilage layer)
Function of articular cartilage as a whole?
-Provides smooth/frictionless surface for joint movement
-Absorbs and disperses everyday compressive forces passing through joint to underlying bone
Articular health/function requires consistent matrix balance between what?
Anabolic and catabolic stimuli
What allows nutrients to pass in and out of articular cartilage/reach the chondrocytes?
Repetitive loading/unloading of compressive forces
What activity pushes fluid (water/synovial fluid) out of the cartilage?
Weight bearing: fluid flow slows/resistance becomes harder when cartilage is compressed
What activity pulls fluid back into the cartilage matrix (acts like a sponge)?
Non-weight bearing forces: proteoglycans, proteins & collagen can regulate fluid flow in/out of cartilage
What maintains articular cartilage matrix homeostasis/turnover?
Cytokine signaling/enzymes, hormones, mechanical stimuli
How does anabolic cytokine signaling/enzymes help maintain articular cartilage matrix homeostasis/turnover?
Chondrocytes will secrete enzymes and anti-inflammatory cytokines to promote in-matrix homeostasis (anabolic)
How does catabolic cytokine signaling/enzymes help maintain articular cartilage matrix homeostasis/turnover?
Chondrocytes may secrete/synovial fluid may contain enzymes & pro-inflammatory cytokines which inhibit in-matrix homeostasis (catbolic)
How do hormones help maintain articular cartilage matrix homeostasis/turnover?
Growth hormone and insulin-like growth factor (IGF-1) stimulate chondrocytes/play a role in regulating matrix turnover (anabolic signaling)
How does mechanical load help maintain articular cartilage matrix homeostasis/turnover?
Normal weight bearing of daily activity: required to maintain matrix homeostasis (anabolic signaling)
Does articular cartilage have direct blood supply?
No
What parts of the articular cartilage do have blood supply?
Subchondral bone below cartilage, tidemark, joint capsule
Is articular cartilage innervated by nerves?
No
What parts of the articular cartilage are innervated by nerves?
Subchondral bone below cartilage, tidemark, joint capsule
Does articular cartilage have good healing properties?
No, poor healing/ability to regenerate after injury due to poor blood supply
Is articular cartilage pain sensitive?
No, pain insensitive
*pain associated w/ joint injuries/pathology does not originate from articular cartilage
Where does pain from joint injuries/ pathology originate?
Damage to other structures of the joint that are pain sensitive (joint capsule, subchondral bone/periosteum)
What is Osteoarthritis (aka degenerative joint disease)?
Non-inflammatory joint disease
Yet when acute trauma/physical stress occurs in a joint w/ OA, it signals pro-inflammatory cytokines contribute to further cartilage degeneration
What is the most common joint disease?
Osteoarthritis (OA)
How does normal cartilage appear?
Smooth/glossy surface
How does cartilage appearance change in osteoarthritis?
Becomes a dull yellow/brown color w/ surface flaking fissures & fibrillations
What is the primary defect of OA?
Cellular disruption of articular cartilage matrix (catabolic signaling exceeds anabolic signaling leading to matrix destruction)
Etiologies of OA?
- Genetics
- Hx of cartilage trauma
- Lifestyle (smoking, obesity, etc.) increase risk
Catabolic enzymatic changes of OA?
Chondrocytes and synovium secrete catabolic enzymes that lead to matri breakdown
Which catabolic enzyme disrupts proteoglycans by breaking down proteins that anchor glycosaminoglycans to HA?
Proteinases
Which catabolic enzyme breaks down collagen fibrils and portions of the proteoglycans?
Collagenases
Pro-inflammatory cytokine signaling in OA?
Chondrocytes and synovium secrete IL-1, TNF, other cytokines, nitric oxide that lead to matrix breakdown
Role of IL-1 beta and TNF-alpha and others in OA?
promote inflammatory catabolic processes
**IL-1 inhibits normal cytokine secretion and stimulates nitric oxide secretion
Role of nitric oxide in OA?
Not normally found in healthy synovial joint - when present, promotes chondrocyte apoptosis
Role of hormone changes in OA?
Chondrocytes will become less sensitive to GH/IGF
How do catabolic enzyme and cytokine changes lead to cartilage function loss?
Loss of proteoglycans, proteins, collagen –> disrupts fluid regulation
*water flows in/out too easily, cartilage loses ability to resist compressive weight bearing force
How do catabolic enzyme and cytokine changes lead to cartilage loss?
Loss of collagen –> disrupts physical structure of cartilage
*flaking/thinning of cartilage
What happens in weight bearing function in OA?
Cartilage unable to resist compressive force, water flows out too easily/rapidly
What happens to non-weight bearing function in OA?
Cartilage will “pull back” too much water, can contain 90+% water
What can result from OA promoting damage to surrounding structures?
Subchondral bone sclerosis and bone cysts, synovial thickening, osteophyte formation
Subchondral bone sclerosis and bone cysts may be asymptomatic until when?
They become severe
Subchondral bone sclerosis and bone cysts have the potential to communicate with what in the cartilage?
Fissures of cartilage (releasing content into synovial fluid of joint space)
What can contribute to the loss of gross movement of a joint?
Synovial thickening and sometimes osteophyte formation
What can occur due to osteophyte formation?
Irritation of synovium, may contribute to loss of gross movement
What are Herberden’s nodes (OA)?
Bony enlargement of the DIP joints from cartilage destruction/osteophytes
“hip-dip”
What are Bouchard’s nodes (OA)?
Bony enlargement of PIP joints from cartilage destruction/osteophytes
Does exercise (running, walking) have any risk for development of OA?
Very low or no risk
*high impact sports may increase risk due to traumatic forces/injuries –> twisting high impact movements increase stress
Risk factors for the development of OA?
-Previous trauma and genetics are MC**
-Age 40/50 and up
-Obesity
-Females > Males
-Others: joint/ligament laxity, inflammatory conditions, neurological disorders
How can neurological disorders contribute to development of OA?
Loss of normal sensory pathways can result in abnormal movement/damage joint
What are the provoking pain patterns of OA?
-Morning pain
-Prolonged postural positions
-Increased pain with extreme/intense activity
Relieving pain patterns of OA?
Feels better w/ easy low impact activity, heat and sometimes cold, OTC NSAIDs
Referred pain from OA?
-OA of the spine (potential nerve root entrapment)
-OA of LE joints (hip may refer to knee, hip to ankle, knee to hip)
How is the joint deformed in OA?
Joint capsule thickening
What loss of function/mobility is present in OA?
-Limited ROM (decreased joint congruency, osteophytes, pain)
-OA of lower extremity: gradual loss of wt bearing activity
Treatment strategies for OA?
-Lifestyle changes (conservative)
-Pharmaceutical (targeted @ sx relief)
-PT
-Injections (steroids or viscosupplementation)
-Surgery
Which surgery options are available for treatment of OA?
Arthroscopic lavage/debridement (limited evidence to support use), and joint replacement (arthroplasty) as a last resort if all other tx fails
Which injection for OA contains gel-like substances (hyaluronates) thought to improve viscous properties of synovial fluid? How many injections are given over several weeks?
Hyaluronic acid injection (viscosupplementation),
1-5 given over several wks
Which injection for OA contains growth factors such as fibroblast GF, epidermal GF, vascular endothelial GF, transforming GF-B, and platelet derived GF?
Platelet rich plasma (PRP) injection
Which injection for OA has better pain relief?
PRP injection (yet results not conclusive)
Are injections for OA high or low risk procedures?
Low risk
Which procedure has limited evidence effectiveness for routine use for OA according to the American Academy for Orthopedic Surgeons?
Arthroscopic lavage and debridement - used as temporary relief for sx, does not repair cartilage
Criteria for joint replacement for OA is determined by what?
Pain and QOL
Does joint replacement for OA have positive outcome rates?
Yes
Cost of joint replacement in U.S. as of 2020?
30k-50k
What are treatment options for cartilage injury?
Marrow stimulating techniques (microfracture)
Osteochondral transplants (OATS)
Autologous chondrocyte implantation (ACI)
What are marrow stimulating techniques for cartilage injury?
Microfracture with growth factor/cytokine augmentation:
Use of a bone pick to penetrate subchondral bone (below tidemark exposing BV and promotes bleeding),
bone marrow bleeding allows fibrocartilage to fill defect
Are the long term outcomes of marrow stimulating techniques good or bad?
Poor w/ microfracture alone
*current approaches include GF and cytokines!
What are osteochondral autograft transplants for cartilage inury?
Autografts (from patients own body):
-Osteochondral plugs are taken from non-wt. bearing area of the knee and inserted into pre-drilled holes in the chondral defect
*plugs comprised of hyaline cartilage, but small space around plugs fill w/ fibrocartilage
What are osteochondral allograft transplants for cartilage injury?
Grafts that come from another person/cadaver:
same as OATS procedure just from cadaver
What is an advantage of allografts?
Allows for more osteochondral tissue to be taken, larger areas of defect can be repaired
What are the phases of autologous chondrocyte implantation (ACI) for cartilage injury?
Phase 1: harvest chondrocytes from non-wt bearing area of joint, culture/grow more chondrocytes in lab for 3-6 weeks
Phase 2: Prepare chondral defect/implant new chondrocytes from lab