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337 Cards in this Set
- Front
- Back
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types of forces |
tension (we apply) shear (we apply) compression (more careful) torsion (more careful) |
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tissues types that forces effect (fundamental tissue types) |
muscular, nervous, epithelial, CT |
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extrinsic factors related to forces |
orthotics, taping, assistive devices, footwear, desk work, what they are doing at gym |
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theory |
predicts/explains phenomena |
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physical stress |
force applied to specific area of tissue |
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organ systems involved w/ guide to PT practice |
MSK Cardiopulm Neuromuscular Integumentary |
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physical stress theory |
changes in relative level of physical stress cause predictable adaptive response in all biological tissue |
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effects of physical stress on tissue (hierarchy) |
death, injury, increased tolerance (hypertrophy), maintenance, decreased tolerance (atrophy) death |
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injury |
tissue damage from excessive stress resulting in pain, discomfort, and/or impaired fxn |
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level of exposure to physical stress is composite value defined by ____,_____,______ of stress application |
magnitude (how much force), time (how long force applied, duration), direction (compression, tension, shear, torsion) |
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excessive physical stress that causes injury can occur through 1 or more of the following 3 mechanisms |
1) high force, short time (car accident) 2) mod force, mod time (running injury) 3) low force, long time (posture) |
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t/f: regardless of mechanism of injury inflammation ALWAYS occurs immediately following tissue injury and renders injured tissue LESS tolerant of stress than it was prior to injury |
True |
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factors affecting level of physical stress on tissues or the adaptive response of tissues to physical stress |
1) mvmt and alignment factors 2) extrinsic factors 3) pysch factors 4) physiological factors |
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mvmt and alignment factors of physical stress |
muscle performance, motor control, posture and alignment, PA; occupational, leisure, and self care activities |
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physiological factors of physical stress |
meds, age, systemic pathology, obesity |
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clinical reasoning in PT is |
-interaction that is collaborative (enable understanding of problem, enable negotiated plan) -pt-centered -deductive and inductive -complex, non-linear, cyclical -allows reflective learning and dev't of clinical expertise |
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types of clinical reasoning |
procedural interactive reasoning about teaching predictive ethical |
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reflective thinking and critical thinking types |
-reflection on action (what you did) -reflection in action (as going through process) -reflection for action (taking next sets in terms of past experience) |
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dialectic thinking |
diagnostic reasoning, deductive reasoning vs. narrative reasoning, inductive reasoning |
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deductive reasoning |
starting w/ known facts, logical reasoning to come up w/ additional facts |
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inductive reasoning |
start w/ general info and try to find patterns in it, try to find patterns in it, generalization |
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8 hypothesis categories |
AL/PR Pathobiological mechanisms Pt perspective impairment/source of sx's Contributing factors mgmt/tx precautions/contraindications Px |
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classifications of injury |
acute subacute chronic acute on chronic |
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acute injury |
immediately after event; macrotrauma and microtrauma when gets to injury level; 7-10 days |
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subacute injury |
12-20 days |
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chronic injury |
not healing way it's supposed to |
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acute on chronic injury |
injury for extended period of time, then reinjuring it |
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physical barriers to invading pathogens |
skin, mucosal membranes |
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innate immune system |
tissue macrophages, neutrophils, NK cells, complement system (membrane attack complex) |
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adaptive or acquired immunity |
B cells: produced in bone marrow T cells: produced in bone marrow, mature in thymus; regulatory T cells, Helper T, Killer T cells |
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T cells |
produced in bone marrow, mature in thymus; bind to MHC complex; MHC I recognized by cytotoxic T cells; MHC II complex recognized by helper T cells |
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CD4 |
helper T |
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CD8 |
killer T |
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B cells |
look for antigens, activated by binding with antigen, may need help from helper T cell to get fully activated, differentiate into clones of itself, turn into memory cells that recognize same antigen quickly, and plasma cells = antibody factories that bind to antigens antibodies bind to antigens = flag antigens to increase rate of phagocytosis |
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neutrophils |
activated as leave blood, most numerous, fastest responders |
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NK cells |
normally in blood, kill what is not human (don't have MHC complex marker) |
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repair |
patched/fixed w/ tissue that is not same as tissue started out as |
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regeneration |
tissue replaced by tissue just like injured tissue |
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phases of wound healing |
hemostasis inflammatory phase repair phase (fibroplasia/proliferative) remodeling phase (maturation) |
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wound healing in general timeline |
inflammatory: acute 0-48 hours, subacute 2-4 wks fibroplasia/repair: day 2-4 to 4-6 wks remodeling/maturation: 2-3 wks up to 2 years |
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inflammatory phase |
essential for orderly, timely healing 3-7 days goal: provide for breakdown and removal of cellular, extracellular, and pathogen debris result: clean wound site for tissue restoration and initiation of repair process |
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fibroplasia/repair phase/proliferative phase |
begins 3-5 days post injury continues for 3 weeks in wounds healing by primary intention goals: fills in wound defects w/ new tissue, restore tissue integrity of skin benchmark: new tissue formation |
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remodeling/maturation phase |
decreasing fibroblasts, increased cross links, type 3 to type I collagen |
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timeline of skin healing |
inflammatory: up to 3 days (most w/in 1st 48 hrs) fibroplasia/repair: day 4-14 remodeling/maturation: 10-14 days to several months |
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prothrombin to clot chart |
draw |
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5 cardinal signs of swelling |
5 cardinal signs of swelling: redness, swelling, heat, pain, loss of fxn |
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key processes in inflammation |
-mitogenesis and chemotaxis of growth factors -controlled tissue degradation -role of perfusion -hypoxia and regulatory fxn of oxygen-tension gradient -complement system activation to control infection -neutrophil, macrophage, mast, and fibroblast cell fxns -keratinocyte activation -current of injury |
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leukocytes |
lymphocytes: T cells and B cells monocytes to macrophages granulocytes: neutrophils, basophils, eosinophils |
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epithelialization phase |
benchmark: resurfacing of wound and changes in wound edges -process of resurfacing is fxn of keratinocytes -response w/in hours of injury -full thickness wounds -tensile strength of remodeled skin |
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epithelialization in chronic wounds |
diminished keratinocyte migration, delayed b/c of need for granulation tissue to fill wound bed |
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key processes in repair phase |
angiogenesis, collagen synthesis, wound contraction |
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angiogenesis |
stimulated by hypoxia; formation of micro vessels to help re establish o2 in area of damage |
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granulation tissue in wound healing |
"patch" replaces provisional fibrin matrix (formed w/ clot) ground substance contains: macrophages, fibroblasts, myofibroblasts, neovasculature capillary budding |
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fibroblastic cell proliferation wound healing |
activated by cytokine GFs released by PDGFs fibroblasts secrete: collagen fibers, GAGs, ground substance, fibronection myofibroblasts: helps w/ remodeling |
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proliferative phase in chronic wound healing |
fibroblast senescence fibronectin composition chronic wound fluid-inhibiting factors plateauing of healing delayed reepithelialization |
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remodeling phase in wound healing |
begins as granulation tissue forms in wound bed during proliferative phase and continues for 1-2 years scar tissue: initially 15-20% tensile strength, end 80% tensile strength collagen conversion Type III to Type I |
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remodeling phase in chronic wounds |
dysregulation of collagen synthesis hypertrophic scarring: thick scar stays in wound margins hypergranulation |
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factors affecting healing process |
local factors: cleanliness, size of injury, mvmt, depth of injury, enviro systemic factors: disease, immune system, alcohol, nutrition extrinsic factors: temp, cleanliness, meds |
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chemical mediators of inflammation |
arachidonic acid leukotrienes thromboxanes PGs |
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arachidonic acid |
metabolism initiated by enzymatic degradation of cell membrane phospholipids forms 3 major substances: leukotrienes, thromboxanes, PGs |
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leukotrienes |
involved w/ allergies and asthma |
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thromboxanes |
involved in clotting/hemostasis |
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Prostaglandins |
produce pain and stimulate pain-producing chemicals produced by nearly all cells in body, released in response to damage to cell membrane, multiple types of PGs (PGe1 and PGE2 primarily affect inflammatory phase of healing) |
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PGE1
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increase vascular permeability; sensitize pain receptors |
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PGE2 |
attracts leukocytes and stimulates production of inflammatory mediators; sensitize pain receptors |
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anti-inflammatory agents, steroids and NSAIDs effect on inflammation |
anti-inflammatory agent: inhibit production of arachidonic acid metabolites steroids: act by inhibiting conversion of cell membrane phospholipids to AA NSAIDs: blocks blocks cyclooxygenase metabolic pathway after AA is formed |
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CT roles |
mechanical support mvmt tissue fluid transport cell migration wound healing control of metabolic processes in other tissue |
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composition of CT |
cells ECM- fibers, proteoglycans, glycoproteins, tissue fluid |
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cells of CT |
chondrocytes osteoblasts/osteocytes fibroblasts tenocytes |
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ECM components |
fibers- collagen, elastin proteoglycans glycoproteins tissue fluid |
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collagen |
19 types common triple helix structure roles: strength and stability of ECM, resists tensile loading |
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structure of collagen in tendons |
parallel alignment; resistance from unidirectional forces, transmission of muscular forces |
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structure of collagen in ligs |
less parallel alignment; resists tension from multi-directional forces |
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structure of collagen in bone |
complex arrangement of orthogonal arrays; provides large amount of multi-directional tensile strength |
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elastic fibers |
allow tissue to withstand repeated stretching and deformation arrangement: concentric fenestrated sheets, individual fibers, 3D honeycomb-like network |
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proteoglycans |
structure: core protein, covalently attached to sulphated GAGs amount and type in CT affect specific biomechanics properties aggregating vs. non-aggregating |
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glycoproteins |
small portion of total matrix components soluble multi-fxnal macromolecule role: stabilizing surrounding matrix, link matrix to cell, regulate cell fxns |
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dense CT |
supports or limits motion examples: bone, lig, tendon, aponeurosis |
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loose CT |
flexible examples: muscles, nerves, fascia, skin |
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articular cartilage (general) |
few chondrocytes in different layers synovial fluid supplies nutrition Type II collagen to anchor to bone large amount of PGs... attract water |
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fibrocartilage |
cells: chondrocytes, fibroblasts dense interwoven collagen fibers: resists multi directional forces, ideal to dissipate loads |
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bone |
cells: osteoblats, osteocytes type I collagen ground substance: mineral salts, proteoglycans |
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local factors affecting healing process |
type, size, location of injury infection vascular supply mvmt/excessive pressure temp deviation topical meds retained foreign body |
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systemic factors affecting healing process |
age/gender sex hormones (estrogen positive) stress ischemia concurrent illness or disease obesity alcoholism smoking immunocompromised conditions nutrition |
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type I collagen |
more mature, stronger, seen predominately in bone, tendons, ligs, annulus fibrosis, joint capsule |
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type III collagen |
sign of immaturity, 1st laid down in healing process; transition to type I as healing occurs |
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type II collagen |
nucleus pulposus, articular cartilage |
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V and XI collagen |
affect diameter, bigger size of fibrils = smaller amounts of V and xI; control how big fibrils become |
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aggregating vs. non aggregating proteoglycans |
aggregating: proteoglycans bind to this and get larger, becoming big complex, resist compression non aggregating: will not bind to this molecule; no role in resisting compression |
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viscoelasticity |
property of substance exhibiting both elastic and viscous behavior, application of stress causing temporary deformation if stress is quickly removed but permanent deformation if it is maintained |
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ductile |
stretch before breaks, failure point far from yield point; allows deformation, big plastic region |
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brittle |
breaks easily, fail point close to yield point, small plastic region |
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creep |
how tissue responds to constant load |
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stress relaxation |
constant deformation; adapting to stretching |
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2 types of fx healing |
intramembranous healing (primary) secondary callus formation |
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phases of fracture healing |
inflammatory phase (0-3 days) reparative phase (3-40 days)- stable vs. unstable remodeling phase (40+ days) |
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inflammatory phase of bone |
WBCs and cytokines to area; macrophages cleaning up junk; mesenchymal cells getting ready to produce cells needed |
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reparative phase of bone |
ORIF (stable): well vascularized area; osteoblasts deposit new bone and jxn btw surfaces unstable fx/insufficient vascularization: not a lot of osteoblasts depositing new bone; more chondrocytes lay down cartilage/callus to stabilize fx and provide structure that bone can work with |
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remodeling phase of bone |
callus replaced by bone; happens as fx site is already mechanically stable |
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factors that affect bone healing |
age, reduction precision, fx type, blood supply, amount of local trauma, degree of bone loss, type of bone involved, type of repair, presence of medical complications, location, general health and nutrition |
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processes that augment bone healing |
ultrasound: energy stresses bone to encourage healing pulsed electromagnetic fileds: for non-unions/mal-unions direct current: stimulates proteoglycans and collagen synthesis capacitive coupling: electrodes on skin affecting Ca channels demineralized bone: biologic added at time of ORIF to form scaffold |
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primary bone healing steps |
stage I, phase I: fx f/b clot + granulation tissue formation stage II, phase II: granulation tissue to bone stage III, phase III: restores normal bone contour |
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secondary bone healing steps |
stage I/II, reactive phase: fx f/b clot + granulation tissue formation stage III/IV, reparative phase: granulation to callus to lamellar bone stage V, remodeling phase: restore normal bone contour |
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S-H type I |
physis separation good px for growth |
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S-H type II |
metaphysis side of physis good px for growth |
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S-H type III |
epiphysis side of physis fair px for growth; may require surgery; physis often fuses |
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S-H type V |
physis crushed physis often fuses |
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colles' fx |
posterior displacement of distal radius |
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jones fx |
fx of diaphysis 5th met in foot, more towards distal end |
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boxer's fx |
5th metacarpal, hitting something with closed fist |
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lisfranc fx |
fx at lisfranc joint (metatarsal and mid foot) |
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march fx |
fx of metatarsal shafts |
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stress fractures |
repeated loading/unloading leading to fatigue failure secondary to accumulation of micro damage compression side of fx may lead to fx more slowly (more time allowed for repair) tension side of fx may quickly become complete fx |
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stress fx risk |
enviro, bone mass, muscle/fitness, nutrition, structure, gender |
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response: return to fxn after stress fx |
graduated loading program, progressive changes, limit variables, allow time btw changes, use cyclic training (w/ rest), vary load |
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relationship btw Ca intake and health risk |
goldilocks pattern (U) |
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OP pharmacological tx + other drugs that negatively impact bone |
biphosphonates: Fosamax, most commonly rx PTH: stimulates bone formation, starts remodeling process calcitonin: reduces blood Ca (more in bone) raloxifene: increases bone thickness corticosteroids: inhibit obsteoblast fxn, inhibit Ca resorption in GI tract, not good for bone health Cox-2 inhibitors: higher rates of non union fx's |
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plagiocephaly |
flat skull |
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osteogenesis imperfecta |
genetic abnormality in type I collagen primary impairments: bone fragility, short stature, scoliosis, lax ligaments, weak muscles, failure of postnatal growth, recurrent fx's Type I most common |
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blount's disease |
tibial vara compressive forces on medial knee = etiology RFs = obesity tx = braces and surgery |
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legg-calve-perthes disease |
avascular necrosis at femoral head occurs in young boys more frequently synovitis repeatedly before; kid limping exposed to smoke increases risk |
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slipped capital femoral epiphysis |
slippage at growth plate femoral head off femoral neck see in metabolic disorder, related to acute trauma more common in older children, boys kids that are obese or big growth spurt pain w/ walking in hip and knee |
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sever disease |
lots of pain in heels self-limiting and lots of stretching apophysitis = driver; place where tendons attach common during growth sports |
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osgood schlatter disease |
apophysitis of tib tuberosity need to offload tendons |
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club foot |
hindfoot varus equinus at ankle defective talus dev't neurologic factors don't see much in 1st world countries |
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rickets |
children; large amounts of unmineralized osteoid; bone becomes more ductile; vitamin D deficiency |
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osteomalacia |
adults; decrease mineralization of bone; bone becomes more ductile; deficiency of vitamin D; don't see bowling b/c bone already formed, bone more likely to fx |
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diabetes- alterations in fx healing |
tissue level changes: decreased bone formation, decreased cartilage formation, increased loss of cart, decreased vascularity and angiogenesis molecular level changes: decreased growth factors, decreased matrix proteins, increased pro inflammatory genes, increased pro osteoclastogenic factors, increased pro apoptotic genes |
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hypothyroidism and bone |
decreased chondrocytes proliferation, decreased hypertrophy, decreased vascular invasion, healing at slower pace |
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osteoporosis |
bone production < bone absorption RFs: aging, women, genetics, thinner frame, post menopausal DEXA scans osteopenia precedes OP estrogen therapy prevents but increased risk of stroke |
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mechanisms of control of bone growth |
systemic: bilateral synchronization local: variable by growth plate mechanical control: alignment w/ predominant forces |
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wolff's law |
every change in form and fxn of bone or of their fxn alone is followed by certain definite changes in their internal architecture, and equally definite secondary alterations in their external confirmation, in accordance w/ mathematical laws bone changes according to stresses applied to it |
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increase bone SA results in |
bigger changes in response to use or disuse; trabecular bone has profound changes in response to exercise/disuse vs. cortical bone (small changes) |
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what happens in mild genu varum? |
higher medial compressive forces, medial growth rate increased, bone wedge formed which realigns axis, equilibrium is restored; extreme deformities do not correct self as in this case |
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properties of bone |
anisotropic composite viscoelastic |
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how is bone anisotropic? |
cortical bone: best set up to take longitudinal stresses (WB), less set up to take transverse stresses, bad at shear stress trabecular bone: tolerates lower stresses overall than cortical bone |
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how is bone a composite? |
inorganic component resists compression; organic component resists tension; direction fibrils deposited influenced by stress |
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how is bone viscoelastic? |
mechanical properties of bone dependent on rate it is loaded rapid loading = increased stiffness higher loads = can be taken before fx occurs slower loads = less stiff, fx occurs at lower load |
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total area under stress strain curve |
energy required for failure to happen (fx) |
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brittle |
low ability to tolerate strain before failure |
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ductile |
able to take lots of strain before failure, low stress, resist propagation of microfx's |
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osteomalacia (Stress strain) |
poorly mineralized bone, weak, more ductile |
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osteoporosis (stress strain) |
hyper mineralized, very brittle bone |
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cortical bone (stress strain) |
more brittle, doesn't tolerate deformation |
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trabecular bone (stress strain) |
can't tolerate a lot of stress but can take a lot of deformation |
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t/f: how much resistance to bending is dependent on bone diameter/hoe much deposition on periosteal bone, and how wide outer ring is |
true |
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length and width effect on stability |
bone same length but diameter is different = resistance to bending related to cube of diameter larger bone 2x diameter = 8x bending as thinner bone same diameter, 2x length = 1/8 bending strength of shorter bone |
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bone is strongest in which forces/direction? |
longitudinal direction (WB), compression in cortical bone shear does ok less strong against transverse tension and compression trabecular significantly less strong |
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viscoelasticity of bone |
with rapid loading = bone responds w/ more stiffness, tolerates more stress before failure, behaves more brittle slow loading = ductile behavior; tolerate lower stresses, not as stiff more compliant |
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function of skeletal system |
protection leverage for mvmt mineral storehouse blood production |
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bone stores what minerals |
99.9% body's Ca, PTH and vitamin D3 hormone control of serum Ca; Na, phosphate, K stored in bone |
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blood production in bone |
bone marrow in medullary cavity; red bone marrow present in infants and young children and ribs, sternum, vertebrae, and coccyx in adults; yellow bone marrow everywhere (doesn't produce RBCs) |
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components of bone |
ECM: fibers, proteoglycans, glycoproteins, tissue fluid cells: osteoblasts, osteocytes, osteoclasts |
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osteoblasts |
cuboid in shape, have central nucleus, form single layer on periosteal and endosteal surfaces; secretory abilities, polarized; have gap jxns; secrete organic components of bone matrix (90% collagen); have proteoglycans and glycoproteins; adhesion, migration and proliferation and differentiation of cells; have gamma-carboxylated proteins |
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following period where osteoblasts are secretory, they will undergo |
apoptosis or differentiate permanently into osteocytes |
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osteoblasts what % of mature bone |
90% |
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nascent osteocyte |
-in direct contact w/ bone lining and osteoblasts -organelles analagous to osteoblasts -cell volume decreased by ~30% -pseudopodia toward previously embedded cells -develop gap jxns |
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mature osteocyte |
embedded w/in bone matrix simplified organelles cell volume decreased by ~70% projections through canaliculi long cell processes extended toward vasculature lacunocanalicular network links have 1/2 life of 25 years |
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osteoclasts |
giant cells multinucleated formed from many hematopoietic (macrophage/monocyte) precursors mature osteoclasts from fusion of 10-20 precursors have ruffled border to increase SA motile form tight jxns btw bone SA and basement membrane external vacuole is acidified and proteolytic enzymes secreted into resorption pit (how ship's lacunae) after degradation products processed, released into circulation |
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bone matrix composed of |
organic components: collagen 90% (Type I) inorganic components: 70-90%; stores 99% Ca, 85% body's phosphorous minor components |
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minor components of bone |
fibronectin osteonectin thrombospondin osteocalcin osteopontin matrix-ala-protein small integrin-binding ligand proteoglycans |
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fibronectin |
relatively abundant in bone, helps regulate osteoblast differentiation... lethal problem if something going wrong |
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osteonectin |
bone connector, regulate mineralization, if taken away = OP |
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thrombospondin |
inhibit bone cell precursors, if not there = see dense bone |
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osteocalcin |
bind Ca; if no osteocalcin = bones seem normal |
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osteopontin |
increases angiogenesis, enhance bone resorption; if not present, resistant to PTH |
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matrix gla protein |
inhibit mineralization; if not there = may see normal bones but calcified blood vessels |
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parts of long bone |
label picture |
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mature bone |
aka lamellar/primary cortical: 80% of bone trabecular bone: 20% of bone structure but has 90% bone SA |
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woven bone |
immature; 1st bone formed, also formed in fx repair |
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main unit of cortical bone |
osteon |
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what lies centrally in osteon? |
haversian canal: blood vessels lined w/ single layer of endosteol or osteoprogenitor cells, lamellae |
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lamellae |
houses number of osteocytes in lacunae; canaliculi allow communication btw adjacent lamellae |
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Volkmann's canal |
connect haversion canals |
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trabecular bone located primarily |
at ends of long bones, vertebral bodies, flat bones ; bone marrow fills in spaces |
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mesenchymal progenitors differentiate into |
pre osteoblasts... osteoblasts pre chondrocytes... proliferating chondrocytes... pre hypertrophic chondrocytes... hypertrophic chondrocytes |
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stages of long bone dev't |
1) mesenchymal condensation 2) cartilage model 3) bone collar 4) replacement of cart by bone (primary ossification center) 5) diaphysis/metaphysis, vascular tissue enters 6) secondary ossification center, gets larger 7) epiphyseal cart disappears, bone stops growing longer, bone marrow cavity becomes continuous along length of bone |
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endochondral ossification |
chondrocytes form cart bone model chondrocytes in center of diaphysis hypertrophy transformation to bone |
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ossification zones of endochondral ossification |
reserve cart chondrocyte proliferation chondrocyte hypertrophy cart calcification |
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principal nutrient artery |
comes from major branches of systemic circulation, enters medullary cavity via nutrient foramen- ascending and descending medullary arteries |
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metaphysial and epiphysial a |
numerous, supply ends of bones, supply ends of bones, arise mainly from periarticular plexus, supplies adjacent bones; terminate in bone marrow, trabecular bone, cortical bone, articular cart |
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periosteal arterioles |
reach cortical surface of diaphysis along ligamentous attachments, supply outer 1/3 of diaphysial cortex |
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TH on bone |
not enough = decrease chondrocyte proliferation, decreased hypertrophy, decrease vascular invasion |
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glucocorticoids on bone |
inhibit chondrocyte proliferation; slow longitudinal growth |
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GH on bone |
increase local and liver production of IGF I; increase chondrocyte proliferation |
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estrogen on bone |
fusion of growth plates; stops bone growth after puberty in males and females |
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testosterone on bone |
converted to estrogen in males to allow for stoppage of growth |
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progesterone on bone |
partner w estrogen (fusion of growth plates; stops bone growth after puberty in males and females) |
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growth factors (FGF, indian hedgehog) on bone |
paired w/ other hormones to result in controlled stimulation to help w/ process of proliferation |
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intramembranous ossification |
typical of flat bone formation no cart bone model required occurs w/ condensed plate of mesenchymal cells osteoblasts secrete osteoid osteoid calcifies to become primitive trabecular bone osteoblasts trapped become osteocytes in lacunae as calcifies- bony spicules become surrounded by mesenchymal cells - periosteum |
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hypercalcemia |
depression of nervous system |
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hypocalcemia |
excitable nervous system; tetany, seizures |
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released in response to low Ca in blood |
PTH |
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draw bone remodeling diagram |
notes |
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4 stages of bone remodeling |
activation resorption reversal formation |
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role of osteoblasts in bone remodeling |
regulators for bone formation and resorption, deposition, regulation of differentiation and activity of osteoclasts, formation of bone |
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remodeling phase of collagen |
controlled degradation of collagen occurs as excess collagen is removed and Type III collagen is replaced w/ Type I collagen as maturation of newly repaired tissues occur |
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biosynthesis of collagen |
write out process |
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mechanotransduction |
stimulation of integrin is responsible for causing adaptive rxn in cell in response to mechanical stresses |
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whole process of biosynthesis of collagen facilitated by |
ascorbic acid/Vitamin C |
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if person has genetic abnormality in pro collagen chain... |
deficiency in enzymes that control posttranslation modification processing, or deficiency in ascorbic acid ---- defective collagen is formed that is unable to tolerate normal stresses |
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degradation of collagen |
enzymes called collagenases degrade covalent bonds of tropocollagen molecule causing it to split and be further broken down by various proteases, which are enzymes that break down proteins collagen is normally resistant to proteases unless tropocollagen is denatured or degraded |
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functions of cartilage |
1) provides viscoelastic structure that 2) transmits and disperses forces to underlying subchondral bone 3) allows virtual frictionless motion of joint 4) improves congruity of joint surfaces, dispersing forces over large area 5) provides stability and structure but w/ flexibility to move and conform |
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types of cart |
hyaline elastic fibrocartilage |
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fibrocartilage |
type I collagen- preponderance intermediate btw CT and hyaline cart IV discs, pubic symphysis, menisci |
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elastic |
Type II collagen and matrix plus abundance of elastic fibers auricle of ear, eustachian tube, epiglottis |
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locations of HAC |
ends of bones of diarthroidal joints epiphyseal plates- developing infant to young adulthood walls of respiratory passages rib articulation w/ sternum embryological template for bone |
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HAC characteristics |
viscoelastic high tensile strength resistant to compressive and shear forces can undergo large deformations while still being able to return to its original shape and dimension |
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cell elements of HAC |
chondrocytes fibroblasts chondroblasts |
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chondrocytes |
make up 2-5% cart by volume responsible for manufacturing proteoglycans, growth factors, cytokines, collagen, and maintaining ECM |
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chondroblasts |
immature chondrocytes which are derived from prechondrogenic mesenchyme are similar to chondroblasts of bone fx callus and growth plates |
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chondrocytes in HAC have receptor for |
basic fibroblast growth factor (bFGF) hypertropic chondrocytes in callous, growth plate do not have bFGF receptor |
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chondrocyte fxns |
produce proteoglycans, GFs, cytokines, collagen tissue, produce and degrade ECM works anabolically to build up ECM works catabolically to degrade cart use metalloproteinases |
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shape of chondrocytes |
normally round or polygonal; close to articular surfaces may be flattened or discoid in shape |
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t/f chondrocytes possess hardware to produce and maintain multiple components of ECM |
true |
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layers of articular cart (superficial to deep) |
tangential layer transitional layer radial layer calcified cartilage subchondral bone |
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cell density is highest at |
articular surface (decreases w/ age) |
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metabolic slugs of body |
chondrocytes |
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HAC ECM characteristics |
avascular, aneural, alymphatic, CT resists static and dynamic loading stresses manufactured by chondrocytes hydrophilic- attracts water |
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contents of ECM |
fibrous collagen- mainly type II ground substance- proteoglycans, non collagenous protein water- 65-80% (more in superficial vs. deep layers) |
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aggregan |
proteoglycans + glycosaminoglycans |
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ground substance |
aggregan and hyaluronic acid |
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_____ accounts of 90-95% of collagen content in HAC |
type II |
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2 major types of GAGs in HAC |
chondroitin 4 and 6 sulfate keratin sulfate (looks like bristles on wire brush and are negatively charged) |
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higher concentration of chondroitin sulfate the better resistance to ____ loading |
compressive loading |
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proteoglycans + GAG + water = |
hydrated tissue that resists compression |
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___ content is larger in HAC than in other joint structures |
proteoglycan |
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articular cart zones normally spans how deep on ends of bones? |
1-7 mm on ends of bones in majority of joints |
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anisotropic tissue |
example is HAC zones; tissue that exhibits properties w/ different values when measured along axes in different directions |
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tangential zone |
10-20% HAC zone lamina splendens- fibrillar sheet densely packed collagen in parallel to surface purpose= resists shear forces low fluid permeability = deforms more |
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transitional zone |
purpose: provides bridge btw superficial and deep layers large loose diameter packed collagen and oblique shaped chondrocytes arranged perpendicular to surface higher compressive modulus than superficial zone |
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deep layer/radial zone |
purpose: plays role in load distribution and resists compression chondrocytes arranged perpendicular to surface highest proteoglycan concentration lowest water concentration **highest compressive modulus than any other zone |
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calcified layer |
characterized by presence of tide mark contains small cells in matrix w/ apatitic salts |
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tide mark |
division btw deep radial layer and calcified cart and subchondral bone |
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biomechanical forces on HAC equation |
CP = CF/CA contact pressure = contact force/contact area |
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contact pressure |
total force on joint surfaces per square area |
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contact force |
determined by GRF and soft tissue force across joint (ligs, capsules, and muscle forces across joint) |
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contact area |
determined by alignment and intervening soft tissue (menisci), and surface in question |
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most pathologies act to ___ permeability, resulting in _____ delta t or loading across joint |
increase; decrease |
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deformation ____ contact area which ______ articular cartilage pressure which leads to ____ stress transmitted to subchondral bone |
increases; decreases; decreased |
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load-bearing equilibrium of HAC |
swelling on solid matrix created by expansion of proteoglycan sln tensile forces w/in collagen network resist swelling pressure external load balanced by forces w/in ECM- no deformation of cart, no fluid flow |
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3 major forces ac to balance external load on HAC (intrinsic properties) |
1) stress w/in collagen matrix- negatively charged 2) pressure w/in fluid phase 3) frictional drag due to fluid flow |
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HAC during loading |
pressure differential is created external forces > internal forces at site of compression temporary creep as fluid is continually displaced to other unloaded areas of HAC and joint space (strain softening) overt time get gradual increase CP of subchondral bone (strain hardening) |
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during articular cartilage loading, interstitial fluid diffuses out of matrix, creating frictional drag on solid matrix and decreasing ____ |
tensile stress (strain hardening) |
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2 methods of HAC growth |
interstitial appositional |
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interstitial HAC growth |
chondroblasts divide to form small groups of cells called isogenous groups- they secrete ECM |
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appositional HAC growth |
differentiation of stem cells to chondrocytes |
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HAC contains ___% chondrocytes |
<2% |
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how does lumbar facet orientation protect disc? |
biplanar orientation limits both forward translation and axial rotation and protects IV discs form both twisting and shearing forces |
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articular cart is sensitive to/ can be destroyed by |
1) impact loading- large delta V = increased acceleration 2) high CP 3) frictional abrasion |
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RFs for dev't of OA |
skeletal malalignment obesity (increased mass, F = ma) increased labor loads |
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damage to HAC may result from |
microtrauma (degeneration) macrotrauma (falling) inflammatory process |
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synovial joints consist of what components? |
diarthroidial joint joint capsule joint cavity synovial lining synovial fluid HAC |
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stratum fibrosum |
outer layer of joint capsule of synovial joint Sharpy's fibers- at ends as joint capsule attaches to periosteum of adjacent bones poorly vascularized joint receptors- high concentration- signal CNS regarding tension, pressure |
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stratum synovium |
highly vascularized, plexus of blood vessels and lymphatics poorly innervated- however many autonomic fibers of adventitia of blood vessels synoviocytes- synovial lining cells- 2 types: macrophage derived and fibroblast derived |
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synovial fluid composed of |
hyaluronic acid lubricin thixotropic |
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hyaluronic acid |
viscous, lubricates synovium, synovium need stop move and glide |
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lubricin |
surface active phospholipid lubricating factor |
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thixotropic |
decreasing viscosity w/ increased mvmt |
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lubrication of synovial fluid |
boundary lubrication: lubricin fluid lubrication: compress of cart = weep that lubricates articular surfaces hydrodynamic lubrication = wedge of fluid created |
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in healthy cartilage, collagen matrix bears only ___% of load |
15% |
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joint lubrication methods (2 main types) |
usually going on at same time to different degrees depending on load, speed of loading, and amount of fluid available 1) boundary 2) fluid film |
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boundary lubrication method |
hyaluronic acid glycoprotein molecule complex layer on each articulating surface |
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fluid film lubrication method |
larger volume of synovial fluid trapped btw 2 joint surfaces |
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synovial fluid has solute pressure that is balanced by |
plasma hydrostatic and osmotic forces |
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effusion is result of |
imbalance |
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effusion |
can occur after injury to structures w/in joint capsule due to influx of proteins from plasma to SF and affecting osmotic pressure causing fluid to build in joint capsule |
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hormone influences on HAC: growth enhanced |
HGH (human growth hormone) thyroxine testosterone- anabolic hormone |
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hormone influences on HAC: growth suppressed |
cortisone- catabolic hormone hydrocortisone estradiol |
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how is OA thought to result from progressive failure mechanism? |
-single high-magnitude trans-articular impact causing perforation of cart tissue (high impact loading) -decreased fluid pressurization in region of defects leads to load transfer from interstitial fluid to solid matrix -increase stress on solid matrix = further damage (think of cathedral model) |
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OA |
chronic degenerative disorder of diarthroidial joints |
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OA characterized by |
-activation of inflammatory and catabolic cascades at molecular level -gradual deformation of articular cart -mechanical and biochemical stress- lead to local production of pro inflammatory cytokines and mediators (interleukin IB, TNF, nitrous oxide, prostaglandins, matrix degrading) |
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RA RFs |
female 2-3x more likely <50 years old possible gene related predisposition |
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OA RFs
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age= 75% people > 70 have OA female obesity heredity trauma NM dysfxn metabolic disorders prior surgery and injury to joint (ACL, repeated ankle sprains) |
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natural hx of OA |
progressive cart loss subchondral thickening marginal osteophytes formation distribution of joints affected: C and L spine facets MCP, PIP, DIP, CMC hips, knees, 1st MTP |
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natural hx of RA |
chronic inflammatory arthritis can affect any organ system usually affects 3+ joints at same time distribution of joints: R/L PIP, MCP, wrist, elbow, knee, ankle, MTP |
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repair of articular cart |
avascular response- VERY SLOW necrosis of cells no inflammatory response unless bone involved no migration of cells for repair, rely on existing chondrocytes almost no ability to regenerate cart |
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superficial vs. deep insult to cart |
superficial: no healing, no OA deep: healing from subchondral bone; hyaline w/ fibrocart elements- not same as articular cart- Type I collagen primarily |
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clinical concerns of single insult to cart |
little concern |
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clinical concerns of multiple insults to cart |
treat by shaving and must violate bone |
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stages of OA |
early: increased cell number of fibroblasts; PGs decreased in zone 1 (tangential) = reduced capacity to resist compressive load moderate: increased number of fibroblasts; PGs decrease in zone II and III advanced: apoptosis, extensive PG loss, thickened subchondral bone |
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how do we treat OA? |
sufficiently decrease stress to augment healing decrease overall loading of joint = brace, surgery increase WB area of joint = varus or valgus osteotomy mechanical stimulation of fibrocartilagenous healing |
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osteochondritis dissicans |
-separation of articular cart subchondral bone segment from articular surface -etiology: ischemic necrosis as result of repetitive microtrauma -presentation: pain w/ WB, (knee) stair climbing, PA, males > females, 11-20 year olds |
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chondrosarcoma |
higher incidence in pelvis and upper femur and ribs malalignment tumor of cart age > 40 tumor matrix made up of chondroid cells survival rate > 90% grade I, <29% for grade 3 |
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t/f: aspirin as destructive consequences on AC |
true |
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effects of aging on HAC |
-increased H20 w/ DJD cart -increased displacement w/ loading due to increased permeability to lower resistance to fluid flow -decreased ground substance and decreased collagen density -delta t preserved to lesser degree -increased stiffness of subchondral bone = increased compressive stress -PG loss = decreases cross links btw collagen fibers = mechanical wear |
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implications for interventions of aging on HAC |
-attenuate contact forces and increase contact area -select exercises that may involve fluid film lubrication (high velocity + low loading/cyclical loading) -bracing -repair ligamentous insufficiencies -activity mod |
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surgical mgmt options of HAC damage |
-initial surgery = debridement and leavage (palliative) -micro fx = fibrin clot that brings scar tissue to fill deformity -osteochondral autograft transplant -autologous chondral implant |
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debridement and levage |
arthroscope cleaning up rough areas damaged usually initial type of surgery for less serious articular damage |
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microfx HAC repair |
-stimulate bone marrow -use awl to tap into deep subchondral bone to stimulate vascular response and blood into area -scar formation occurs filling in defect -scar filled in by fibrocart w/ higher concentration of type I collagen w/ inferior qualities of resisting shear and compression |
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microfx rehab considerations |
min WB 4-6 weeks no closed chain exercises initially low impact loading exercises |
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osteochondral autograft transplant |
-plugs of bone and cart taken from non WB portion of joint -site of lesion is derided down to subchondral bone -site is measured -correct number of plugs used and placed w/ snug fit flush w/ surrounding articular cart -only one procedure = advantage |
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protective phased rehab |
-progression of activities and exercises based on soft tissue healing constraints (tissue that is repaired) -need to consider tissue that was repaired and forces imparted to that tissue to facilitate healing but not break down or fail |
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non protective rehab |
no repair of tissue, usually debridement of offending tissue; progressions usually based on pt response |
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HAC primarily composed of |
water |
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t/f: HAC has uniform distribution of its components throughout its layers |
false |
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HAC is best at resisting what type of forces |
compression |
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fibrocartilage has much higher component of ___ collagen than HAC |
type I |
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chondrocytes in fibrocartilage produce mainly type 1 collagen but in HAC, chondrocytes produce mainly what collagen? |
type II |
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t/f: both fibrocartilage and HAC are completely avascular |
false |
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the IVD is aneural, however, can cause pain if presses on nerve root |
false |
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number of tidemarks ____ with age (> 60) |
increases |
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_____is a boundary in metabolically active zone between the noncalcified and calcified articular cartilage |
tidemark |
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t/f: Variations in subchondral bone volume are thought to influence the tidemark region |
true |
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in vivo the tidemark advances in the direction of the ______ |
noncalcified cartilage |
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The following are all characteristics of synovial lining tissues except: Synthesize biological lubricants and lubricate articular cartilage Control synovial fluid volume and compositionRemove metabolic waste Have clearly defined basement membrane |
have clearly defined basement membrane |
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protects deeper layers from the shear stresses involved with articulation |
superficial layer |
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provides the first line of resistance to the compressive forces. |
middle layer |
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provides the primary resistance to compression |
deep layer |
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secures the cartilage to the bone. |
calcified layer |
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fxns of fibrocart |
-increase joint congruity- increase SA of CP equation -assist in joint lubrication- synovial fluid and models of lubrication -protects edges of joint against extensive forces on periphery -acts as shock absorber- architecture of fibrocart resists tensile and compressive forces -transmits loads -protects HAC from excessive wear |
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locations of fibrocart |
meniscus IVD labra of GH joint, hip SC joint, TMJ, pubic symphysis TFCC (triangular fibrocart complex) |
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menisci made up of what type of collagen |
type I |
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menisci absorb what loads and collagen arranged in what pattern |
compression; circumferential |
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arrangement of collagen fibers in menisci allow them to resist what stresses? |
hoop stresses during WB |
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medial meniscus |
-fibrocart structure that have bony attachments to A-P tibial plateau -AP diameter of post horn is greater than anterior horn |
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lateral meniscus |
-semicircular -covers larger area of articular surface of tibia than medial -A and P horns much closer -attaches just adjacent to ACL anteriorly -lateral meniscus has greater mobility |
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why is posterior portion of lateral meniscus difficult to repair |
where popliteal tendon passes by lateral meniscus- meniscus is avascular |
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t/f: entire meniscus is vascular at birth and decreases until age 10 at which time it reaches adult condition |
true |
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what parts of med/lat meniscus is vascular/neural |
10-25% lat 10-30% med periphery neural: most abundant in outer portions |
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fxns of menisci |
load sharing- 50-70% ext, 85-90% flex reducing joint contact forces (by increasing contact SA) distribute synovial fluid shock absorption passive joint stabilization limiting extremes of flex and ext proprioception during compression, decreased ability to tolerate shear forces |
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removal of ___ results in 50-70% decrease in femoral condyle surface contact area; increase of 100% in joint rxn forces |
meidal meniscus |
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removal of ____ results in 40-50% decrease in contact area and increase of contact stresses by 200-300% |
lateral meniscus |
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fairbanks sign |
smaller medial space on knee, bone spur, sclerotic changes of OA |
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gold standard of dx imaging of meniscus |
arthroscopy |
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rehab considerations of repair vs menisectomy |
outer 1/3 has blood supply during healing, meniscus unable to take normal stresses likely non-WB for 4-6 weeks avoid hyperext and end range flex may be partial WB w/ immobilized ext |
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IVD increases from ___ to ____ |
cervical to lumbar (lumbar supports more weight) |
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ratio btw thickness of disc and vertebral body is greatest in C region. why? |
move mvmt |
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IVD allows for what degrees of freedom? |
6 DOF |
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annulus fibrosis vs. nucleus pulposus collagen types |
annulus = Type I nucleus = Type II (resists compressive and tensile loads better) |
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IVD components |
proteoglycans- GAG's linked to proteins fluid- varies w/ age, time of day collagen innervation: outer 1/3 of C and L discs |
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recurrent meningeal (sinu-vertebral) nerve has 2 possible routes |
segmentally: through adjacent posterior (dorsal nerve root) extrasegmentally: through paravertebral sympathetic chain |
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cartilage end plant of IVD |
HAC, 1 mm thick, caps end surface of vertebra attached to vertebral body by thin calcified layer pathway for diffusion of nutrients to disc and removal of waste products barrier btw avascular proteoglycan rich nucleus and vascular sponges of vertebra |
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2 parts of annulus fibrosus |
outer annular lamellae-ligamentous: resists tensile, some vascularity inner annular lamellae- cartilaginous : load bearing role and high PG content (similar fxn to HAC) |
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composition of nucleus pulposus |
90-70% water (decreases w/ age) soft and more deformable than HAC Type II collagen hydrophilic in closed system = lift and separation of vertebrae |
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how is adult IVD nourished and what are clinical implications |
diffusion from vascular buds and vertebral body disc; slow system = injury to area leads to increased swelling that sticks around for long time; why the next morning couldn't get out of bed from yard work the previous day |
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intradiscal pressure in supine standing sitting bending forward and lifting loads |
intradiscal pressure in supine: 25 standing: 100 sitting: 150 bending forward and lifting loads: 220 |
