Intro

movement and alignment
extrinsic factors
physiological factors
psychosocial factors

muscle performance - force generation + length
motor control
posture and alignment
physical activity
occupational, leisure and self care activities

orthotic devices, taping, assistive devices
footwear
ergonomic environment
modalities - used to augment the bodies adaptive capabilities
gravity

medications
system pathology
obesity
age

ligaments
joint capsule
musculotendinous
bone

hemorrhage
hemostasis

ruptured blood vessels

vascular response to stop bleeding

effusion
edema
erythema
hyperthermia

proliferation of phagocytic white blood cells - initial defense
normally resolves with acute inflammation
chronic inflammation can develop - phagocytic activity continues, and immunologic responses are elicited

muscle spasm + nociception
-loss of function (ROM and strength deficits)

more active

contraction - increase in stiffness

epithelial tissue
muscle tissue
nervous tissue
connective tissue

collagen
elastin
reticular fibers

provides stiffness and strength
most abundant

provides tensile strength and recoil ability
found most in skin and blood vessels

provides supporting network for body organs and glands
not common in musculoskeletal system

ECM
Amorphous gelatinous material
supporting framework for cells
lubricant to reduce friction between connective tissue
contains two types of large molecules (glycoproteins and proteoglycans)

fibroconectin
formation of cross links with collagen fibers
provide strength and stability to connective tissue

protein and carbohydrate core
-Glycosaminoglycans (GAGs) maintain hydration and prevent excessive collagen formation
-excessive cross linkage of collagen = too stiff

mast cells
macrophages
fibroblasts
plasma cells

vasoactive mediators in actue inflammation

phagocytosis
immune function
active during subacute, and chronic inflammation
attract fibroblasts to injured tissue

synthesis of collagen during repair process

immune function - produce antibodies to specific pathogens

loose connective tissue
dense connective tissue - dense irregular and dense regular

thin loosely woven fibers

thick tightly woven fibers
less flexible but stronger
collagen - strength

provides resistance to tissue loading from all directions (joint capsules)

provides optimal resistance to loading from one direction (tendons)

regeneration
repair

restoration of tissue that is identical in structure and function
ideal wound healing

division of cells that have survived the original trauma and remained functional
restores anatomical continuity of damaged tissue
functional restoration may be incomplete
less ideal

undergo continual division and replication
bone marrow, epidermis
excellent regeneration potential

potential divide but only in response to specific stimuli
fibroblasts, osteoblasts, chondroblasts
some injured connectve tissue has repair capacity

no ability to divide
neurons of CNS, cardiac muscle, skeletal muscle

excessive forces is applied causing both cellular and vascular disruption

connective tissue repair
-promote hemostasis

serotonin mediates inital vasoconstriction
ADP promotes platelet adhesion
vasodilation and changes in vascular permeability
-significantly impacts edema formation
-prostaglandins increase sensitivity of peripheral nociceptors

plasma
formed elements
-leukocytes (WBCs)
-- Granular: Neutrophils, Eosinophils, Basophils
-- Agranular: Monocytes (macrophages), Lymphocytes
-erythrocytes (RBCs)
-thrombocytes (platelets)

promotes tissue growth
replacement of damaged tissue
(minerals, vitamins, proteins, carbs, lipids, water)

released from platelets
mediates development of hemostatic plug
essential in coagulation of clotting blood - can't clot without

also need for bone regeneration and remodeling - hard callus formation and bony union

essential in biosynthesis of collagen by fibroblasts

essential coagulation factor

essential in cellular function of fibroblasts

regulates absorption of calcium and phosphorus

essential for normal metabolic function
provde amino acids necessary for collagen synthesis
major structural component of scar formation
immunological function
primary contituent of hemoglobin

combine with proteins to form proteoglycans and glycoproteins, contribute to tissue strength and stability

control detrimental effects of hemorrhage and edema, limit nociception and muscle spasm, enhance physiological mechanism of connective tissue repair, prevent contractures and adhesions, enhance definitive structure and function of scar tissue

pharmalogical agents, physical agents, psychosocial considerations

influence vascular and cellular events

influence vascular and cellular events - therapeutic exercise, thermotherapy, electrotherapy

affect of language, patient expectations, and experiences

characteristic vascular and cellular responses during a particular stage of wound healing, specific physiological or neurological response to be modified, capability of physical agent to affect the desired response (indications), potential detriental affect of therapeutic agent on normal diseased or surgically repaired tissue (contraindications)

trauma, microtrauma, stress-related

inflammation, fibroplasia, scar maturation

with injury blood vessels are disrupted and hemorrhagic effusion occurs, hemostasis

arrest of bleeding by physiological properties - vasoconstriction and coagulation, surgery; primary and secondary hemostasis

occurs within seconds after blood vessel trauma - vasoconstriction and development of temporary hemostatic plug; platelets accumulate along the wall of the damaged vessel and become activated due to morphological and functional changes; activated platelets release serotonin, thromboxane, calcium, and ADP (makes platelets clot) - platelet release reaction; serotonin and thromboxane mediates vasoconstriction, smooth muscle fibers of vascular wall contract, initial vasoconstriction is transient and lasts seconds to minutes

1-3 mins post injury; platelet adhesion and platelet aggregation

platelets adhere to sub endothelial connective tissue which has been exposed due to trauma

adhesion and aggregation of large number of platelets; formas main mass of the plug; basis for subsequent clot formation

initial platelet plug is reinforced, coagulation

coagulation is initiated by a release of hemostatic mediators from damaged tissue and disrupted blood vessels; formation of a stable insoluble fibrin clot in the damaged vessels; cascade of coagulation factors

activated coagulation factor functions as an enzyme to activate the next factor; fomation of prothrombinase, conversion of prothrombin to thrombin, conversion of soluble fibrogen to insoluble fibrogen

extrinsic pathway, intrinsic pathway, completion of first tstage

thromboplastin infiltrates the blood from damaged tissues that are extrinsic to the blood vessel - initiated by thromboplastin sequential activation of Factors VII and X

Factor XII (Hageman) is activated by exposure to sub endothelial collagen intrinsic to the blood vessel

conversion of prothrombin to thrombin - prothrombinasein the presence of calcium ions catalyzes the conversion of prothrombin to thrombin

conversion of soluble fibrogen to insoluble fibrin - thrombin converts fibrogen into fibrin, network of soluble fibrin filaments is developed, insoluble clot is formed

clot retraction occurs minutes after formation - strengthens the clot, prepares the vessel for repair; fibrinolysis - clot dissolved by proteolytic enzymes

predictable

type of tissue injured, extent of tissue damage, region vascularity, general nutrition of person with injury, age of person with injury, persistent inflammation

first stage of wound healing, natural nonspecific response of vascularized tissue to irritant or injury

acute (0-3 days), subacute (4 days - 2 weeks), chronic, systemic inflammation (lymphangitis - lymph vessel and lymphadenitis - lymph nodes)

bodies initial response to injury - characterized by pagocytotic activity; short in duration - hours to 3 days; vascular responses - result in fluid accumulation; cellular responses - proliferation of white blood cells and phagocytosis

vasodilation, increased vaascular permeability, increased blood viscosity, increased blood viscosity with slowing of blood flow; results in - increased intersitial fluid, obstruction of local lymph vessels, decreased lymphatic drainage; essential prelude to phagocytic function of WBC's

histamine; increased vascular permeability, short lived (<1 hr) so other things don't get in, leukocytes and plasma proteins escape vessels causing extravascular fluid to become more viscous (Exudation), RBC's become more concentrated, blood viscosity increases, slowing of blood flow - allows contact of circulating WBC's with epithelium of vascular wall, WBC's (neutrophils) emigrate to injured tissue

vascular response responsible for 3/5 cardinal signs of clinical inflammation; hyperthermia (heat), erythema (redness), edema (swelling)

interstitial pressure increases causing impairment of local circulation and decreased oxygen supply; secondary hypoxic injury

elevation, soft tissue mobilization, compression

defense system against pathogenic agents, proliferation of WBC's (leukocytes), phagocytosis of pathogenic microorganisms, leukocytosis

increased production and release leukocytes from red bone marrow, occurs within hours of injury

margination, adhesion/pavementing, emigration, chemotaxis, phagocytosis

accumulation of leukocytes to endothelial surface

leukocytes become attached to vascular wall

movement of leukocytes through vessel wall - bc of vasodilation

leukocytes attracted to damaged tissue in preparation for phagocytosis

primary mechanism - recognition of invading organism (bacteria); adherence of phagocytic cell to surface of pathogenic agent; engulfment of microorganism; degradation of pathogenic agent; neutrophils are most active during first 24 hours

formation of purulent exudate - pus; doesn't have to be an infection, just high phagocytic activity

favorable environment for connective tissue repair

destroy pathogenic agents -> specific immunological responses are elicited

provoked by persistent pathogenic microorganisms; agents or materials that cannot be phagocytized; represents an extension of the acute inflammatory response; may last for several months; can be prolonged by recent injury; clinically - tenosynovitis, bursitis, synovitis

second stage of connective tissue repair; proliferation of fibroblasts; collagen synthesis and fibrogenesis; formation of granulation tissue; wound contraction; dense scar formation

fibroblasts arise from undifferentiated mesenchymal cells; main supportive protein of connective tissue; normal collagen synthesis is altered to allow more built up and less lysis (decrease breakdown which happens all the time); fibroblasts become entrapped in the fibrin threads of the clot and become positioned for development of new tissue matrix

tensile

initial collagen fibrils merge to become fibers, collagen fibers form collagen bundles, collagen bundles become major structural support

can use intermittent tension for the fibrils to lay down in the right direction

temporary connective tissue matrix at injury site which is immature and structurally weak; represents normal function of connective tissue healing and indicates that normal repair is occuring; includes neovascularization - angiogenesis (new blood vessel formation), new lymph vessels, granular tissue appears red

reduction in size of tissue defect; approximation of newly formed or existing fibers in the wound margins; soft connective tissue utilizes mechanism of repair and contraction

performed by myofibroblasts that have contractile properties; appear 3-4 days post injury and reach peak at 2 weeks; can reduce a defect by up to 70%

tissue matrix gradually becomes dense fibrous tissue; scar formation does not replicate structural or biomechanical properties of the normal connective tissue; scar formation required the transition from Type III to Type I collagen, increase in overall collagen deposition, resorption of small blood vessels in vascular bed

begins 3 weeks after injury; structure, strength, and biomechanical properties of the scar are determined; may continue for several months

tensile strength of the initial tissue

rate of collagen turnover, number of collagen cross-links, realignment of collagen fibers