2Inflammation What is Inflammation A vascular and cellular response to trauma. Its purpose is to initiate the healing of the injured tissueThe body’s attempt to dispose of micro-organisms, foreign material and dying tissues so that tissue repair can occurAn inflammatory response may result from external or internal factors (infection)Protects to the body by localizing and removing the injuring agent
3Signs of Swelling Redness (Rubor) Swelling (Tumor) Pain (Bolar) Warmth (Calor)Loss ROM
4Signs of Inflammation (Cardinal Signs) Redness (Rubor):Caused by blood vessel dilation (the arterioles)Chemical mediators promote the vessel dilation (contained in the capillary walls or endothelium resulting in immediate response)HistamineSeritoninBradykininsProstaglandinsNote: a 1x increase in arteriole diameter yields a 4x increase in blood flow
5Signs of Inflammation Cont. Swelling (tumor)Edema fluid varies with the stage of inflammationinitially vessel permeability is only slightly altered and no cells or protein escapes and the fluid is mainly water and dissolved electrolytes (transudate): like synovial fluidAs capillary permeability increases and plasma proteins escape the extravascular fluid becomes cloudy and more viscous. This is called exudate (contains a large amount of leukocytes (called pus)
6Causes of Edema/Swelling- bleeding from torn vesselscell death due to anoxia, allows fluid leakage (permeability increases)increased proteins raise extracellular osmotic pressure, drawing fluids from the capillariesChemicals alter cell permeability to proteins and fluidGravity may increase swelling (Capillary filtration pressures)
7This is what we try to do as therapists through modality use Edema/SwellingTo cease hemorrhage/swelling/edemaMust reverse the conditionpressure gradientvessel repairThis is what we try to do as therapists through modality use
8Signs of Inflammation Cont. Pain (bolar)Results from irritation of nerve ending by physical or chemical factorsPhysical trauma may irritate pain receptorsChemical mediators release when cell damage occurs sensitize pain receptorsTrauma may result in cell anoxia because of interference with blood flow due to capillary damage
9Signs of Inflammation Cont. Warmth (calor)The result of chemical activity and increased blood flow in the injured area.Loss of FunctionMay occur due to pain causing reflex guarding or muscle spasm, spasm decreases metabolic activity and constricts blood flow which causes more pain due to ischemia; thus the pain cycle
10Phases of the Inflammatory Process Phase I: Acute Phaseinflammatory response: lasts 2-4 days but is complete in 2 weeksPhase 2: Tissue Formation (Proliferation)Subacute phase, Tissue rebuilding approximately 2-3 weeksThis does not include chronic inflammationPhase 3: Remodeling PhaseAdapt to original tissueContinues for up to 1 year post injury
11Phase I: The Inflammatory Process Early PhaseInsult occurs - may be internal (infection) or external (trauma)Vasoconstriction to decrease blood flow (first 10 minutes)VasodilatationLate PhaseTissue RepairRegeneration
13Inflammatory PhasesChart Designates Percent of phase over time
14Phase I: Early Phase Inflammation - Vasodilatation Chemical mediators are released:histamine, bradykinis, serotonin, prostaglandin's - increase vascular permeability released from mast cells and blood platelets into traumatized tissue.As fluid filtrates through “gaps in the extravascular spaces this is calls exudation.
15Phase I: Vasodilatation Cont. The accumulation of excess fluid is called edema (Swelling)Vascular permeability due to action of the histamine is short-lived, lasting less than 1 hour
16Phase I: Early Phase Inflam. - Lymphatic channels are blocked Local lymphatic channels are blocked by fibrin plugs formed during coagulation. Obstruction of the local lymphatic channels prevents drainage of fluid from the injured site, thus localizing the inflammatory reaction.
17Phase I: Early Phase Inflammation - Margination When trauma occurs the endothelial wall is disrupted exposing collagen fibers creating a “stickiness”WBC’s concentrate in the injury site to rid the body of foreign substances and dead (necrotic) tissue
18Phase I: Margination Cont. As circulation slows, leukocytes migrate and adhere to the walls of post-capillary venuels (for approx 1 hour)The leukocytes pass through the walls of the vessels (diapedesis) and travel to the site of injury (Chemotaxis)
19Phase I: Early Phase Inflammation - Phagocytosis Body’s cellular defense to remove toxic material via lymphatic systemPhagocytosis: a process when leukocytes capture and digest foreign matter and dead tissue1st line of defense: neutrophiles(in most abundance from 1-3 days) - phagocytic activity reaches maximum effectiveness within 7-12 hours
20Phase I: Phagocytosis Cont. 2nd line of defense: monocytes (which convert into large cells called macrophages) and lymphoctes consume large amounts of bacteria and cellular debris. Monocytes are critical in the initiation of tissue repair because the attract fibroblastsBacteriaMacrophage
21Phagocytosis Cont.Pus is the end result - it contains leukocytes, dead tissue and phagogenic materialProlonged puss accumulation can prevent fibroplasia which begins the wound healingFibrobalsts are connective tissue responsible for collagen synthesisLigaments, joint capsule, tendonOsteoblasts: responsible for bone synthesisFibropblastMacrophages
22Phase I: Late Phase Blood Clotting Ruptured vessels release Enzyme (Factor X)Factor X reacts with prothrombin (free floating in blood)Thrombin then stimulates fibrogen into its individual form fibrinFibrin grouped together to form “lattice” around injured areaFibrin lattice contracts to remove plasma and compress platelets forming a “patch”
23Phase I: Late Phase Blood Clotting Factor XProthrombinFibrin Forms SealThrombinFibrin MeshFibrogen and Thrombin MeetFibrin Monomer
24Phase II: Regeneration: The replacement of destroyed cells by reproducing healthy cells adjacent to the wound (humans capacity to regenerate tissue is limited and further affected by age and nutritional state).
25Phase II: Stages of Regeneration: Stage starts with peripheryRe-eptheliaization is proliferation of peripheral epithelial tissue which then migrates to the wound until the area is covered.Capillarization (Capillary buds proliferate and connect forming new capillaries which gives the red, granular appearance to the scar (granular tissue)
26Phase II: Stages of Regeneration: Cont. Fibroplasia occurs due to fibroblasts which arises from undifferentiated mesenchymal cells and migrate into the area along fibrin strands and begin to synthesize scar tissue. Scar tissue is CT and mostly collagen and mucopolysaccharides. Fibroblasts secrete both, contributing tensile strength to the repair. Scar tissue very inelastic compared to surrounding tissue.
27Phase II: Stages of Regeneration: Cont. Vascularization - occurs with the proliferation of collagen synthesisFormation of blood vessels (angiogensis)
28Phase II: Collagen Synthesis: Occurs within 12 hours of injury to 6 weeks (average 3 weeks)Type I: collagen: associate with muscular tissue (larger and stronger fibers)Type III collage: smaller fibers, less cross linking and highly disorganized (ligamentous, tendinous)Type III with time is replaced by Type I collagen
29Phase II: Collagen Synthesis Cont. Tissue Healing TimesMuscle : approximately 3 weeksTendon: 4-6 weeksExtent of the tissue damage and vascularity will aid in determining healing timeAge may also be a factor in healing
30Phase II: Stages of Regeneration: Cont. Wound Contraction:Wound contraction begins to occur in CT as the myobroblasts (actin-rich fibroblasts) contract. Myofibroblasts move toward the center of the wound, helping reduce the size of the area to be covered.Outside-in
31Phase III: Maturation/Remodeling Phase Purpose of this phaseStrengthen the repaired tissueFiroblasts, myofobrpb;asts & Macrophages reduced to preinjury stateType I fibrin continues to be replaced by type III
32Phase III: Maturation/Remodeling Phase (day 9 onward) Blends in with the repair phase, original collagen fibers were randomly oriented. During remodeling, the fibers become more organized, parallel to the wound surface which provides greater tensile strengthThe type of tissue involved will determine the duration and extent of remodeling activity
33Phase III: Maturation/Remodeling Phase Cont. Strengthening of scar tissue continues from 3 months to 1 year, but fully mature scar in only 70% as strong as intact tissue.Motion will influence the structure and functional capacity of scar tissue (controlled stress increases functional capacity, allows healing and reduces adhesion formation).
34Chronic Inflammation Inflammation which continues past 1 month Marked by a loss of functionFibroblast activity continues forming granuloma
35Chronic Inflammation Complications Granuloma: large mass of weaker scar tissue (usually due to large inflammation and activity without regard to healing time)Retardation of muscle fiber: with excessive granuloma fibroblasts cannot reach damaged tissueAdhesions/contractures in tissueKeloid/hypotrophic scars
36Abnormal scarring:Hypertophic scar or keloid scar. Biological difference not well understood, but clinically hypertrophic scar is contained within the boundaries of the original wound while a keloid scar extends beyond the borders of the original wound.