KIN 188KIN 188Prevention and Care of Prevention and Care of
Athletic InjuriesAthletic InjuriesTissue HealingTissue Healing
Tissue HealingTissue Healing
Soft tissue healingSoft tissue healing
Bone/fracture healingBone/fracture healing
Nerve healingNerve healing
Phases of Soft Tissue HealingPhases of Soft Tissue Healing
Phase I – Inflammatory ResponsePhase I – Inflammatory Response
Phase II – Repair/RegenerationPhase II – Repair/Regeneration
Phase III – Remodeling/MaturationPhase III – Remodeling/Maturation
Phase I – Inflammatory ResponsePhase I – Inflammatory Response
OnsetOnset Immediate and typically progresses x 3-5 daysImmediate and typically progresses x 3-5 days
Signs and symptoms Signs and symptoms Redness (rubor)Redness (rubor) Pain/point tenderness (dolor)Pain/point tenderness (dolor) Warmth (calor)Warmth (calor) Swelling (tumor)Swelling (tumor) Limited ROM (functio laesa)Limited ROM (functio laesa)
Phase I – Inflammatory ResponsePhase I – Inflammatory Response
Tissue damage – initiates inflammationTissue damage – initiates inflammation
VasocontrictionVasocontriction Initial attempt to limit bleeding at siteInitial attempt to limit bleeding at sitePlatelet reactionPlatelet reaction Provokes clotting at site to “plug” ruptured Provokes clotting at site to “plug” ruptured
vascular structuresvascular structuresCoagulationCoagulation Clot/hematoma is formedClot/hematoma is formed
Phase I – Inflammatory ResponsePhase I – Inflammatory Response
White blood cell infiltrationWhite blood cell infiltration Neutrophils and macrophages attracted to area via Neutrophils and macrophages attracted to area via
chemical processes to rid waste, debris and infectious chemical processes to rid waste, debris and infectious agents (phagocytosis)agents (phagocytosis)
VasodilationVasodilation Additional blood flow to area via chemical processesAdditional blood flow to area via chemical processes Increases cell permeability causing swelling/edema Increases cell permeability causing swelling/edema
from tissue exudate – allows for further arrival of from tissue exudate – allows for further arrival of “good stuff” and removal of “bad stuff”“good stuff” and removal of “bad stuff”
Inflammatory ResponseInflammatory Response
Phase II – Repair/RegenerationPhase II – Repair/Regeneration
OnsetOnset 48 hours – 8 weeks48 hours – 8 weeks Somewhat dependent upon tissue type – Somewhat dependent upon tissue type –
quicker proliferation with greater blood supplyquicker proliferation with greater blood supply
Signs and symptomsSigns and symptoms Decreased sx of inflammationDecreased sx of inflammation
Phase II – Repair/RegenerationPhase II – Repair/Regeneration
Proliferative phaseProliferative phase New blood supply allows for waste removal and arrival of New blood supply allows for waste removal and arrival of
fibroblastsfibroblasts
FibroplasiaFibroplasia Process of generating collagen tissue via fibroblast activityProcess of generating collagen tissue via fibroblast activity
Progression of phase – changes in cellular Progression of phase – changes in cellular activityactivity
Proliferation of new blood supply and fibroblast activity reinforce Proliferation of new blood supply and fibroblast activity reinforce new connective tissue matrix - each fuels the othernew connective tissue matrix - each fuels the other
Phase III – Remodeling/MaturationPhase III – Remodeling/Maturation
OnsetOnset 6-8 weeks6-8 weeks May last months/years - unknownMay last months/years - unknown
Signs and symptomsSigns and symptoms Minimal sxMinimal sx Resolution of sx of inflammation unless Resolution of sx of inflammation unless
complications have arisencomplications have arisen
Properties of Scar TissueProperties of Scar Tissue
Structurally weakStructurally weak
Decreased elasticityDecreased elasticity
Contractures/adhesionsContractures/adhesions
Sensory impairmentSensory impairment
Factors Affecting Rate of HealingFactors Affecting Rate of Healing
Blood supplyBlood supply
Degree of immobilizationDegree of immobilization
Foreign substancesForeign substances
Vitamin/mineral deficiencyVitamin/mineral deficiency
Steroid useSteroid use
Phases of Fracture HealingPhases of Fracture Healing
Phase I – Inflammation and Hematoma Phase I – Inflammation and Hematoma Formation Formation
Phase II – Cellular ProliferationPhase II – Cellular Proliferation
Phase III – Callous FormationPhase III – Callous Formation
Phase IV – Bony Union/OssificationPhase IV – Bony Union/Ossification
Phase V – RemodelingPhase V – Remodeling
Phase I – Inflammation and Phase I – Inflammation and Hematoma FormationHematoma Formation
Bleeding from periosteum, endosteum, Bleeding from periosteum, endosteum, bone marrow and surrounding soft tissuebone marrow and surrounding soft tissue
Typically lasts approximately 4 daysTypically lasts approximately 4 days
Phase I – Inflammation and Phase I – Inflammation and Hematoma FormationHematoma Formation
Hematoma accumulates in area to form matrix Hematoma accumulates in area to form matrix for healing – blood clotting initially occludes for healing – blood clotting initially occludes normal blood flow and local cells dienormal blood flow and local cells die
Secondary to cellular death, inflammatory Secondary to cellular death, inflammatory response occurs similar to soft tissue injuriesresponse occurs similar to soft tissue injuries Vasodilation, inflammatory cell arrival, swellingVasodilation, inflammatory cell arrival, swelling
Phase II – Cellular ProliferationPhase II – Cellular Proliferation
Vascular proliferationVascular proliferation Capillary buds in callous and surrounding soft tissueCapillary buds in callous and surrounding soft tissue Bring endosteal cells to areaBring endosteal cells to area
Osteogenic (endosteal) cells proliferate intoOsteogenic (endosteal) cells proliferate into Osteoblasts - formation of callous (bone)Osteoblasts - formation of callous (bone)
Osteoblasts more numerous in highly vascular areasOsteoblasts more numerous in highly vascular areas Chondroblasts - formation of callous (cartilage)Chondroblasts - formation of callous (cartilage) Osteoclasts - reabsorption of boneOsteoclasts - reabsorption of bone
Phase II – Cellular ProliferationPhase II – Cellular Proliferation
Fibrous junction between ends of bones at Fibrous junction between ends of bones at fracture site is built fracture site is built First it’s callous then progresses to cartilage First it’s callous then progresses to cartilage
and finally boneand finally bone
Phase III – Callous FormationPhase III – Callous Formation
External callous from periosteal cellsExternal callous from periosteal cells
Internal callous from endosteal cellsInternal callous from endosteal cells
Soft callous forms externally and internally Soft callous forms externally and internally to bridge the fracture site (internal callous to bridge the fracture site (internal callous grows faster to create natural grows faster to create natural immobilization)immobilization)
Phase III – Callous FormationPhase III – Callous Formation
Hard callous starts forming at 3-4 weeks Hard callous starts forming at 3-4 weeks and continues for 3-4 monthsand continues for 3-4 months
Unsatisfactory immobilization leads to Unsatisfactory immobilization leads to cartilagenous union vs. bony union due to cartilagenous union vs. bony union due to incomplete formation of hard callousincomplete formation of hard callous
Phase IV – Bony Union/OssificationPhase IV – Bony Union/Ossification
Callous replaced by boneCallous replaced by bone InternalInternal ExternalExternal Influx of new Haversian system/blood supplyInflux of new Haversian system/blood supply
Callous “comes together” in bony unionCallous “comes together” in bony union Fracture site is bridged by boneFracture site is bridged by bone
Phase V - RemodelingPhase V - Remodeling
Callous reabsorbed by osteoclasts and bone Callous reabsorbed by osteoclasts and bone assumes normal formation/appearanceassumes normal formation/appearance
Complete remodeling may take yearsComplete remodeling may take years
Remodeling complete when fractured bone is Remodeling complete when fractured bone is restored to normal shape or has developed a restored to normal shape or has developed a shape that can withstand imposed stressesshape that can withstand imposed stresses
Fracture HealingFracture Healing
Factors Affecting Bone HealingFactors Affecting Bone Healing
InfectionInfection Especially with open fractures but also may Especially with open fractures but also may
arise with systemic infections of closed fracturesarise with systemic infections of closed fractures
Metabolic disorders/diseasesMetabolic disorders/diseases Vitamin and mineral deficienciesVitamin and mineral deficiencies
Steroid useSteroid use Interferes with collagen synthesisInterferes with collagen synthesis
Factors Affecting Bone HealingFactors Affecting Bone Healing
Unbridgeable gapsUnbridgeable gaps Loss of bone tissue, interposition of soft tissueLoss of bone tissue, interposition of soft tissue
Vascular destruction/poor vascular supplyVascular destruction/poor vascular supply Avascular necrosis (carpal navicular/schaphoid, head of Avascular necrosis (carpal navicular/schaphoid, head of
femur)femur)
Inadequate reduction/poor immobilizationInadequate reduction/poor immobilization Not only may impact healing but may contribute to Not only may impact healing but may contribute to
development of permanent deformitydevelopment of permanent deformity
Nerve HealingNerve Healing
When nerve severed, healing does not When nerve severed, healing does not occur and loss of function typically occur and loss of function typically permanentpermanent
If nerve fibers ruptured but surrounding If nerve fibers ruptured but surrounding myelin sheath intact, it’s possible for myelin sheath intact, it’s possible for regeneration to occurregeneration to occur Very slow process (<1mm/day, Very slow process (<1mm/day,
~2.5cm/month)~2.5cm/month)