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Pathoph Tiss Healing
| Question | Answer |
|---|---|
| What are the phases of tissue healing? | Inflammatory Proliferation Remodeling |
| What are the three phases of bone healing? | Reactive Reparative Remodelling |
| Reactive phase of bone healing | Impaction Induction Inflammatory |
| Name the subphases of reparative phase of bone healing | soft callus hard callus |
| What happens during impaction? | dissip of the energy from an insult (perpedndicular) impact of insult is proportional to energy applied and inversely proportional to the volume of bone more injury if force is great or small bone as age, decrease elasticity greenstick frx (children) |
| 2 phases of reactive phase | induction(1 week) inflammatory (2-8 weeks) |
| WHat happens in the induction phase? | Osteoblastic/osteoclastic activity is stimulated at site of blood supply disruption Hemotoma develops |
| What happens in the inflammatory phase? | Resorption of necrotic bone Creation of early fibrous or cartilaginous callus Loss of fracture line visualization Fracture site gapping Peak at 4-6 weeks |
| What activates induction phase? | (unknown time frame or when it starts) activated by oxygen gradients, forces, bone morphogenic, proteins or noncollagenous proteins |
| What happens in the inflammatory phase? | 1. increase vascularity (form hemtoma) scaffold for bone 2. invaded by neutrophils, macrophages and phogocytes 3. elim necrotic tissue 4. fracture line more visible |
| describe reparative phase | 3-12 weeks differentiation of cells Fx hematoma is invaded by chondroblasts and fibroblasts, which lay down the matrix for the callus Initially the soft callus Increased vascularity during this phases |
| what is the soft callus made of? | Initially the soft callus is composed mainly of fibrous tissue and cartilage with a very small amount of bone |
| Describe the reparative phase | 5012 weeks osteoblasts destroy soft callus, make hard one of woven bone, increase stability Immature and wk Bridging of the fx complete when stable clinical and radiological healing |
| Describe the remodeling phase | 4 weeks to months Osteoblastic and osteoclastic activity Immature bone replaced by mature bone Stability increases |
| wolf's law | a bone in a healthy person or animal will adapt to the loads it is placed under. |
| Primary bone healing | Occurs with direct or intimate contact between the fracture fragments Bone grows across compressed bone ends slow proc. Fixation devices: compression screws and plates |
| Secondary bone healing | callus formation evident motion at fx external bridging callous occur with castin or external fix or rod most common |
| Factors that affect healing | Severity of fracture Location of the fracture Soft tissue damage Type of fixation Extent of overall trauma Age Co-morbidities |
| How to assess fx for healing? | clinical judgement pt sx and phys findings overtime pres, absence or diminution of pain with activities eval of fx site for TTP and motion assess pt during funct, activity |
| radiographic evidenced of fx healing assessment | Callus formation Disappearance of fracture line (4 cortices) A fx is considered healed when there is progressive callus formation with blurring and disappearance of the fracture line |
| time lines for bone healing | Child 4-6 weeks Adolescent 6-8 weeks Adults 10-18 weeks |
| time from fracture to full bone resorption | Keep in mind that the process from fracture to full bone resorption takes weeks to months |
| factors that influence bone healing | Age Degree of local trauma Degree of bone loss Type of bone involved Degree of immobilization Infection Local malignancy Avascular necrosis Hormones Weightbearing stress |
| How does location of tear affect healing? | midsubstance heals slower because of less vascularity |
| Factors that affect healing | Depends on the makeup of the tendon: proportion of collagen to elastin; Degree of tear & amount of loading applied(small/partial verse total) |
| What is the healing time for tendons? | Healing time is typically 4-6 weeks with some early mobilization at 2 weeks |
| What must you consider for rehab in relation to the tensile strength of the repaired tendon? | Avoid aggressive motion/strengthening that is greater than the tensile strength of the repair should be avoided |
| Characteristic of healing of ligaments | Vascularity is poor Heal by scarring location: fingers 3 weeks, knee 3 mos, ankle moths to >1yr Degree of tear |
| Healing for the joint capsule | poor vascularity, other factors immobilization, degree of tear 3-5 weeks |
| Contusions | when sudden, heavy compressive force (direct blow to muscle) |
| Strains | excessive tensile force leads to overstraining of the myofibers; more likely to occur during eccentric contractions (higher tensile stress) and on muscles that cross 2 joints |
| What injuries are the most? | 90% contusions and straings |
| what is the myotendinous junction? | Myotendinous junction: end of muscle fiber and tendon |
| Where does skeletal muscle usually occur? | myotendinous junction |
| How does muscle repair? and what is needed for regeneration | repair with scar regeneration requires intact basement membrane |
| What could affect the basement membrane? | Severe infection Transection of a muscle Contused or strained muscle |
| healing of articular cartilage | Limited healing ability: no lymph, no blood, no nerves Articular cartilage only versus with subchondral bone involvement |
| What happens in healing process if just cartilage? | don’t form clot, no recruitment macrophages or neutrophils |
| What happens if bone is involved wth articular cartilage injury? | If bone involved vascularization of bone allows for fibrin-fibronectingel giving access to the inflammatory cells and permitting the formation of granulation tissue has low proteoglycan content which predisposed it to degeneration and erosive changes |
| What happens if no bone is involved in articular cartilage injury? | less likely to heal |
| Zone 1 of articular cartilage | Outermost layer Collagen (type II) fibers are oriented parallel to the joint surface Reduces friction between opposing joint surfaces |
| ZOne II and III of articular cartilage | Collagen fibers are randomly arranged, form an open latticework more proximal and aides in additional shock absorption In the third layer some of the fibers lie perpendicular and extend across the interface between the uncalcified and calcified portions |
| ZOne iV of articular cartilage | Calcified cartilage layer |
| SUrgical interventions for articular cartilage repair | Lavage and debridement 40-66% good results after 3 years Marrow Stimulation 50-60% satisfactory improvement 3-5 years Autologous Perichondral Grafts Good: 1-2 year f/u Poor to fair > 8 years |
| Other surgical interventions | Osteochondral Autographs Good 2 year f/u Autologous Chondrocytes Implantation Good to excellent results at 39 months (Brittenberg et al) Good to excellent results at 4 years (Petersen et al) Cartilage similar to surrounding cartilage |
| Factors influencing healing | Type: surg incision faster than blunt trauma Size: sm faster than bif Location: vascularized vs ischemic areas |
| how does vascular supply affect healing | Vasc sply: nutrition, O2, inflammatory response requires this. w/o it increased risk of infection infection,increase lysis n decrease collagen production n get excessive granulation tiss |
| how do physical agents affect healing? | Physical agents: thermal, electromagnetic, mechanical forces, cryotherapy, thermotherapy, US, radiation, light, electrical currents mechanical pressure |
| how does movement affect healing? | Early mobilization is preferred: muscle significant strength loss in 4 weeks collateral ligaments: 50% strength in 4 weeks cruciates: 30% in 8 weeks CPM- can get rid of edema, and increase ROM, and decrease pain (short term) |
| How does age affect healing? | Age: sun exposure, decrease density and cross-linking ability of collagen (reduced tensile strength), decreased mast cells and fibroblasts, lower rate of epithelialization, poor organization of cutaneous vessels |
| how does disease affect healing? (DM) | DM: impaires collagen synthesis, increases risk infection, dampened immuned response, decreased phagocytosis, decreased blood flow (PVD), increased risk for injury due to neuropathy |
| Immunosupressed.immunocompromised affects healing how | Immunosuppressed/immunocompromised: infection due to inadequate inflammatory response (person with transplant, HIV) |
| CV and diabetes affect healing how | CV: decreased oxygen from poor supply diabetes- decreased phgocytosis, decreased collagen production, increase risk of neuropathy |
| Meds affect healing glucocorticosteroids | block inflammatory cascade via inhibition of inflammatory molecules cytokines, enzymes, receptors, adhesion molecules) cortisone or hydrocortisone |
| corticosteroids | decrease margination, migration, accumulation of monocytes to site of inflammation & induce anti-flammatory actions (inhibit wound contraction, decrease rate of epithelialization, decreased the tensile strength of closed/healed wounds) |
| NSAIDs | interrupt prostaglandins but don’t interupt fibroblast or macrophages; they cause vasoconstriction & suppress inflammatory response |
| Vit A THiamine (B1) B5 Vit C | Vit A retard epithelialization, rate of collagen synthesis, cross-linking Thiamine (B1) decreases collagen formation B5 decreases tensile strength, reduces fibroblasts Vit C impairs collagen synthesis, capillary rupture , risk of infection |
| ZInc Mg Copper | Zinc decreases epitheliazation, reduces collagen synthesis and decrease tensile strength Mg decreased collagen synthesis Copper alter cross linking (decreased tensile strength) |
| Intervetion considerations (stages of healing) | P.R.I.C.E. Estim Gentle ROM within painfree range Massage vs STM vs compression US: continuous vs intermittent Phonophoresis Iontophoresis Ther ex Heat vs cold |
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