Response and Wound Healing Flashcards
What are the signs and symptoms of vasovagal syncope?
Loss of consciousness
Warm sweaty extremities
Fast pulse
How to manage VVS?
Head down posture
What are the phases of physiological response to trauma and their respective lengths?
Ebb, flow, recovery
Hours, days, weeks
What is the ebb phase of trauma response?
Hypovolemic shock
Priority is to maintain life/homeostasis by reducing cardiac output, oxygen consumption, BP, and therefore tissue perfusion
Body temperature drops
Metabolic rate drops
What is the flow phase of trauma response?
Increase in catecholamines, glucocorticoids, glucagon and release of cytokines and lipid mediators
Acute phase protein production
Basically catabolism causing hypermetabolism, breakdown of skeletal muscle protein, lipid stores, glycogen stores, insulin resistance
What is the significance of the flow phase?
Prolonged metabolic stress without provision of adequate calories and protein leads to impaired body functions and ultimately malnutrition due to the catabolic phase
What are the 4 categories of wounds?
Clean
Clean/contaminated
Contaminated
Infected
What is a clean wound
Operative incisional wound following nonpenetrative (blunt) trauma
What is a clean/contaminated wound
Uninfected wound with no inflammation but respiratory, GI, genital and/or urinary tract has been entered
What is a contaminated wound
Open, traumatic wound or surgical wound involving a major break in sterile technique showing evidence of inflammation
What is an infected wound
Old, traumatic wounds containing dead tissue and wounds with evidence of clinical infection like purulent discharge
What are the categories of wound closure
Primary intention (all layers close quickly and cleanly)
Secondary intention (deep layers close but superficial layers left to heal from inside out)
Tertiary intention (delayed primary closure)
What causes inflammation in wounds?
Damaged endothelial cells release cytokines to increase integrand expression in circulating lymphocytes
Histamine, serotonin and kinins cause vessel contraction, decreases blood loss, and causes chemotaxis of neutrophils (most abundant cell in initial 24h)
What is proliferative phase of wound healing?
After neutrophils have removed cellular debris and released cytokines to attract macrophages
Lasts for up to 3 weeks
Fibroblasts migrate into wound and secrete collagen type III
Angiogenesis occurs by 48h
Macrophage remodelling and secretion
Greatest increase in wound strength
What is maturation phase of wound healing
Final phase, from 3rd week to 9-12 months
Collagen III is converted to collagen I, tensile strength increases up to 80% of normal tissue
What type of healing occurs in extraction wounds?
Secondary intention
- Wound edges separated
- Gap between them cannot be bridged directly
- Extensive loss of epithelium
- Severe wound contamination or
- Significant subepithelial tissue damage
Immediately after extraction:
Blood fills extraction site
Intrinsic and extrinsic clotting cascade pathways activated
Fibrin meshwork forms containing entrapped RBCs, sealing off torn BV and reducing wound size
First 24-48h after extraction:
Clot organisation
Engorgement and dilation of BV in PDL remnants
Leukocytic migration
Formation of fibrin layer
V impt as if blood clot disintegrates healing may be greatly delayed and may be extremely painful
First week after extraction:
Clot forms temporary scaffold for inflammatory cell migration
Epithelium at periphery grows over surface of clot
Inflammatory stage - WBCs enter socket to remove bacteria and debris like bone fragments
Fibroplasia - ingrowth of fibroblasts and capillaries
Epithelial migration down socket wall until it contacts epithelium from the other side of the socket or encounters the bed of granulation tissues under the clot, over which it can migrate
Osteoclasts accumulate along crestal bone
Second week after extraction:
Large amount of granulation tissue fills socket
Osteoid deposition along alveolar bone lining socket, in smaller sockets epithelium may already be fully intact
Trabeculae of osteoid extends into clot from alveolus, and osteoclastic resorption of cortical margin of alveolar socket is more distinct
These processes continue into week 3 and 4, along with completion of epithelialization of most sockets
Third week after extraction
Filled with granulation tissue with poorly calcified bone at wound perimeter
Surface completely reepithelialized with minimal or no scar formation
Active bone remodeling by deposition and resorption continues for several more weeks
Histological phases of the healing continuum
Inflammatory
Proliferative
Remodeling
Inflammatory phase of the healing continuum
Initial transient vasoconstriction followed by vasodilation
Initiation: tissue trauma and bleeding activates factor XII (Hageman factor) initiating healing cascade effectors such as complements, plasminogen, kinins and clotting systems
Aggregation of circulating platelets at injury sites, adhering together and the exposed vascular subendothelial collagen to form a primary platelet plug within a fibrin matrix, achieving hemostasis
Clot serves as a reservoir of cytokines and growth factors that are released as activated platelets degranulate (interleukins, TGF-8, PDGF, VEGF) to regulate subsequent healing
Adjacent epithelium begins to migrate
Undifferentiated mesenchymal cells begin to transform into fibroblasts
Proliferative phase of the healing continuum
Cytokines and growth factors of inflammatory phase stimulate proliferative phase
Starts as early as 2nd day and lasts up to 3 weeks
Formation of pink granulation tissue, with establishment of local microcirculation to supply oxygen and nutrients for elevated metabolic needs of regenerating tissues
Epithelial thickness increases, collagen fibers haphazardly laid down by fibroblasts, building capillaries establish contact with their counterparts from other sites in wound
Remodeling phase of the healing continuum
Proliferative phase is progressively replaced by a phase of progressive remodeling and strengthening (balance between matrix degradation and formation) of the immature scar tissue
Can last for several years
As metabolic demands decrease, capillary network regresses, vascular integrity is reestablished
Fibroblasts start to disappear and type III collagen is replaced by stronger and more organized type I collagen
Epithelial stratification is restored
Local factors affecting healing
Wound sepsis
Location (poor blood flow, tension)
Foreign bodies
Previous irradiation
Poor technique
Immobilization (formation of connective tissue is not hindered?)
Systemic factors affecting healing
Nutritional deficiencies (proteins, vitamins A, C, D)
Systemic disease
Therapeutic agents
Age
Complications of extraction wounds
Localized alveolar osteitis
Delay
Slower rate of apposition of regenerate bone to remaining alveolar bone due to absence of healthy granulation tissue matrix
If infected, remains open or is partially covered by hyperplastic epithelium for extended periods
Fibrous healing
What is dry socket?
Inflammation involving either whole or part of condensed bone (lamina dura) lining the tooth socket
Empty socket, which may have evidence of broken down blood clot and food debris inside
Intense odor
Painful socket arising 24-72h after extraction, may last 7-10 days
About 3% of extractions
Predisposing factors in dry socket
Infection
Trauma
Blood supply
Site
Smoking
Sex
Systemic factors like oral contraceptives
Fibrous healing of extraction wound complication
Uncommon
Usually following difficult, complicated or surgical extractions, when accompanied by loss of both lingual and labial/buccal plates along with periosteum
Radiographically see well circumscribed radiolucent area in site of extraction site
Treat by excising the lesion
Sequelae of cortical bone / lamina dura
After removal, remaining empty socket consists of cortical bone covered by torn PDL with a rim of oral epithelium (gingiva) at the coronal portion
Cortical bone is resorbed from the crest and walls of the socket as new trabecular bone is laid down across the socket. Radiographically evident after 6-8 weeks.
4-6 months after, cortical bone is fully resorbed, loss of distinct lamina dura radiographically. Normal bone fills the socket and epithelium moves towards the crest and becomes level with adjacent gingiva
What are the types of healing in bone grafts
Osteogenic: viable osteoblasts/cytes in graft, direct healing and formation of new bone and BV
Osteoconductive: inorganic bone material conducts a path for osteoclasts to resorb HAP crystals and osteoblasts from host to form new osteons
Osteoinductive: organic bone material induces formation of new osteoblasts from osteoprogenitor cells (BMP)
What are the types of bone grafts
Autogenous (live bone, osteogenic)
Allogenous (human)
Xenogenous (bovine)
Alloplastic (beta tricalcium phosphate)
Bone healing in fracture stages
Immediate: acute inflammation, migration of vessels and osteogenic cells, fibrovascular invasion and hematoma organization
Callus formation: osteogenic cells from periosteum proliferate, forming a thin rim of bone to bridge the gap between fragments. Fusiform swells, hyaline cartilage forms beneath the rim of bone. Eventually replaced by woven bone via endochondral ossification
Remodeling of woven bone until compact lamellar bone forms.
If movement occurs only fibrous tissue bridges the gap, causing exuberant callus formation to stabilize the fragments.
If there is a large gap between fragments, persistent movement, avascular necrosis or interposed soft tissue, there may be non-union (persistent fracture gap, fibrous/fibrocartilaginous bridging and pseudoarthrosis)
Primary bone healing
When fragments are stable and well aligned. Compression leads to better adaptation, frictional stability, direct cortical bone-bone contact and osteoinduction
Depends on fracture gap size and stability
Cancellous bone healing
- If bony trabeculae aligns anatomically, capillaries proliferate, traversing the gap and reconstituting the torn medullary network
- Local osteogenic cells cross fracture site to form new trabeculae, which thickens with woven bone to create clinical union with little fibrosis and no cartilage precursors after 4 weeks
Cortical/contact healing
- If bone is in direct cortical contact, osteoclasts widen haversian canals on either side, oriented longitudinally towards site
- Capillary ingrowth
- Osteoblasts lining tunnels lay down osteoid which matures directly into lamellar bone
- Wider gaps bridged by woven bone
- Cortical bridging occurs by 8 weeks, finishing by 16 weeks, with clinical union by 6-8 weeks due to cancellous healing
Nerve injury types
Neurapraxia
Axonotmesis
Neurotmesis
Neurapraxia
Reversible physiological nerve conduction block, some loss of sensation and muscle power for a few days/weeks
Due to mechanical pressure causing demyelination
Neurotmesis
Division of nerve trunk
If injury is more severe, where nerve is no longer in continuity, recovery will not occur
Classes of nerve injuries
First degree injury - transient, reversible ischemia and neurapraxia
Second degree injury - axonotmesis, with axonal degeneration, but as endoneurium is preserved, regeneration without need for intervention can result in complete or near complete recovery
Third degree injury - Endoneurium disrupted but perineural sheaths intact and internal damage is limited. Fibrosis and crossed connections limit recovery.
Wallerian degeneration
Distal axon regeneration following sectioning or severe injury with myelin degradation, occurring within 7-10 days of injury
This portion of nerve is inexcitable
Axon degeneration
Distal degenerated nerve is inexcitable
Regeneration can occur as basement membrane of Schwann cell survives
Demyelination
