Lesson 1: Wound Healing & Response To Injury Flashcards
What can happen before/during an extraction?
Vasovagal Syncope (most common)
Carotid Sinus Syndrome
Situational Syncope
What is VVS? Name the signs and symptoms, management. Who most commonly gets VVS?
Sudden drop in BP/HR due to overreaction and reflex of vagus nerve in response to triggers (emotional stress, pain, fear, dehydration)
LOC, warm, sweaty, fast pulse
Mx: head down posture
Most common in populations with young people without structural heart disease
How has the body’s metabolism changed post trauma?
• Trauma alters body’s metabolism of micronutrients
• Body’s hormonal situation changes -> increasing demand for energy, proteins and micronutrients
• Loss of body mass, protein or impairment and loss of body functions can take place if nutritional requirements are not met
Name 5 types of responses of the body to trauma
1) Endocrine
• Pituitary Gland (increase GH, ACTH)
• Adrenal Gland (increase cortisol, aldosterone)
• Pancreas (increase glucagon, decrease insulin)
• NET EFFECT: increased secretion of catabolic hormones
2) Afferent neuronal impulses from site of injury -> Hypothalamus
3) Efferents to sympathetic nervous system -> Adrenal medulla -> increase catecholamines [stress hormones] (causing tachycardia, hypertension)
4) Cytokines produced by endothelium, activated leukocytes and fibroblasts -> produce different proteins
5) Acute Inflammatory Response
• Cellular activation and inflammatory mediators (TNF, IL1)
Describe Ebb Phase post injury.
- Hypovolemic shock
- Priority to maintain life/homeostasis
- Decrease cardiac output, oxygen consumption, BP, tissue perfusion
- Decrease in metabolic rate may be protective mechanism during hemodynamic instability)
Describe Flow phase post injury.
- Catabolism (breaking down energy stores)
- Increase catecholamines, glucocorticoids, glucagon
- Release of cytokines, lipid mediators
- Acute phase protein production
- Hyper metabolism
- Alterations in skeletal muscle and liver proteins
- Insulin resistance
Net effect from flow phase post injury.
mobilisation of tissue energy reserves, body temp increases, fatty acids produced from lipid reserves, glucose from hepatic glycogen and muscle glycogen (only glucose provided for involved muscle), gluconeogenic precursors (amino acids) produced from muscle
Name the Classification of Wounds
1) Healing by Primary Intention
• All layers closed, heals in a minimum amount of time with no separation of wound edges and minimal scarring
2) Healing by Secondary Intention
• Deep layers closed but superficial layers left to heal -> wound edges separated
• Gap between wound edges cannot be bridged directly
• Extensive loss of epithelium
• Severe wound contamination or subepithelial tissue damage
• Cases of infection, excessive trauma, tissue loss or imprecise approximation of tissue
3) Healing by Tertiary Intention
• Delayed primary closure
Extraction Wound healing is by ___ intention?
Secondary intention
Describe wound healing in 3 steps.
1) Inflammation
- damaged endothelial cells release cytokines that increase expression of integrates in circulating lymphocytes
- histamine, serotonin cause vessel contraction, decrease in blood loss and act as chemotactic factors for neutrophils
2) Proliferative phase (after neutrophils removed cellular debris)
- fibroblasts migrate into wound and secrete collagen type 3
- angiogenesis occur
- segregation of collagen and macrophage remodeling
- greatest increase in wound strength
3) Maturation
- collagen 3 converted to collagen 1
- tensile strength continues increasing up to 80% of normal tissue
Describe the wound healing of extraction socket (immediate)
- blood fills site
- both intrinsic and extrinsic pathways of clotting cascade are activated
- resultant fibrin meshwork containing entrapped RBCs seal off torn blood vessels
- size of extractions wound decreases
Describe the wound healing of extraction socket (first 24-48h)
- organisation of clot
- dilation of blood vessels in PDL remnants
- leukocytic migration
- formation of fibrin layer
Describe wound healing of extraction socket (in the first week)
- clot forms temporary scaffold upon which inflammatory cells migrate
- epithelium at wound periphery grows over surface of organising clot
- WBCs enter socket to remove bacteria and break down debris and bone fragments
- fibroplasia begins (in growth of fibroblasts and capillaries)
- epithelial migrates down socket wall to contact epithelium on other side of socket or encounters granulation tissue
- osteoclasts accumulate along crestal bone
Describe wound healing of extraction socket (2nd week)
- large amount of granulation tissue fills socket
- osteoid deposition along alveolar bone lining socket (epithelium fully intact for small sockets)
- trabeculae of osteoid slowly extend into clot from alveolus
- continue during 3rd and 4th week
Describe the wound healing of extraction socket (3rd week)
- extraction socket filled with granulation tissue and poorly calcified bone forms at wound perimeter
- surface of wound completely reepithelialised with minimal or no scar formation
- active bone remodeling by deposition and resorption continues for several more weeks
What are the 3 phases of wound healing
1) inflammatory
- vasoconstriction
- platelet plug
2) proliferative
- formation of granulation tissue
- establishment of local micro circulation to supply oxygen and nutrients for increased metabolic needs of regenerating tissue
3) remodeling
- strengthening of immature scar tissue
- type 3 collagen gradually replaced by stronger type 1 collagen
Name the local factors affecting wound healing
- Wound sepsis (infection)
- location (poor blood or wound tension)
- foreign bodies
- Previous irradiation
- poor technique
- immobilisation (so that formation of connective tissue not hindered)
Name systemic factors affecting wound healing
- nutritional deficiencies (proteins, vitamins)
- systemic diseases (diabetes)
- therapeutic agents (e.g. drugs that prevent osteoblast activity)
- younger patients heal faster
Describe the complications in healing of extraction wounds
1) localised alveolar osteitis
2) delay
3) regeneration of bone happens at slower rate due to absence of healthy granulation tissue
4) infected socket remains open or partially covered with hyperplastic epithelium for extended periods
5) fibrous healing of extraction wound
What is localised osteitis?
- inflammation involving whole or part of condensed bone lining tooth socket (laminandura)
- empty socket
- intense odour
- painful 24h-72h after extraction and may last for 7-10 days
- overall incidence 3%
Name the predisposing factors in a dry socket
1) infection
2) extraction trauma
3) less blood supply at posterior areas (bone denser)
4) site
5) smoking
6) females
7) systemic factors (e.g oral contraceptives)
Describe fibrous healing of extraction wound
- uncommon complication
- after difficult/complicated extraction
- commonly occurs when extraction accompanied by loss of both lingual and labial/buccal plates along with periosteum
- radiographically well circumscribed radiolucent area of previous extraction
- treatment: excision of lesion
What happens to the cortical bone post extraction
- bone is resorbed from the crest and walls of the socket
- new trabecular bone is laid down across the socket
- takes 4-6 months for full resorption (loss of distinct laminate dura radiographically)
- epithelium moves toward crest and becomes level with adjacent crestal gingiva
- 6-8 weeks for bone formation to show on radiograph
- rim of fibrous scar tissue remains on edentulous alveolar ridge
Describe the bone healing process in bone grafting
1) osteogenic
- presence of viable osteoblasts in graft with direct healing and formation of new bone and blood vessels
2) osteoconductive
- bone inorganic material conducts path for osteoclasts to resorb hydroxyapatite crystal and osteoblasts from host bed to form new osteons
3) osteoinductive
- organic portion of bone induces formation of new osteoblasts from osteoprogenitor cells
What are the typesof Bone Graft? What to take note about bone graft
1) autogenous
2) allogenous - human
3) xenogenous - from external body
4) alloplastic-beta tricalcium phosphate (e.g. osteon) (man made)
*graft must be fixated in place because micro motions will disrupt angiogenesis
Describe bone healing in fracture
1) acute inflammation
- migration of vessels and osteogenic cells
- fibrovascular invasion and organisation of haematoma
2) callus formation (soft fibrous tissue and cartilage)
- osteogenic cells from periosteum proliferate and form thin rim of bone to bridge gap between fragments -> leads to fusiform swelling
- hyaline cartilage forms beneath bone rim
- callus eventually replaced by woven bone through endochondral ossification
3) remodeling of woven bone until compact lamellar bone formed in previous fracture
4) osteogenesis extends into fracture gap when stable conditions exist
- if movement occurs, only fibrous tissue bridges the gap, leads to exuberant callus formation to stabilise fragments
5) non-union (persistent fracture gap, fibrous/fibro-cartilaginous bridging & psuedoarthrosis) occurs if there is large gap between fragments
- persistent movement
- avascular necrosis
- interposed soft tissue
What is primary bone healing?
- occurs when fragments are stable and interfragmentary surfaces are well aligned
- compression at fracture site leads to bone adaptation, frictional stability, direct cortical bone to bone contact and osteoinduction
- depends on size of fracture gap and stability
- divided into cancellous bone and cortical bone/contact healing
What is cancellous bone healing?
- if ORIF (open reduction and internal fixation - surgery) can align bony trabeculae anatomically, capillaries proliferate and traverse gap to reconstitute torn medullary network
- local osteogenic cells cross fracture site
-> new trabeculae forms and existing ones thicken with woven bone until clinical union with little fibrosis and no cartilage precursors - cancellous surfaces form clinical union in 4 weeks
What is cortical/contact healing?
- occur when bone is in direct cortical contact
- begins with osteoclastic widening of Haversian canals on either side of fracture
- initial healing in viable bone some distance from injury
- widened canals oriented longitudinally towards site, osteoclasts excavating towards and across fracture (1mm in 2-3 weeks)
- osteoblasts line tunnels laying down osteoid that matures directly into lamellar bone
- wider gaps bridged by woven bone
- cortical bridging occurs by 8 weeks, completed by 16 weeks
- clinical union by 6-8 weeks due to cancellous healing
What is gap healing?
- critical distance bridged by primary healing is MAX 20micro meter
- larger gaps up to 100 micro meter heal by gap healing with deposition directly by new lamellar bone parallel to fracture, transverse to long axis of the bone
- eventual remodeling to become parallel to long axis of bone
What are the 3 basic pathological processes
- Wallerian degeneration
- distal axon degeneration after section or severe injury, with degeneration of myelin
- process occurs within 7-10 days of injury and this portion of nerve is inexcitable electrically - Axon degeneration
- distal degenerated nerve is inexcitable electrically
- regeneration can occur since basement membrane of Schwann cell survives and act as skeleton along which axon regrows up to rate of 1mm/day - Demyelination
- segmental destruction of myelin sheath occurs without axonal damage
- primary lesion affects Schwann cell and causes marked slowing of conduction or conduction block
- local demyelination caused by inflammation e.g. Guillain-Barre syndrome
What are the 3 types of nerve injuries?
- Neurapraxia (temporary numbness)
- reversible physiological nerve conduction block
- loss of some sensation and muscle power with spontaneous recovery after a few days or weeks
- due to mechanical pressure causing segmental demyelination
- seen typically in ‘crutch palsy’ and milder tourniquet palsy
- first degree injury - Axonotmesis
- part of nerve trunk injured
- axonal degeneration takes place
- endoneurium is preserved so regeneration can lead to complete recovery without intervention - Neurotmesis
- division of the nerve trunk
- endoneurium is disrupted but perineurial sheaths are intact and internal damage limited
- chances of axons reaching their targets are good but fibrosis and crossed connections will limit recovery
