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wound repair Flashcards

1
Q

WOUNDS IN THE WORLD

A
  • Anytime you perform SURGERY you create a WOUND
  • Leaves underlying tissue vulnerable to infection
  • Wound healing remains problematic →why and what can we do to lessen this?
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2
Q

CAUSES OF INJURY

A
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3
Q

EPITHELIALIZATION
* Noted with what injuries?
* Renewal of? occurs within?
* Completion occurs at?
* Free edge of epithelium migrate until?
* Signal is terminated in?
* Occurs over?
* Occurs faster with?
* Epithelium does cross over?

A
  • Noted with abrasions, most superficial
  • Renewal of epithelium occurs within hours after injury
  • Completion occurs at 24 – 48 hours
  • Free edge of epithelium migrate until it contacts the opposite edge=Signal is terminated in CONTACT INHIBITION
  • Occurs over wound bed but under scabbing/superficial blood clot
  • Occurs faster with moisten substrate over wound
  • Epithelium does cross over desiccated surface
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4
Q

OROANTRAL COMMUNICATIONS

A

fistula may form as a result of extraction if sinus floor exposed/down to oral cavity

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5
Q

PHASES OF WOUND HEALING

time frames of each

A
  • Inflammatory phase: Day 1-6
  • Fibroplastic phase: Days 4- 3 weeks
  • Maturation/remodeling phase: 3 weeks – 1 year
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6
Q

INFLAMMATORY PHASE:
days?
* Also called?
* increase in wound strength? due to?
* principle material holding wound together?
* tensile strength?
* phases?

A

DAYS 1- 5ISH
* Also called LAG PHASE:
* No increase in wound strength, Due to little collagen deposition
* FIBRIN principle material holding wound together
* Has little tensile strength
* 2 phases of the Inflammatory Phase: Vascular
and Cellular

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7
Q

VASCULAR PHASE of inflamm phase
damaged vs non damaged vessels?
mediated by?
results?

A
  • Vasoconstriction of disrupted vessels: Coagulation (platelets and fibrin) and Clot formation 5-10 minutes
  • Vasodilation of non-disrupted vessels
  • Increases permeability to site to allow healing factors and cells to reach injury site
  • Mediated by histamine and prostaglandins (E1 and E2) from WBCs
  • Causes EDEMA
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8
Q

CELLULAR PHASE of inflamm phase

A
  • PMN (neutrophils) arrive within 24 hrs of injury
    • Margination: PMNs stick to side of blood vessels
    • Diapedesis: PMNs migrate through vessel walls
    • Degranulation: PMNS releasing lysosomal enzymes to destroy bacteria/foreign materials/necrotic tissue
    • Macrophages continue clearance of debris
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9
Q

FIBROPLASTIC PHASE:
time frame?
* dominant cell?
* cell function
* content? →purpose?
* Secretes? functions?

A

DAY 4 – 3 WEEKS
* Fibroblasts are the dominant cell
* Deposits ground substance and TROPOCOLLAGEN over fibrin lattice
* Ground substance contains mucopolysaccharides →cement collagen fibers together

  • Secretes FIBRONECTIN:
    1. * Stabilize fibrin
    1. * Assists in recognizing foreign material
    1. * Chemotactic factor to aid recruitment of fibroblasts and macrophages
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10
Q

FIBROPLASTIC PHASE
* vascular event? why? causes?

A
  • Angiogenesis occurs:
  • Increase vascularity (from wound edges inward)
  • Causes raised and red color of wound
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11
Q

FIBROPLASTIC PHASE:
* Superfluous fibrin strands?
* collagen deposotion? result
`

A
  • Superfluous fibrin strands removed by plasmin
  • Excessive collagen deposited in haphazard manner:
    1. * Increases tensile strength (~ 5-7 days after injury →timing for suture removal)
    1. * 70%-80% tensile strength compared to uninjured tissue
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12
Q

REMODELING PHASE:
time frame? collagen? wound strength?

A

3 WEEKS TO 1 YEAR/INDEFINITE
* Increase in collagen ORGANIZATION AND STRENGTH
* Collagen oriented in direction to better resist tension
* Type III collagen replaced by Type I
* Excess collagen removed →scar softens
* Wound strength never reaches above 80% - 85% of uninjured tissue (NEVER ABOVE 90)
* Peak tensile strength at 60 days

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13
Q

REMODELING PHASE:
wound eryhtema changes and wound contraction

A
  • Wound erythema decreases as vascularity decreases to site
  • Wound contraction occurs by migration of wound edges toward each other
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14
Q

why keep PDL in socket with extraction?

A

will attract fibroblasts, decrease odds for infection

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15
Q

ant man flaps?

A

no, mental nn present

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16
Q

implant compressing nn, what to do?

A

remove implant

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17
Q

does neurotemesis recover?

A

no

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18
Q

factors impairing wound healing

A

any foreign material
necrotic tissue
ischemia
tension

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19
Q

foreign material and healing

A
  • Dirt, wood, glass, suture, bacteria
  • “Non-self” material causes chronic inflammation —Decreases fibroplasia
  • Bacteria proliferation causing infection
  • Destroys host tissue with bacteria byproducts
  • Non-bacteria causes a harbor for bacteria
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20
Q

necrotic tissue and wound healing
* classic example?
* Barrier to?
* Serves as a?
* Hematoma?

A
  • Free bony fragment in extraction site is classic example
  • Barrier to ingrowth of reparative cells
  • Serves as a protected niche for bacteria
  • Hematoma formation:
  • Nidus for bacteria, as well as food source for bacteria
  • Blood clot is small and functional, hematoma is large and of no use
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21
Q

ischemia and wound healing

results of this

A
  • Decreased blood supply, resulting in poor oxygen delivery to needed site
  • Increases wound infection by halting delivery of PMNs, WBCs, antibodies, ABX
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22
Q

causes of wound ischemia

A
  • Poorly designed flaps
  • Tight sutures
  • Internal pressure from edema/hematoma
  • Hypotension during surgery
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23
Q

tension and wound healing

effect of this on early suture removal?

A
  • Wounds closed under tension will cause ischemia at margins with eventual opening (dehiscence)
  • If suture removed too early, the wound under tension will reopen and heal with excessive scar formation
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24
Q

HYPERTROPHY (scar)
demo?
common in?
with time?
where common?

A
  • Overgrowth of tissue within border of wound edges
  • Any race
  • Common in pediatrics
  • Regresses with time
  • Common on flexor surfaces
25
KELOID * Common in? * pediatrics? * Grows for? * Common areas
* Overgrowth beyond border of wound edges * Common in darker skin/hereditary * Rare in pediatrics * Grows for years * Common on upper body, head/neck
26
KELOID/HYPERTROPHY TREATMENT
* Similar strategy for both findings: Keloid significantly more difficult to eradicate * Triple therapy: 1. Surgical excision 2. Corticosteroid injection * 40 mg/cc injection intralesional * 2-3 times per month for 6 months 3. Silicone pressure dressing * Worn 12-24 hours per day * For 2-3 months
27
forms of wound healing
primary, secondary and tertiary intention
28
PRIMARY INTENTION * loss of tissue? * scarring? * Closure stabilized and accomplished with?
* Edges of wound returned to anatomic position * Wound edges directly next to each other * Little loss of tissue * Minimal scar * Closure stabilized and accomplished with sutures/staples/adhesives
29
examples for 1 intetnion healing
* Lacerations * Well reduced bone fractures
30
SECONDARY INTENTION
* Wound is allowed to granulate in * May be packed by surgeon with gauze or drain * Granulation results in broad scar * Slower healing process
31
examples 2 intention
* Gingivectomy * Tooth extraction * Poorly reduced fracture
32
TERTIARY INTENTION
* Delayed primary closure * Related to contaminated wounds * Wound cleaned, debrided and observed * Closure attempted after 4-5 days * Purposely left open to observe for any signs and symptoms of infection or further tissue necrosis
33
how can we cover 3 intention wounds?
* Skin grafting or flaps can be used to cover these type of wounds
34
primary vs secondary intention table
35
HEALING OF EXTRACTION SOCKETS
Most cases healing is by SECONDARY INTENTION
36
healing process Immediately after extraction:
* Remnants of periodontal ligament remain attached to the lamina dura * Gingival epithelial margin is separated at the crest * Coagulated blood seals socket
37
healing of extraction sockets in the first week phase? what begins? dry sockets? epithelium action?
* Inflammatory phase: WBCs break down and digest bacteria and debris * Fibroplasia begins * Fibroblast proliferate forming granulation tissue * Neovascularization penetrates clot- Clinical correlation: Localized osteitis, “dry socket,” occurs if this phase fails * Epithelium begins to migrate down towards first granulation tissue it comes into contact with
38
second week healing of extraction sockets | what increase? time frame?
* Granulation tissue increase and matures * Small socket may close off at 14 days, molars by 3 weeks
39
Third and Fourth week socket healing | closure? deposition of?
* Almost all sockets will have epithelial closure by 21 days * Deposition of early bone (osteoid) within the socket
40
healing of sockets 4-6 months | alveoulus? LD? clinical correlation?
* Continued resorption and recontouring of alveolus * Total resorption of lamina dura by 1 year * Clinical correlation: What is time frame to wait before building a final prosthesis?
41
* Where do osteogenic cells responsible for bone repair come from?
* Periosteum * Endosteum * Circulating pluripotential mesenchymal cells
42
bone healing 1 vs secondary intent
43
factors important to proper bone healing
vascularity and immobility
44
vascularity and bone healing * If low oxygenation? * If severe?
* If low oxygenation →cartilage will form instead of bone * If severe →fibrous tissue may never calcify →fibrous union
45
IMMOBILITY and bone healing * ways to do this? * Mobility prevents?
* Intermaxillary fixation (IMF), bone plates, direct wires * Mobility prevents fibrous tissue from ossifying →fibrous union, non-union,
46
NERVE REPAIR considerations for which nn's?
* OMS considerations with inferior alveolar or lingual nerves
47
* Prognosis for return of sensory function with nn repair is related to:
* How bad was the damage (severed, crushed, stretched, pinched) * Condition of epineurium * Amount of separation between nerve ends
48
phases of nn repair
* Degeneration * Regeneration
49
nn repair: degeneration forms? symptoms?
**Segmental demyelination** * Myelin sheath dissolved in isolated segments (slows nerve conduction) * Symptoms: paresthesia, dysesthesia, hyperesthesia, hypoesthesia ** Wallerian Degeneration** * Axons and myelin sheath of nerve distal to site of interruption undergo disintegration in their entirety * Axons proximal to the site of interruption undergo some degeneration generally a few Nodes of Ranvier away
50
nn growth/regeneration
* Growth cone (growth of new nerve fibers from proximal nerve stump) starts growing down remnant Schwann cell tube * Progresses 1 mm per day * Continues until site innervated by the nerve is reached * New myelin sheaths may form as axons increase in diameter
51
neuroma
* Abnormal nerve healing →NEUROMA * Mass of aimless nerve fibers * Painful when disturbed (temperature, pressure, etc...)
52
neuropraxia
mild injury to nn
53
axonotmesis
more severe injury
54
neurotmesis
most severe nn injury
55
Paresthesia
* Spontaneous and subjective altered sensation that IS NOT PAINFUL/UNCOMFORTABLE
56
Dysesthesia
* Spontaneous and subjective altered sensation that IS PAINFUL/UNCOMFORTABLE
57
Hyperesthesia
* Excessive sensitivity of a nerve to stimulation
58
Hypoesthesia
* Decreased sensitivity of a nerve to stimulation
59
Anesthesia
* No sensation when stimulated

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