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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
Q

KELOID
* Common in?
* pediatrics?
* Grows for?
* Common areas

A
  • Overgrowth beyond border of wound edges
  • Common in darker skin/hereditary
  • Rare in pediatrics
  • Grows for years
  • Common on upper body, head/neck
26
Q

KELOID/HYPERTROPHY TREATMENT

A
  • Similar strategy for both findings: Keloid significantly more difficult to eradicate
  • Triple therapy:
    1. Surgical excision
  1. Corticosteroid injection
    * 40 mg/cc injection intralesional
    * 2-3 times per month for 6 months
  2. Silicone pressure dressing
    * Worn 12-24 hours per day
    * For 2-3 months
27
Q

forms of wound healing

A

primary, secondary and tertiary intention

28
Q

PRIMARY INTENTION
* loss of tissue?
* scarring?
* Closure stabilized and accomplished with?

A
  • 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
Q

examples for 1 intetnion healing

A
  • Lacerations
  • Well reduced bone fractures
30
Q

SECONDARY INTENTION

A
  • Wound is allowed to granulate in
  • May be packed by surgeon with gauze or drain
  • Granulation results in broad scar
  • Slower healing process
31
Q

examples 2 intention

A
  • Gingivectomy
  • Tooth extraction
  • Poorly reduced fracture
32
Q

TERTIARY INTENTION

A
  • 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
Q

how can we cover 3 intention wounds?

A
  • Skin grafting or flaps can be used to cover these type of wounds
34
Q

primary vs secondary intention table

A
35
Q

HEALING OF EXTRACTION SOCKETS

A

Most cases healing is by SECONDARY INTENTION

36
Q

healing process Immediately after extraction:

A
  • Remnants of periodontal ligament remain attached to the lamina dura
  • Gingival epithelial margin is separated at the crest
  • Coagulated blood seals socket
37
Q

healing of extraction sockets in the first week
phase?
what begins?
dry sockets?
epithelium action?

A
  • 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
Q

second week healing of extraction sockets

what increase?
time frame?

A
  • Granulation tissue increase and matures
  • Small socket may close off at 14 days, molars by 3 weeks
39
Q

Third and Fourth week socket healing

closure? deposition of?

A
  • Almost all sockets will have epithelial closure by 21 days
  • Deposition of early bone (osteoid) within the socket
40
Q

healing of sockets 4-6 months

alveoulus? LD? clinical correlation?

A
  • 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
Q
  • Where do osteogenic cells responsible for bone repair come from?
A
  • Periosteum
  • Endosteum
  • Circulating pluripotential mesenchymal cells
42
Q

bone healing 1 vs secondary intent

A
43
Q

factors important to proper bone healing

A

vascularity and immobility

44
Q

vascularity and bone healing
* If low oxygenation?
* If severe?

A
  • If low oxygenation →cartilage will form instead of bone
  • If severe →fibrous tissue may never calcify →fibrous union
45
Q

IMMOBILITY and bone healing
* ways to do this?
* Mobility prevents?

A
  • Intermaxillary fixation (IMF), bone plates, direct wires
  • Mobility prevents fibrous tissue from ossifying →fibrous union, non-union,
46
Q

NERVE REPAIR considerations for which nn’s?

A
  • OMS considerations with inferior alveolar or lingual nerves
47
Q
  • Prognosis for return of sensory function with nn repair is related to:
A
  • How bad was the damage (severed, crushed, stretched, pinched)
  • Condition of epineurium
  • Amount of separation between nerve ends
48
Q

phases of nn repair

A
  • Degeneration
  • Regeneration
49
Q

nn repair: degeneration
forms?
symptoms?

A

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
Q

nn growth/regeneration

A
  • 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
Q

neuroma

A
  • Abnormal nerve healing →NEUROMA
  • Mass of aimless nerve fibers
  • Painful when disturbed (temperature, pressure, etc…)
52
Q

neuropraxia

A

mild injury to nn

53
Q

axonotmesis

A

more severe injury

54
Q

neurotmesis

A

most severe nn injury

55
Q

Paresthesia

A
  • Spontaneous and subjective altered sensation that IS NOT PAINFUL/UNCOMFORTABLE
56
Q

Dysesthesia

A
  • Spontaneous and subjective altered sensation that IS PAINFUL/UNCOMFORTABLE
57
Q

Hyperesthesia

A
  • Excessive sensitivity of a nerve to stimulation
58
Q

Hypoesthesia

A
  • Decreased sensitivity of a nerve to stimulation
59
Q

Anesthesia

A
  • No sensation when stimulated

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