Tissue Injury and Repair 3 Flashcards
Healing by first and second intention. -How granulation tissue can go wrong in horses, and a major differential diagnosis. -Definitions of wound healing by first and second intention and the details of each stage in these processes. -How to draw a graph of the basic stages of wound healing. -How to describe healing of deep and shallow corneal ulcers. -Causes of delayed wound healing. -Differences between mammals and reptiles.
PROUD FLESH
A frequent complication of LIMB wounds in HORSES (not body, not ponies)
Too much granulation tissue produced by protracted fibroblast proliferation.
Most common non-neoplastic proliferative cutaneous lesion.
Continued low level neutrophilic inflammation.
DIFFERENTIAL DIAGNOSIS FOR PROUD FLESH
SARCOIDS.
Can have same gross appearance, seen in horses, donkeys and mules.
Flat, verrucous or nodular.
Can be:
-Bovine Papilloma Virus in horses- Nonproductive.
-Locally aggressive, non-metastatic fibroblastic tumours.
Sarcoids are the most common skin tumour of horses (most often 3-6 years of age)
CUTANEOUS WOUND HEALING
Involves epithelial regeneration AND formation of connective tissue scar.
Is illustrative of the general principles of wound healing.
PHASES OF WOUND HEALING
Three main overlapping phases:
- INFLAMMATION.
- FORMATION OF GRANULATION TISSUE.
- DEPOSITION OF ECM AND REMODELLING.
Larger wounds also contract during the process, though this is not really seen in humans.
HEALING BY FIRST INTENTION
aka. PRIMARY UNION.
Seen in surgical, sutured wounds. Very rarely in natural wounds.
Only focal disruption of basement membrane.
Only a small number of epithelial cells and CT cells die.
Minimal fibrosis, as epithelial regeneration predominates.
Some inflammation round sutures is normal, but should not be excessive.
HEALING BY FIRST INTENTION- 24 HOURS TO 7 DAYS
Neutrophils migrate into fibrin clot, followed by macrophages.
basal cells at cut edge of epidermis begin to show mitotic activity.
Epithelial cells start to migrate. and proliferate across the dermis, depositing BM as they progress.
cells meet in midline, under a scab.
Epidermis is thickened (Hyperplastic).
Fibroblasts migrate in, proliferate and start to produce collagen.
Blood vessels for,
-> granulation tissue.
HEALING BY FIRST INTENTION- EARLY WEEKS
Continued collagen accumulation.
Fibroblasts start to reduce in number.
Decreased leukocytes/oedema/vascularity.
Blanching seen due to increased collagen and decreased vascularity.
Epidermis should be intact/closed when sutures are removed (10 days)
Some inflammation round sutures is normal, but should not be excessive- few/no inflammatory cells should be present.
HEALING BY FIRST INTENTION- MONTHS TO YEAR.
SCAR- Dense connective tissue, covered by an essentially normal epidermis.
Gradually increases in strength.
Dermal appendages are permanently lost (eg. hair follicles)
HEALING BY SECOND INTENTION
Seen in most natural wounds, as MORE TISSUE IS LOST.
eg. Abscesses, ulcers, larger wounds.
More intense inflammation.
Abundant development of granulation tissue.
Wound contracts by action of myofibroblasts.
Large defect in epithelium and underlying tissue.
Blood clots, necrotic slough and acute inflammation.
RAPID PROLIFERATION OF GRANULATION TISSUE lasts for 1-2 weeks.
-Slough and scab
-Epidermal proliferation
-Vascular granulation zone
-Zone of hyperaemia- may persist for some time.
GRANULATION TISSUE MATURATION AND WOUND CONTRACTION- 3-6 weeks.
- Epithelial proliferation across granulation tissue surface by before gradual shedding of scab.
- Granulation tissue begins to contract, bringing edges of wound closer together.
- Hyperaemia.
Forms a larger, fibrous scar (cf. the linear fibrous scar seen in first intention)
Puckering caused by wound contraction.
Dermal appendages are again permanently lost.
WOUND CONTRACTION
Large defects should be reduced to 5-105 of original size within 6 weeks.
Due to MYOFIBROBLASTS contracting the wound.
These modified fibroblasts have some of the features of smooth muscle contractile cells eg. Actin filaments.
CORNEAL ULCERS
Cornea has very regular stroma; mostly collagenous with no blood vessels.
Mild, persistent irritation will cause CUTANEOUS METAPLASIA- becomes skin.
Rapid and/or severe injury will cause ULCERATION.
MILD CORNEAL ULCERATION
Hyperplastic epithelium- rete pegs are seen.
Hyperpigmentation.
Stromal scarring.
SHALLOW CORNEAL ULCERS
Caused by injury that is too rapid/severe for metaplasia to occur.
Necrosis seen, usually results in ulceration.
IMMEDIATE oedema seen due to absorption of tear film through ulcerated corneal surface.
This allows neutrophil absorption.
Epithelial cells flatten and slide across the ulcer surface.
DEEP CORNEAL ULCERS
Oedema (tear film absorption- neutrophils)
Neutrophilic inflammation
Neutrophil mediated stromal (CT) lysis.
Fibroblasts and blood vessels grow in from limbus (edge of cornea) at 1mm day. This is normal! Allows repair of stroma.
Epithelial regeneration follows stromal rebuilding.
Very susceptible to opportunistic infection.
Specific lamellar stucture is never replicated on regeneration.
Corneal clarity is permanently impaired.
WOUND HEALING- HORSES VS PONIES
Pony wounds heal more favourably and cost less to treat.
Inflammatory phase is faster and more intense.
Granulation tissue is formed, but WOUND CONTRACTION has a great contribution to wound healing.
Epithelialisation contributes less to contraction.
Horse wounds show weaker but persistent inflammation. There is lower initial production of inflammatory mediators.
Granulation tissue formation is fast, excessive and persistent, due to prolonged inflammatory response.
More extensive scar formation is seen, as epithelialisation is the main method of wound closure.
Differences in wound healing between horses and ponies are more obvious in LIMB wounds than body wounds.
