Wound healing

Moderator Dr. Tewodros T; consultant(OCMFS)

Presenter; Dr. Alelign A.( R-I)
 contents

• Introduction
• The Healing process
• Wound healing stages
• Wound healing complications
• Phases of healing and complications in specialized tissue
• Factors in suboptimal wound healing
• Take home message
• Reference

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 Learning Objectives

 At the end of this presentation, we are expected to know

 Process of wound healing in cutaneous tissue and specialized
tissues
 Complications of wound healing
 Factors affecting wound healing

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 Introduction to wound healing

• A wound is a disruption in the normal anatomic structure and function

of tissue and is accompanied by cellular damage.
• Healing is sequence of cellular and biochemical responses directed
toward restoring tissue integrity and functional capacity following
injury.

• The process by which healing occurs in a tissue is dependent on several

factors – Type of cell , extent of injury etc.
 There are 3 pathways of healing; primary intention, second intention &
by tertiary intention

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 Acute wound

 Acute wounds have surgical, traumatic, pathologic, or ischemic causes.

 Other mechanisms of traumatic y include tissue exposure to extremes
of temperature, radiation, or caustic chemicals that cause injury by
ltering tissue pH, denaturing proteins, and causing local ischemia.
 Pathologies( neoplasms and nonhealing ulcers.

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 Chronic wound

 Local factors impairing wound healing include the presence of foreign

bodies or necrotic tissue within the wound, a high microbial burden,
ischemia secondary to venous or arterial insufficiency and tissue
hypoxia secondary to radiation fibrosis.

 Some systemic factors aging, malnutrition, vitamin deficiencies,

diabetes, immunocompromised states, atherosclerosis, peripheral artery
disease, collagen vascular disease, and chemotherapy

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 The Healing Process

• Normal tissue healing-repair

• The healing response depends primarily on the type of tissue involved

and the nature of the tissue disruption.
• At cellular level it depends on labile, stable, or permanent cells
• At macro level; primary, secondary, teritiary

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 ...

 patterns of biochemical and cellular events ie, the healing continuum of

coagulation, inflammation, reepithelialization, granulation tissue, and
matrix and tissue remodeling is typically broken down into three distinct
overlapping phases:
 Inflammatory(reactive)
 Proliferative(regenerative or repair)
 Remodeling(scarring, contraction,

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 Phases of cutaneous wound healing

Phases of repair pic

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 1. Inflammatory phase

 lasts for 3–5 days.

 Sequence of events of Vasoconstriction to achieve clot form
 followed by persistent vasodilation mediated by histamine,
prostaglandins,kinins, and leukotrienes and diapedesis blood cells
 Neutrophils, monocytes & macrophages various roles continue

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 2. Proliferative phase(3rd day-3wk)

 distinguishing pink granular tissue formation by inflammatory cells &

capillary angiogenesis secondary to wound hypoxia & native growth
factors, particularly VEGF, fibroblast growth factor 2 (FGF-2), and TNF-
β
 The fibroblasts start synthesizing new extracellular matrix (ECM) and
immature collagen (Type III)
 Collagen deposition rapidly increases the tensile strength of the wound
and decreases the reliance on suture material to hold the wound edges
together.
 At surface of wound reepithelialization which is facilitated by underlying
contractile connective tissue, which shrinks in size to draw the wound
margins toward one another.

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 3. Remodeling phase(6th month- yrs)

• Involves choreographed balance between matrix degradation and

formation regulated to a large extent by serine proteases and matrix
metalloproteinases (MMPs) under the control of the regulatory
cytokines and tissue inhibitors

• Capillary angiogenesis regress, fibroblast disappear, collagen Type III

deposited during the granulation phase is gradually replaced by
stronger Type I collagen increasing about 80% of original tensile
strength

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 Complications of cutaneous wound healing

1. Proliferative scaring
 All proliferative scaring are characterized by hyper-vascularity and
hyper-cellularity, Excessive scarring, persistent inflammation, and an
overproduction of ECM glycosaminoglycans and collagen Type I
 Cause apoptotic dysregulation
 sustained elevation of growth factors including TGF-β, platelet-derived
growth factor, IL-1, and IGF-I

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 ...

 3types a)Hypertrophic scar b)Keloid formation c)Exuberant granulation,

 Hypertrophic scar
 Arise shortly after injury & eventually recede.
 It is raised, erythematous, and remains within the boundaries of the
original trauma or wound.
 A keloid, on the other hand, manifest months after the injury, grow
beyond the wound boundaries, and rarely subside and is more nodular.

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 Cont…

 Wound dehiscence or ulcers

 Infection(signs of erythema, warmth, swelling,pain, and accompanying
odor and pus &>100,000bacteria/gm
 Rarely – neoplasia may develop Squamous cell carcinoma following
burns
 Incisional hernia
 Excessive contraction Formation of contractures
 Implantation cyst

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 Specialized tissue healing

 1.Bone
 2.GIT
 3.Nervous system
 4.Liver
 5.Kidney
 6.Muscle

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 WOUND REPAIR IN OTHER TISSUES OF
THE HEAD AND NECK

NORMAL BONE HEALING (REPAIR)

1. Procallous formation
2. Osseous callous formation
3. Remodeling
1) Procalus formation • Haematoma forms at the site of fracture • Fibrin clot
forms the framework • Local inflammatory response- PMN ,
macrophages • In growth of granulation tissue • Callus formed of
woven bone forms ( fusiform shape)

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 Bone healing

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 Complications in bone healing

• Mal union,
• nonunion,
• infections,
• osteomyelitis,

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 Tooth Extraction socket healing

Tooth extraction site healing by secondary intention

Involves, clot formation, osteoblast & osteoclast activity and full
reepi5heliazation completed in 4th week & bone remodeling up to 6
months

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 cartilage

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 Factors in suboptimal Wound Healing

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 …

 Immune compromise; lymphpcyte1200-1800, and levels below 800 are

considered severe total lymphocyte deficits.
 Radiation
 Age
 Nutrition
 Growth factors; exogenous growth factors, such as PGDF, angiogenesis
factor, epidermal growth factor (EGF), TGF, basic fibroblast growth
factor (bFGF), and IL-1, directly to the wound, recombinant human
platelet-derived growth factor-BB [rhPDGF]; Regranex, 0.01% gel
applied to wound
 Dermal and Mucosal Substitutes

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 nutrition

• Nutritional deficiencies severe enough to lower serum albumin to <2

g/dL are associated with a prolonged inflammatory phase, decreased
fibroplasia, and impaired neovascularization, collagen synthesis, and
wound remodeling.
• Serum prealbumin has shorter half-life & hence indicative.
• Normal serum prealbumin is about 22.5 mg/dL, a level below
17 mg/dL is considered a mild deficit, and a severe deficit would be
below 11 mg/dL.

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 TRAUMA-, STRESS-, AND SEPSIS-INDUCED MALNUTRITION
PHYSIOLOGY

Hypermetabolic
Characteristic Fasting Starvation
Catabolism

Neuroendocrine activation - +

Resting energy expenditure - ++

Protein catabolism + +++

Protein anabolism

Total body - -

Hepatic + +++

Amino acid oxidation + +++

Ureagenesis + +++

Gluconeogenesis + +++

Ketone production ++++ +

Malnutrition development
+ +++
rate

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 Carbohydrate requirement

• In fasting starvation nutritional support; carbohydrate 5mg/kg/min,10%

of energy source fat, body spares aminoacids
• In hypermetabolic starvation metabolic support; carbohydrate(resting
energy expenditure,high glucose prodn & utilization), 30% of energy
source fat, body spares amino acids

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 Protein requirement

• daily protein losses approximate 20 to 30 g/day.

• In a critically ill patient in a hypermetabolic state, the protein losses are
greater.
• The net losses can be 1% of the total body protein each day.
Therefore, daily protein supplementation should be 1.5 to 2.0 g/kg of
ideal body weight

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 ELECTROLYTE REQUIREMENTS

 The phosphorus-dependent metabolic pathways are numerous.

 The clinician should be aware that refeeding will cause shifts of the
already depleted electrolytes (phosphorus, magnesium, and potassium)
intracellularly, and thus must be monitored closely to avoid
cardiovascular complications.

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 Vitamins

Vitamin A deficiency impairs B cell and T cell function and antibody

production during the inflammatory phase.
Vitamin A supplementation counteracts the delay in wound healing caused
by corticosteroids for the treatment of inflammatory diseases
Decrease epitheliazation, collagen synthesis, and granulation tissue
development
Vitamin B deficiencies impairing antibody production and white blood cell
function, which in turn increase the risk of infectious complications

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 ...

Vitamin C – have role in cell migration, collagen synthesis, antioxidant

response and angiogenesis.
Forms extra bound between collagen fibers that increase stability and
strength of collagen matrix
Vitamin D and its receptor (i.e., VDR)—which is ubiquitously expressed in
several tissues—modulate structural integrity and transport across
epithelial barriers

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 Vitamin D deficiency among venous and pressure ulcer patients has
suggested the potential involvement of vitamin D in the wound healing
process
Vitamin E might negatively affect collagen synthesis, antioxidant response,
and the inflammatory phase

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 Minerals

Zinc is essential for DNA replication in cells with high cell division rates,
such as inflammatory and epithelial cells, and fibroblasts
Zinc promotes immune response
Activates lymphocytes and producing antibodies

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 Take home message

 Wound healing is an intricate, tightly choreographed continuum of

overlapping inflammatory, proliferative, and remodeling phases.
 With distinctive variations, all tissues including skin, bone, and nerve
underdo similar pathways to tissue repair or regeneration.
 Many local and general factors can affect wound healing, and an
improved understanding of modifiable risk factors will help the surgeon
optimize the healing process and outcomes.

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 References

1. Raymond J Fonseca, oral & maxillofacial trauma 4th ed, Elsevier

2. Peterson's principle of oral & maxillofacial surgery 4th ed, Elsevier

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