wound Healing

1. WOUND HEALING

2. Definitions • A wound is a disruption in the normal anatomic structure and function of tissue. • A cut or break in the continuity of any tissue, caused by injury or operation. • Wound healing is an intricately coordinated series of processes that involve cellular and subcellular responses to tissue injury.

3. Classification of tissues • Based on their healing capabilities, tissues are categorized as: • Labile tissues-eg,keratinocytes of epidermis • Stable Tissues-eg-bone, liver cells • Permanent tissues-eg nerve ,cardiac cells • Therefore, healing depends on: • Tissue involved • Extent of injury • Nature of injury

4. Cont. • BASED ON DURATION OF HEALING: Acute wounds- that heal in a predictable manner and time frame • with few complication. Chronic wound – No clear time frame • tissue’s normal healing process experiences a disruption,compromised or delay. • Delays usually arrest healing at the inflmmatory phase • Wounds that have failed to epithelize and close in reasonable amount of time(>3months).

5. Open and closed wound • Based on Involvement of the skin or covering tissue Closed wounds • Contusion- minor soft tissue injury • Abrasion- epidermis of the skin is scraped away • Hematoma- bleeding sufficient enough to create a localized collection in the tissue Open wounds • Laceration- the result of sharp object injury • Penetrating- stab injury • Crush • Avulsion injuries • Animal bites

6. Classification: By Etiology • Traumatic • Mechanical trauma • Thermal trauma (Burn, freezing) • Chemical trauma (Acid, Base) • Surgical (Intentional) • Infectious

7. Classification: Risk of infectionusually for traumatic wounds Tidy (Non-tetanus prone) Untidy (Tetanus prone) Crushed or avulsed Contaminated Devitalized tissues Often tissue loss Older than 6 hours Animal bites Puncture wounds deeper than 1cm • Incised • Clean • Healthy tissues • Seldom tissue loss • Younger than 6 hours • Puncture wounds which are not deeper than 1cm

8. Classification of wounds:-based on mechanism Blunt injuries- swelling in the subcutaneous or muscle Clean cut injuries- vascular response is not intense can damage important structures like nerve & arteries Avulsion injuries-vascular response is intense local damage is greater and contracture is expected. Punction injuries - dog bite, knife or needle

9. Classification by contamination(surgical wound) Clean wound:- are those produced by sterilized blades No need of Abxs &suture is enough Clean contaminated wound-No evidence of infection or major break in aseptic technique Contaminated wound:- produced by non sterilized materials in normal condition consider debridement, secondary healing,topical antiseptics & Abx Dirty wound:- wounds are clearly infected or plenty of necrotic tissue clean the wound with a saline soap soln. debridement, immediate or delayed surgery, secondary healing& proper Abx

10. Wound healing • It is a physiologic process whereby the body attempts to restore the integrity and function of the injured part • Occurs as a cellular response to tissue injury • All tissues follow similar mechanisms, even though individual tissues may have unique healing characteristics. • The tissue produce some substance, cells and structure that allow the organ to continue its physiologic work. • never be the same as the original.

11. THE HEALING PROCESS The healing response depends primarily on the type of tissue involved and the nature of the tissue disruption regeneration - restitution by means of tissue that is structurally and functionally indistinguishable from native tissue. repair - tissue integrity is reestablished primarilythrough the formation of fibrotic scar tissue.

12. Wound healing physiologic phase 1. Inflammatory Phase :- takes 3 – 5 days -the more inflammatory reaction the longer would be the scar formation.has two different reaction: Vascular reaction :- due to exposure of endothlia, collagen and bleeding -Vasoconstriction to avoid bleeding followed by vasodilatation and leakage of plasma components. -local release of histamine, bradykininand prostaglandins modulate this change while stimulate fibroblast proliferation. • coagulation cascade is activated and fibrn clot is formed.

14. Cont……………….. Cellular reaction 1) PMN -1st infiltrate cells -Peaks 24-48 hrs -Factor stimulating their migration -Role (phagocytosis of & tissue debris and cytokine release- TNF- α) 2) Macrophages - derived from monocytes - max. 48-96 hrs post injury - until wound healing complete - role…. 3) T-lymphocytes - Max 1 week post injury - Truly bridge the transition from inflammation to proliferative phase of healing.

15. 2. Proliferative Phase:- after the inflammation proliferation of substances and cells for repairing occurs(4-5days to 2-3wks). 2.1 Fibroblast phase Fibroblast cells are predominant derived from specialized stem cells in the adventitia of small blood vessels • many factors including blood oxygen stimulate them to produce procollagen which later converted to collagen 2.2 Angiogenesis stimulated by macrophages chemotactic factors, endothelial buds normally takes place at the 4th day.

16. 2.3 Epithelialization phase This is the process in which an open wound is finally covered by a layer of epithelial cells. So by itself it does not provide enough protection. There are four stages for the epithelialization to occur; cell dedeferentiation, mitosis, migration and contact inhibition. 2.4 Matrix formation:network of collagen on the wound surface primary collagen molecules will form the fibrils and fibbers that will provide the tensile strength to the scar.

17. 3. Remodeling of collagen Starts during 3rd week and lasts several months to years Final phase of wound healing Besides collagen degradation vascularization decline gradually Scar become soft, elastic & pale. The equilibrum between synthesis and degradation of collagen result in a normal scar with adequate tensile strength, size & colour. Not only accumulation of collagen but also cross linking and fibbers realignment are important for adequate tensile strength. Collagenase enzyme plays a vital role in remodeling of collagen.

18. Wound contraction • Contraction of a wound is a dynamic biologic process in which the healing area decreases in its size. • Contracture is the final result of the contraction Not always referred to a bad scar affecting the function and aesthetics of the surrounding area. • Myofibrolast cells derived from fibroblast play a vital role in wound contraction.

19. There are three types of wound healing or wound closure— • primary intention, • delayed primary closure and • secondary intention.

20. Healing by primary intention -edges of the wound are approximated by the surgical sutures. -rapid healing and minimal scarring. -It is not recommended in grossly contaminated wounds -Clean and uninfected - --Surgically incised -minimal loss of cells and tissues -Wound with opposed edges

21. DELAYED PRIMARY CLOSURE The wound edges are apposed only after a period of wound management to optimize healing. • Tissue grafts may also be used for wound closure. • The avulsive or contaminated wound is débrided and allowed to granulate and heal by second intention for 5 to 7 days. • Once adequate granulation tissue has formed and the risk of infection appears minimal, the wound is sutured to heal by first intention.

22. Healing by secondary intention • Wounds with separated edges • more extensive loss of cells and tissue. • Abundant granulation tissue grows to complete the repaire. • Inflamatory reaction is more intense • Much larger amounts of granulation tissue are formed • Wound contraction occurs in large surface wounds • Substaintal scar formation and thinning of the epidermis occurs.

23. Healing by primary intention: Healing by secondary intention Healing by tertiary intention

24. NORMAL BONE HEALING • Normal bone healing parallels soft tissue healing. • Both types undergo three phases of wound healing—inflmmation, proliferation, and remodeling. • However, bone healing also undergoes calcifiation. • A hematoma is formed within the fractured bone. • Inflmmationis stimulated by vessel injury in the haversian canals and periosteum and by the presence of bony debris or necrotic material in the fracture site.

25. The proliferative/ firoblastic stage • Pleuripotentialmesenchymal cells and firoblasts enter the site of injury to lay down fibrous tissue, cartilage, and immature bone fibers. • leaving a residual space between the two bony segments, the fracture will heal by secondary intention. • The soft cartilage callus calcifis into woven bone. • The callus as rudimentary splint, offers stability • Healing by primary intention -no cartilaginous callus is formed minimally displaced fractures a/c # reduction without a gap immobilized with rigid fixation Dental extraction sites heal by secondary intention.

26. Remodeling phase • The callus completely ossifis as osteoclasts gradually resorb the immature bone and it becomes remodeled into lamellar bone. • The gradual resorption of immature woven bone with bone formation and maturation to lamellar bone is known as creeping substitution.

27. COMPLICATIONS IN BONE HEALING • Malunion • Nonunion • Infection especially in open fracture • osteomyelitis

28. NORMAL CARTILAGE HEALING • In the maxillofacial region, cartilage is found in the articular surfaces of the TMJ and in the auricular and nasal cartilages. • Facial cartilaginous defects are generally caused by traumatic injury, infection, pathology, or chronic degeneration. • Cartilage has limited inherent capacity for self-repair 2nd to its low cellular density and minimal vascular supply. Although cartilage is a metabolically active tissue, it has no inherent vascularity or lymphatic vasculature. • A poor inflmmatory response is elicited after cartilage injury because progenitor cells from the blood or bone marrow are unable to access the damaged cartilage.

29. NORMAL NERVE HEALING • Nerve injuries can be categorized by the Seddon or Sudderland classification. • The Seddonclassifiation describes three types of nerve injury: 1,neuropraxia, 2 axonotmesis 3,neurotmesis

30. Cont……………….. • Neuropraxia/ nerve bruising - a transient interruption/block in nerve conduction. • Axonal continuity is preserved,Recovery is spontaneous but may take weeks to months. Axonotmesis-individual axons are damaged within the nerve, with the epineurium being preserved. Wallerian degeneration, the degradation of distal axons with concomitant loss of Schwann cells, occurs. • neurotmesis -Complete nerve transection + Wallerian degeneration ensues.

31. Sudderlandclassifiation The original encompassed five degrees of nerve injury. 1st degree injury/ neuropraxia 2nd degree-some nerve fibers are damaged, w/o injury to endoneurium. 3rd-degree injury- Endoneurium involve w/o perineurium damage. 4th degree injuries- Perineurial damage within an intact epineurium. 5TH degree injuries are complete nerve transections. Surgical intervention is recommended for 4th - and 5th-degreeinjuries.

32. Factors stimulating wound healing Growth hormones Hyberbaric oxygen Vitamin A,iron,cu Growth factors, Zn, arginine Factors that facilitates wound healing Slight increase in local temprature Some degree of humidity Coverage (dressing) of the wound Stability (dressing, splinting) Non aggressive antiseptics No tension on the wounds borders.

33. FACTORS IN SUBOPTIMAL WOUND HEALING • Common risk factors for poor healing in the inpatient or trauma setting are advanced age, wound infection, diabetes, smoking, and malnutrition.

34. AGING - the capacity for wound repair declines with age. • Aging results in generalized tissue thinning caused by collagen loss, as well as vascular compromise and poor perfusion. • older patients are more likely to have associated health conditions that adversely affect healing. INFECTION-is a major cause of impaired wound healing.If not properly addressed, contaminated wounds can become infected . • A high microbial burden in a wound increases the host’s inflmmatory response to the area. • bacterial infection and increased inflmmation can lead to further tissue damage.

35. Cont…………….. • Bacteria also compromise wound healing by competing with the healing tissue for nutrients and oxygen. • Infected wounds should be addressed with adequate débridement, removal of foreign bodies and necrotic tissue, and irrigation. • Infected soft tissues wounds are characterized by erythema,edema,warmth,andtenderness,leukocytosis and fever. • Fluid collections, abscesses, and hematomas should be drained to avoid bacterial growth. • Targeted antibiotic therapy should be instituted based on the risk of developing antibiotic-resistance.

36. SMOKING causes tissue hypoperfusion and hypoxia. • Nicotine reduces oxygen delivery to peripheral tissues secondary to vasoconstriction by epinephrine and norepinephrine. • Hypoxia is exacerbated by carbon monoxide binding to hemoglobin. • Nicotine also causes collagen deposition and prostacyclin formation. • It increases platelet aggregation, causes neutrophil dysfunction, and increases blood viscosity. • Prior to elective surgery, patients should be advised todiscontinue tobacco use for at least 8 weeks and shouldrefrain from smoking until wound healing is complete.

37. DIABETES • poor glucose control leads microvascular disease. • Microvascular disease adversely affects the blood supply of healing tissue. • reduced Release of oxygen to tissues. • Hyperglycemia - impairing neutrophil and lymphocyte function, chemotaxis, and phagocytosis. • poor cell recruitment and wound ischemia creates a suboptimal healing environment. • peripheral neuropathy - decreased pain sensation and are more prone to develop pressure ulcers. • Tight serum glucose level control is recommended to improve the likelihood of wound healing.

38. ImmunosuppressionI IMMUNOSUPPRESSION • medical conditions/medications may cause immunosuppression . • the hall mark of HIV /AIDS and may be seen in cancer patients and poorly controlled diabetics. • can also be encountered in older and malnourished patients • Medication-induced immunosuppression is seen in transplant recipients and in patients being treated for autoimmune and collagen vascular diseases. • Use of glucocorticosteroids can cause : delayed wound healing and susceptibility to infection. • Glucocorticoids reduce the normal inflmmatory response and adversely affect wound healing by suppressing protein synthesis and cell proliferation.

39. RADIATION AND CHEMOTHERAPY • Radiation therapy induces many deleterious effects in tissue:hypocellularity, hypovascularity, and hypoxemia. • The adverse effects of radiation are dose dependent. • Radiation therapy can have acute and chronic effects. • A/C changes in the oral region include mucositis, erythema, and desquamation. • C/C radiation changes are irreversible • Chemotherapeutic drugs inhibit wound repair, causes bone marrow suppression, with decreased production of inflmmatory cells. • Some agents target VEGF- angiogenesis.suppressing VEGF is a good target for combating neoplasia.

40. Management • Examination of the wound • Exploration & diagnosis • Debridement&irrigation • sutures • Skin grafts • Skin closure without tension • Topical&systemic Antibiotics • Dressing • Tetanus prophylaxis

41. wound management Wound care begins by optimizing the healing environment. • Wounds should not be dessicated or exposed to caustic chemicals. • wound closure should be done in a tension-free manner. • All dead space should be obliterated and vital structures covered with well-vascularized tissues. • Bone fractures should be reduced and adequately immobilized. • . Necrotic tissue and foreign bodies should be removed to decrease the bacterial burden. • Hematomas and abscesses should be drained. • Infections can be treated with systemic or topical antibiotics or by débridement of infected tissue.

42. Dressings • Dressings -maintain a moist environment that encourages faster wound resurfacing by allowing migration of epithelial cells over the moist surface and by preserving growth factors exuded at the wound surface. • Dressings can aid in the delivery of topical antimicrobialsor recombinant growth factors to the wound bed, protectthe wound from friction or shearing trauma, and collectexudate or drainage. • Can be used as a form of débridement with frequent dressing changes, especially when used in conjunction with topical agents. • Dry dressings are often not recommended because theyallow tissues to desiccate easily and form dry scabs. • Dressings can be categorized as open (e.g., no dressing withscab formation), semiopen, occlusive, semiocclusive, and biologic.

43. Cont'd Ideal dressing _ absorb and contain exudate _ doesn’t leave particulate contaminants _ provides thermal insulation _ doesn’t traumatise the wound bed when removed _ Impermeable to water & bacteria _ minimizes the frequency of dressing _ provides pain relief & comfort

44. Topical Agents • Topical agents may be benefiial as an adjunctive wound care treatment. • Some commonly used topical antimicrobials are Bacitracin zinc ointment,TTC,neomycine, cadexomeriodine,nitrofurazone and silver sulfadiazine. • They help reduce bacterial load within a wound and keep the wound moist. • topical applications may be used in conjunction with dressings for gentle wound.

45. Skin grafts • Graft _ transfer of devascularised tissue from one area to another • Often used to cover large areas • Classified as; _ full thickness _ split thickness

46. complication • Improperly handled and managed wounds can result in local and systemic complications Local:hematoma,seroma,infection,dehiscence,granuloma,scar,contracture,soft tissue maceration Deficient scar formation- wound dehiscence& ulceration excessive formation of the repaire component - hypertrophic scar & keloid Systemic:Bacteremia , sepsis and death

47. References • Fonseca, oral and maxillofacial trauma, 4th Edition • Peterson Priniciple of Oral and Maxillofacial Surgery 4th Edition.