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W OU ND HE ALI NG
1. 2. 3. 4. 5. 6. 7. INTRODUCTION HEALING BY FIRST INTENTION (WOUNDS WITH OPPOSED EDGES) HEAIING BY SECOND INTENTION (WOUNDS WITH SEPARATED EDGES) WOUND STRENGTH LOCAI AND SYSTEMIC FACTORS THAT INFLUENCE WOUND HEALING PATHOLOGIC ASPECTS OF WOUND REPAIR HEALING FOLLOWING PERIODONTAL THERAPY
a). HEALING FOLLOWING SCALING & ROOT PLANING b) HEALING FOLLOWING Curettage c) HEALING FOLLOWING FLAP SURGERY d) HEALING FOLLOWING OSSEOUS RESECTION e) STAGES OF HEALING OF IMPLANTS 8. SUMMARY
WOUND HEALING INTRODUCTI
Wound healing is a complex but orderly phenomenon involving a number of processes: 1. Induction of an acute inflammatory process by the initial injury 2. Regeneration of parenchymal cells 3. Migration and proliferation of both parenchymal and connective tissue cells 4. Synthesis of ECM proteins 5. Remodeling of connective tissue and parenchymal components 6. Collagenizaton and acquisition of wound strength .
Healing by First Intention (Wounds With Opposed Edges)
1. The least complicated example of wound repair is the healing of a clean, uninfected surgical incision approximated by surgical sutures 2. The incision causes death of a limited number of epithelial cells and connective tissue cells as well as disruption of epithelial Basement Membrane continuity. 3. The narrow incisional space immediately fills with clotted blood containing fibrin and blood cells, dehydration of the surface clot forms the well- known scab that covers the wound. 4. a) Within 24 hours, neutrophils appear at the margins of the incision, moving toward the flbnn clot. b)The epidermis at its cut edges thickens as a result of mitotic activity of basal cells, and within 24 to 48 hours, spurs of epithelial cells from the edges both migrate and grow along the cut margins of the dermis, depositing BM components as they move. c) They fuse in the midline beneath the surface scab, thus producing a continuous but thin epithelial layer. 5. By day 3, the neutrophils have been largely replaced by macrophages. Granulation tissue progressively invades the incision space. Collagen fibers are now present in the margins of incision, but at first these are vertically oriented and do not bridge the incision.
Epithelial cell proliferation continues, thickening the epidermal covering layer. 6. By day 5, The incisional space is filled with granulation tissue. b)Neovascularization is maximal. c) Collagen fibrils become more abundant and begin to bridge the incision. d)The epidermis recovers its normal thickness, and differentiation of surface cells yields a mature epidermal architecture with surface keratinization.
7. During the second week, a) There Is Continued Accumulation Of Collagen And Proliferation Of Fibroblasts. b) The leukocytic infiltrate, edema, and increased vascularity have largely disappeared. At this time, the long process of blanching begins, accomplished by the increased accumulation of collagen within the incisional scar, accompanied by regression of vascular channels. c) By the end of the first month, the scar comprises a cellular connective tissue devoid of inflammatory infiltrate, covered now by intact epidermis. d)The dermal appendages that have been destroyed in the line of the incision are permanently lost. e) Tensile strength of the wound increases thereafter, but it may take months for wounded area to obtain maximal strength. Although most skin lesions heal efficiently, the end product may not functionally perfect. Epidermal appendages do not regenerate and there remains a dense
connective tissue scar in place of the mechanically efficient meshwork of collagen in unwounded dermis.
HeaIing by Second Intention (Wounds With Separated Edges)
When there is more extensive loss of cells and tissue, as occurs in infarction, inflammatory ulceration, abscess formation and surface wounds that create large defects, the reperative process is more complicated .The common denominator in all these situations is a large tissue defect that must be filled. Regeneration of parenchymal cells cannot completely reconstitute the original architecture. Abundant granulation tissue grows in from the margins to complete the repair. This form of healing is red to as secondary union or healing by second intention. Secondary healing differs from primary healing in several respects:
large tissue defects initially have more fibrin d more necrotic debris and exudate that must be removed. Consequently the inflammatory reaction is more intense. Much larger amounts of granulation tissue are formed, when a large defect occurs in deeper tissues, such as in viscous , granulation tissue with its numerous scavenger white cells bears the full responsibility for its closure because drainage to the surface cannot occur. Perhaps the feature that most clearly differentiates primary from secondary healing is the phenomenon of wound contraction, which occurs in large surface wounds. Contraction has been ascribed, at least in part, to the
presence of myofibroblasts, altered fibroblasts that have the ultrastrucrural characteristics of smooth muscle cells. Whether a wound heals by primary or secondary intention is determined by the nature of the wound, rather than by healing process itself
When sutures are removed , usually at the end of the first week, wound srength is approximately 10% of the strength of Unwounded skin, but it increases rapidly over the next 4 weeks. This rate of increase then slows at approximately third month after the original incision and then reaches plateau at about 70 to 80% of the tensile strength of unwounded skin, which may persist for life. The recovery of tensile strength results from increased collagen synthesis exceeding collagen degradation during the first 2 months and from structural modifications of collagen fibers (cross- linking, increased fiber size).
LocaI and Systemic Factors That Influence Wound Healing
SYSTEMIC FACTORS INCLUDE THE FOLLOWING:
has profound effects on wound healing rrotein deficiency, for example, and particularly vitamin C deficiency inhibit collagen synthesis and retard healing. METABOLIC status can change wound healing. Diabetes mellitus, for example, is associated with delayed healing. CIRCULATORY status can regulate wound healing. Inadequate blood supply usually caused by arteriosclerosis or venous abnormalities that retard venous drainage also impair healing. HORMONES, such as glucocorticoids, have well-documented anti-inflammatory effects that influence various components of inflammation and fibroplasia; additionally, these agents inhibit collagen synthesis. LOCAL FACTORS THAT INFLUCENCE HEALING INCLUDE THE FOLLOWING:
is the single most important cause of delay in healing. MECHANICAL FACTORS, such as early motion of wounds,
delay healing. FOREIGN BODIES, such as unnecessary sutures or fragments of steel, glass, or even bone, constitute impediments to healing. SIZE, LOCATION, AND TYPE OF WOUND INFLUENCE HEALING. Wounds in richly vascularized areas, such as the face, heal faster than those in poorly vascularized ones, such as the foot. As we have discussed, small injuries produced intentionally heal faster than larger ones caused by blunt trauma.
Pathologic Aspects of Wound Repair
Complications in wound healing can arise from abnormalities in any of the basic repair processes. These aberrations can be grouped into three general categories: (1) deficient scar formation, (2) excessive formation of the repair components, and (3) formation of contractures. Examples of each of these types of healing abnormalities are : 1. Dehiscence or rupture of a wound is most common after abdominal surgery and is due to increased abdominal pressure. This mechanical stress on the abdominal wound can be generated by vomiting, coughing, or ileus. 2. Wounds can ulcerate because of inadequate vascularization during healing. For example, lower extremity wounds in individuals with atherosclerotic peripheral vascular disease typically ulcerate
3. Non-healing wounds also form in areas devoid of sensation. These neuropathic ulcers are occasionally seen in patients with diabetic peripheral neuropathy
4. Excessive formation of the components of the repair process can also complicate wound healing. 5. Aberrations of growth may occur even in what may begin initially as normal wound healing. The accumulation of excessive amounts of collagen may give rise to a raised tumorous scar known as a KELOID, or hypertrophic scar . 6. Another deviation in wound healing is the formation of excessive amounts of granulation tissue, which protrudes above the level of the surrounding skin and in fact blocks reepithelialization. This has been called EXUBERANT GRANULATION (or PROUD FLESH). 7. Contraction in the size of a wound is an important part in the normal healing process. An exaggeration of this process is called a CONTRACTURE and results in deformities of the wound and the surrounding tissues.
HEALING FOLLOWING PERIODONTAL THERAPY 1.HEALING FOLLOWING
SCALING & ROOT PLANING
Immediately after Scaling of Teeth the epithelial attachment will be severed & junctional & crevicular epithelium Partially removed. Numerous polymorphonuclear leucocytes can be seen between residual epithelial cells & crevicular surface in about 2 hrs. There is dilation of blood vessels, oedema & necrosis in the lateral wall of the pocket. The remaining epithelial cells show very little premitotic activity at that time. 24 hrs. After scaling a widespread & intense labeling of the cells have been observed, in all areas of the remaining epithelium& in 2 days the entire epithelium is covered by epithelium. In 4-5 days a new epithelial attachment may appear at bottom of sulcus. Depending on the severity of inflammation & the depth of the gingival crevice, complete epithelial healing occurs in 1-2 weeks. Immature collagen fibers occur within 21 days. Following scaling, root planning & curettage procedure healing occurs with the formation of a long, thin junctional epithelium with no connective attachment.
2. HEALING FOLLOWING CURETTAGE A blood clot forms between the root surface & the lateral wall of the pocket, soon after the curettage. Large number of polymorphonuclear leucocytes appear in the area shortly after the procedure.This is followed by rapid proliferation of granulation tissue. Epithelial cells proliferate along the sulcus. Epitheliasation of the inner surface of the lateral wall is completed in 2-7 days. The junctional epithelium is also formed in about 5 days.Healing results in the formation of a long junctional epithelium adherent to the root surface.
3. HEALING FOLLOWING FLAP SURGERY Immediately after suturing of the flap against tooth surface a clot forms between the 2 tissues. The clot consists of fibrin reticulum with many polymorphonuclear leukocytes, erythrocytes & remnants of injured clots. At edge of flap numerous capillaries are seen. 1-3days after surgery space between flap & tooth surface & bone appears reduced & the epithelial cells along border of the flap start migrating. By 1 week after surgery, epithelial cells have migrated & established an attachment to root surface by means of hemidesmosomes. The blood clot is replaced by granulation tissue proliferating from the gingival connective tissue, alveolar bone 7 periodontal ligament. By 2nd week collagen fibers begins to appear. Collagen fibers gets arranged parallel to root surface rather than at right angles. The attachment between soft tissue & tooth surface is weak. By end of one month following surgery the epithelial attachment is well formed& the gingival crevice is also well epithealised. The long junctional epithelium forms the attachment of soft tissues to root surface.
In cases where MUCOPERIOSTEAL FLAP has been reflected, superficial bone necrosis have been observed during first 3 days. Osteoclastic Resorption occurs in that areawhich reaches its peak at 4-6 days. Osteoblastic Remodelling occurs subsequently. Loss of alveolar bone height by about 1 mm may be expected after healing. 4. HEALING FOLLOWING OSSEOUS RESECTION Osseous surgery initiates a inflammatory response. Elevation of Mucoperiosteal Flap results in temporary loss of nutrient supply to the bone.In additition surgical resection of bone also contributes to inflammatory changes. Necrosis of the alveolar crest & osteoclastic resorption of the bone takes place initially. The osteoclastic resorption is followed by bone deposition & remodeling. The initial loss in bone height is compensated to some extent by the repair and remodeling. Thus final loss in bone height is clinically insignificant. Osteoblastic activity is even seen after 1 yr. post-operatively. As mucoperiosteum is sutured back on to alveolar process the osteoclastic activity doesn’t lasts for long.
5. STAGES OF HEALING OF IMPLANTS a. Wooven Bone Formation: When bone matrix is exposed to extra-cellular fluid, non-collagenous proteins & growth factors are
set free & initiate repair. Wooven bone is first formed & bridge a gap within a few days. Wooven bone formation dominates the first 4-6 weeks. b. Lamellar Bone Formation : From 2nd month post-operatively the microscopic structure of bone changes to lamellar or parallel fibered bone. c. Bone Remodelling : It begins around 3rd month post-operatively. Initially rapid remodeling occurs which slows down & continues for rest of the life.
The healing wound, as a prototype of tissue repair, is a dynamic and changing process .The early phase is one of inflammation, followed by a stage of fibroplasia, followed by tissue remodeling and scarring. Different mechanisms occurring at different times trigger the release of chemical signals that modulate the orderly migration, proliferation, and differentiation of cells and the synthesis and degradation of ECM proteins. These proteins, in turn, directly affect cellular events and modulate cell responsiveness to soluble growth factors. The magic behind the seemingly precise orchestration of these events under normal conditions remains beyond our grasp but almost certainly lies in the regulation of specific soluble mediators and their receptors on particular cells; cellmatrix interactions; and a controlling effect of physical factors, including forces generated by changes
1. PATHOLOGIC BASIS OF DISEASES 2. WILLIAM F GANGING, REVIEW OF MEDICAL PHYSIOLOGY 3. NEWMAN, TAKEI, FERMIN, A. CARRANZA 4. GYTON, TEXTBOOK OF PHYSIOLOGY
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