Wound Healing

Wound Healing

Steven Engebretson

Department of Periodontology and Implant Dentistry, New York University College of Dentistry, New York, NY, USA

Definitions and Terms for Clinical Outcomes

Repair is defined as healing of a wound by tissue that does not fully restore the architecture or the function of the part. Reattachment means to attach again such as the reunion of epithelial and connective tissues (CT) with root surfaces and bone such as occurs after an incision or injury. New attachment is the union of CT or epithelium with a root surface that has been deprived of its original attachment apparatus. This new attachment may be epithelial adhesion and/or CT adaptation or attachment and may include new cementum. Regeneration is the reproduction or reconstitution of a lost or injured part. Guided tissue regeneration refers to procedures aimed at regeneration of lost periodontal structures by guiding differential tissue responses using barrier materials such as expanded‐polytetrafluoroethylene, polyglactin, polylactic acid, titanium mesh, or collagen to exclude epithelium from the root surface.

Inflammatory Phase

When a surgical wound is created bleeding occurs, the cascade of events leading to hemostasis is initiated and a clot is formed. Collagen attracts platelets to the wound site and a platelet plug is formed, creating a fibrin matrix, providing the basis for tissue repair. Neutrophils are the first immune cells recruited to the wound in response to the activation of complement, the degranulation of platelets and the products of bacterial degradation. Polymorphonuclear leukocyte (PMN) or the “poly band” reaches peak activity 24–48 hours followed by the influx of monocytes, which act to debride the site of bacteria and necrotic tissue. Platelets release growth factors and cytokines and regulate subsequent healing. Platelet‐derived growth factor (PDGF) stimulates chemotaxis of neutrophils and macrophages in the wound site as well as chemotaxis and mitogenesis of fibroblasts and stimulates collagen synthesis. Transforming growth factor beta (TGF‐β) is a key modulator of wound healing and is chemotactic for macrophages, fibroblasts, and smooth muscle cells and stimulate collagen synthesis, while modulating collagenase and tissue inhibitor of metalloproteinases (TIMPS). After two to three days monocytes differentiate into macrophage and secrete factors that stimulate angiogenesis and fibroblast proliferation that promotes the proliferative phase.

During the inflammatory stage flap tensile strength is still weak, as fibrin holds the flap in place (Hiatt et al. 1968). Following hemostasis, vasodilation of tissues adjacent to the wound, mediated by histamine, prostaglandins, kinins, and leukotrienes result in vascular permeability allowing blood plasma and white blood cells to permeate via diapedesis to the extravascular space. The classical signs of inflammation are thus observed: swelling (tumor), redness (rubor), heat (calor), and pain (dolor).

Proliferative Phase

The cytokines and growth factors secreted during the inflammatory phase stimulate the succeeding proliferative phase. The proliferation of fibroblasts from the surrounding tissue induces production of collagen and proteoglycans. Collagen production restores tissue stability and serves to support the newly formed blood vessels supplying the wound. Proteoglycans function as a reservoir of moisture essential for early wound hydration. Angiogenesis is essential for the transport of nutrients and oxygen and begins post injury and lasts up to three weeks. The proliferative phase is distinguished by the formation of granulation tissue containing macrophages, fibroblasts, and budding vasculature in a loose collagen matrix. Angiogenesis induced by vascular endothelial growth factor (VEGF) and fibroblast growth factor 2 (FGF‐2). Epithelialization is facilitated by underlying CT, which draws the wound margins together and contraction begins leading to the remodeling phase.

Remodeling Phase

During the remodeling stage the collagenous matrix is synthesized continually and broken down in an effort to achieve tissue homeostasis. Cross‐links are formed between collagen molecules and tensile strength of the wound increases. Osteoclasts ruffled borders act to resorb the bone, while osteoblasts form new bone tissue in response to mechanical stress. New haversian systems are developed as concentric layers of cortical bone are deposited along blood vessels. The bone has the capacity to undergo regeneration as part of a repair process and can heal without scarring.

Epithelium and Connective Tissue Healing

Following a procedure such as gingivectomy or gingivoplasty, an incision to the gingiva results in a clot formation followed by an infiltrate of PMN, which forms a band around the wound. The acute inflammatory response ensues (Ramfjord et al. 1966). Blockage and withdrawal of cut capillary ends occur during the first day, and by day 2 new sprouts are observed, capillary loops form by day 3–5, and anastomoses and normal vasculature are restore by day 11 (Cutright 1969

Only gold members can continue reading. Log In or Register to continue

Nov 6, 2022 | Posted by in Implantology | Comments Off on Wound Healing
Premium Wordpress Themes by UFO Themes