By D. J. Verret, MD

Skin
The skin is composed of several layers.  The outermost layer is the epidermis.  The epidermis has four cell types in it: keratinocytes, melanocytes, langerhas' cells, and merkel's cells.  These cells are organized into a consistent four layers (stratum germinativum, stratum spinosum, straum granulosum, and stratum corneum) with an additional layer (statrum lucidum) seen in the palms and soles.  Deep to the epidermis is the dermis.  At the dermal-epidermal junction is the basement membrane, anchoring fibrils, and rete ridges.  The dermis itself is composed of two layers: the papillary dermis and the reticular dermis.  The papillary dermis is composed of loose collagen, blood vessels, and fibrocytes.  The deeper reticular dermis is composed of compact collagen, larger feeding blood vessels, nerves, pilosebaceous units, appocrine units, and eccrine unites.  The edge of the skin is formed by the superficial fascial layer which houses a rich vascular network before entering into the subcutaneous tissue.

Closing wounds
Several clinical considerations must be taken into account when closing wounds, from technical factors to systemic diseases.  Care must be taken to use minimal cautery, avoid crushing skin edges with forceps, and avoid excess suture tightness.  Wound dessication should be avoided.  Using occlusive dressings can be useful and have been shown to decrease healing times, but do promote bacterial growth.  Studies have also shown that topical Neosporin and silvadene also decrease healing times without bacterial promotion.  Care must be taken though, not to use petroleum jelly or triamcinolone creams as these decrease healing times.

Infections and other complications
Obviously, care must be taken to avoid infections in wound beds.  Bacterial infection leads to direct damage of repair cell.  In addition, the bacterium will compete with the rebuilding substrate for oxygen and nutrients.  The inflammatory response produced to the bacterial insult will prolong the healing process by reversing the progress made or simply prolonging the inflammatory phase of healing.
Several systemic diseases can also lead to impairments in wound healing.  Diabetes causes microangiopathy and insulin deficiency decreases leukocyte function and collagen synthesis.  Smoking can result in wound healing impairments in many ways.  Smoking limits oxygen uptake, vasoconstriction of small vessels, impaired collagen synthesis, local thrombosis, and altered immune function.  The optimum time to stop smoking before an elective procedure has not been fully elucidated but there are several studies to suggest that patients must quit smoking more than 3 weeks before surgery in order to decrease their risk of complications.  Several other congenital syndromes can cause impairments of wound healing but are beyond the scope of this discussion.

Nutrition
Nutrition plays a vital role in wound healing as well.  Without the building blocks of protein, epidermal rebuilding cannot occur.  Several vitamins also play a crucial role in wound healing, among these are Vitamins A, C, K, and E.  Vitamin A promotes epithelialization and wound closure, increases collagen synthesis rates, and promotes cross-linking of collagen.  Vitamin C contributes to neutrophil function and the hydroxylation of lysine and proline during collagen synthesis.  Vitamin K is essential in the production of clotting factors II, VII, IX, and X - without them, hematom and bleeding are more likely.  Vitamin E increases collage production and tensile strength.
Free tissue transfers, such as skin grafts, heal differently from primary closure sites or those with axial blood supplies. 

Skin Grafts
Skin grafts heal through three phases: imbibition, revascularization, and organization.  Serum imbibition lasts for the first 48 hours and involves the graft tissue receiving its nutrition from fibrinogen free serum from dilated capillaries in the host bed.  The revascularization phase occurs primarily through neovascularization into the dermis of the transplanted tissue with minor contributions from a process known as inosculation whereby there are anastomosis between host and donor blood vessels.  Lymphatic drainage occurs during this phase by the fourth or fifth day.  The final phase, organization, begins within five hours.  This involves an initial leukocyte infiltrate which is then replaced with fibroblasts as revascularization occurs.  By the ninth day, the graft is firmly adhered to the recipient bed by new blood suppl e and fibroblast integration.  Within two months, neural structures begin to regenerate along vacated neurilemmal cell sheaths though full sensation is unlikely.