Regeneration and Repair Mechanisms

The skin has various regeneration and repair mechanisms. These are employed to eliminate any damage caused by external influences and to restore lost function.

Reactions of the horny layer
The action of external mechanical, physical or chemical irritants causes the horny layer to thicken. Typical examples are the thickening found after intensive UV radiation and the formation of calluses on areas subject to mechanical stress (palms of the hands and soles of the feet).

Regeneration following UV-related damage
Intense UV-exposure causes primary damage to the genetic material. Secondary damage is inflicted on the cell proteins and membranes by UV-induced free radicals. The skin has many mechanisms to repair damaged DNA. In humans, the most important are the excision repair and post-replication repair mechanisms: The excision repair mechanism is based on recognition, removal and replacement of the damaged DNA segment. This way mutations are prevented as long as the repair mechanism is not overburdened or defective. The post-replication repair mechanism, on the other hand, works around the damaged DNA segment, meaning that it is ignored when the genetic code is read. Only later is the damage repaired. This mechanism is so faulty however, that often more mutations are caused by the repair than by the original radiation damage.

Chemically-induced calluses can ensue from repeated bathing with lipid-dissolving solvents and water.

Regeneration following skin injury
The layer of epidermal mother cells - the basal layer - ensures a steady renewal of the epidermis, through continual cell division (proliferation). If an injury is confined to the uppermost skin layer, this damage, known as erosion, can heal without scarring. If the damage reaches the dermis (e.g. an ulcer) and thus involves the basal membrane, then healing is usually accompanied by scar formation. In this case destroyed skin cells are replaced by connective tissue. Wound-healing follows in several consecutive stages: in the first phase coagulating blood forms a membrane with a hard surface that adheres to the wound (crust). In the following skin cleansing stage, autolysis and phagocytosis of the damaged and dying cells takes place. In parallel connective tissue fibres are dissolved by enzymes. Mobile immune cells and phagocytes become active and lymphatic fluids flow into the wound.

In the building or proliferation phase, epithelization of the wound base occurs, including the formation of capillary buds, new connective tissue and collagen fibres. Cell division during the proliferation phase can be stimulated and supported by the application of topicals such as dexpanthenol which allows for better and faster healing.

Autolysis is the destruction of dead or dying cells by lysosomal enzymes produced by the cells themselves. Phagocytosis is the active ingestion of particles by phagocytes.