9.5 Skin Ageing, Wound Healing & Scar Formation

9.5 Skin Ageing, Wound Healing & Scar Formation

CIDESCO Exam Tip: The written paper draws on skin structure and how that structure changes over time and after injury. Be able to separate intrinsic from extrinsic ageing by cause and clinical sign, recite the four phases of wound healing in order with their approximate timings, and distinguish a hypertrophic scar from a keloid.

Every aesthetic treatment a therapist performs is applied to skin that is either ageing, healing, or both. Chemical peels, microdermabrasion, extractions and electrical epilation all create controlled injury and then rely on the client's repair mechanisms. Understanding the biology of ageing and repair is therefore what separates a safe treatment plan from one that causes scarring or pigmentation damage.

Intrinsic (Chronological) Ageing

Intrinsic ageing is the genetically programmed decline that occurs in all skin regardless of sun exposure. It is best observed on habitually covered sites such as the inner upper arm or buttock, where the skin becomes thin, dry, finely wrinkled and lax, but retains an even colour.

A second internal mechanism is glycation: circulating glucose binds non-enzymatically to dermal collagen, forming advanced glycation end-products (AGEs) that cross-link fibres and make them stiff, brittle and yellowed.

Extrinsic Ageing (Photo-Ageing & Environmental Damage)

Extrinsic ageing is superimposed damage from the external environment and accounts for the majority of visible facial ageing. Ultraviolet radiation is the dominant driver.

• UVA (315-400 nm) penetrates to the reticular dermis. It generates reactive oxygen species that upregulate matrix metalloproteinases (MMP-1 collagenase, MMP-3, MMP-9), which cleave existing collagen while simultaneously suppressing new pro-collagen synthesis. The net result is progressive dermal matrix loss.
• UVB (280-315 nm) is absorbed mainly in the epidermis, where it forms thymine dimers in keratinocyte DNA, stimulates melanogenesis and causes erythema and sunburn. It is the principal contributor to cutaneous carcinogenesis.
• Solar elastosis is the histological hallmark of photo-ageing: masses of degraded, disordered elastotic material replace normal dermal architecture, producing the thickened, leathery, yellowed appearance seen at Glogau Type III-IV.
• Other extrinsic factors: cigarette smoke (vasoconstriction plus MMP induction), atmospheric particulate pollution, infrared-A heat exposure, poor nutrition, alcohol and chronic sleep deprivation.

The Four Phases of Cutaneous Wound Healing

When the epidermis and dermis are breached by extraction, an electrolysis probe, a lancet or a deep peel, repair follows four overlapping phases.

  HAEMOSTASIS      INFLAMMATION       PROLIFERATION        REMODELLING
  (0-10 min)       (0-4 days)         (day 3 - week 3)     (week 3 - 2 years)
  vasoconstriction  neutrophils then   fibroblasts,         Type III collagen
  platelet plug     macrophages;       Type III collagen,   converts to Type I;
  fibrin clot       phagocytosis       angiogenesis,        fibres realign;
                    of debris          re-epithelialisation strength ~80% max

1. Haemostasis: Immediate reflex vasoconstriction limits blood loss. Platelets aggregate and degranulate, releasing growth factors (PDGF, TGF-beta). The coagulation cascade converts fibrinogen to fibrin, forming a clot that acts as a provisional scaffold.
2. Inflammation (days 0-4): Vasodilation and increased capillary permeability produce the four cardinal signs - redness, heat, swelling and pain. Neutrophils arrive first to destroy bacteria; macrophages follow from about 48 hours, clearing debris and releasing the growth factors that trigger the next phase.
3. Proliferation (day 3 to week 3): Fibroblasts migrate into the clot and lay down Type III collagen and ground substance. New capillaries sprout (angiogenesis), producing red, granular granulation tissue. Keratinocytes migrate from the wound edges and from hair follicle stem cells to restore an intact epidermis (re-epithelialisation), and myofibroblasts draw the wound margins together (contraction).
4. Remodelling / maturation (week 3 to 2 years): Type III collagen is progressively replaced by stronger Type I collagen, fibres realign along lines of mechanical stress, and excess capillaries regress so the scar fades from red to pale. Even a fully matured scar recovers only about 80% of the tensile strength of uninjured skin.

Factors That Delay Healing

Advanced age, uncontrolled diabetes mellitus, smoking, systemic corticosteroids, chemotherapy, protein malnutrition, deficiency of vitamin C or zinc, poor local blood supply, wound tension, repeated trauma and bacterial infection all prolong repair. Several of these are the same conditions listed as electrotherapy contraindications, which is not a coincidence.

Scar Classification & Post-Inflammatory Change

• Atrophic scars: Depressed, caused by loss of dermal tissue. Acne subtypes are ice-pick (narrow, deep), boxcar (wide, sharp-edged) and rolling (broad, tethered by fibrous bands).
• Hypertrophic scars: Raised, red, firm, but confined within the original wound boundary. They often flatten spontaneously over 12-18 months.
• Keloid scars: Raised nodular overgrowth that extends beyond the original wound margins and does not regress. Strongly associated with Fitzpatrick phototypes V-VI, and with the earlobe, sternum, shoulder and jawline.
• Post-inflammatory hyperpigmentation (PIH): Melanin deposition following inflammation, most common in phototypes IV-VI.
• Post-inflammatory erythema (PIE): Persistent capillary dilation after inflammation, more common in phototypes I-III.

Practical Rules for the Therapist

• Never treat over a wound that has not fully re-epithelialised. Waxing, abrasive exfoliation, brush cleansing and electrotherapy are all withheld until the epidermis is intact.
• Fresh scar tissue is treated as a local contraindication for at least 6 months, and only with medical clearance where the scar overlies a surgical site.
• Broad-spectrum SPF 30-50 daily for at least 3-6 months after any controlled injury is the single most effective measure against PIH.
• A client with a personal or family history of keloids should not receive aggressive exfoliation, electrical epilation or extraction over keloid-prone sites.
• Support healing nutritionally: adequate protein, vitamin C for prolyl and lysyl hydroxylase activity, zinc for matrix metalloproteinase regulation.