Controlled light injury makes skin rebuild itself. Strongest gains: smoother, less wrinkled skin, improved depressed acne scars, clearance of rough sun-damaged patches. Brown-spot fading is weaker and reverses soonest. Gains hold a year or two, not permanently. In older people, treated sun-damaged skin developed fewer new skin cancers. Costs are mostly pigment change, pain, redness, herpes flare-ups and occasional scarring. (Full Review)
| Marker | Target | Why |
|---|---|---|
| Glycated haemoglobin (HbA1c) | 4.8–5.4% | High glucose slows surface regrowth and raises infection risk |
| 25-hydroxyvitamin D | 40–60 ng/mL (100–150 nmol/L) | Supports keratinocyte proliferation and barrier restoration |
| High-sensitivity C-reactive protein (hs-CRP) | Below 0.5 mg/L | Baseline inflammation predicts prolonged post-procedure redness |
| Serum ferritin | 50–125 ng/mL (women), 50–150 ng/mL (men) | Iron is a cofactor for collagen cross-linking; low stores slow closure |
| Serum zinc | 90–120 µg/dL | Zinc deficiency delays wound contraction and cell migration |
| Serum albumin | 4.2–5.0 g/dL | Indicates protein availability for new collagen deposition |
| Haemoglobin | 13.5–15.0 g/dL (women), 14.0–16.0 g/dL (men) | Low values reduce oxygen delivery to healing tissue |
| Herpes simplex virus type 1 antibody (HSV-1 IgG) | No established target; positive or negative | Identifies who carries the latent virus that thermal injury reactivates |
Cadence: Wound check at days 3–7, closure confirmation at two weeks, pigment assessment at 4–6 weeks, outcome photography at three and six months. Metabolic markers rechecked only before any subsequent session; actinic keratosis counts every 6–12 months where prevention is the aim.