Skin is largely structural. By dry weight, the dermis is around seventy percent collagen, predominantly type I, with type III playing a key role in younger, more elastic tissue. Collagen gives skin its tensile strength. Elastin lets it recoil. Together they sit in a hydrated extracellular matrix that holds water and signals cells.
What changes with age
From the mid-twenties, fibroblasts, the cells responsible for producing collagen, gradually slow their activity. Net collagen content declines by approximately one percent per year. Existing fibres become more cross-linked and fragmented. The ratio of type I to type III shifts. The extracellular matrix loses hyaluronic acid and water.
The visible result is everything we recognise as ageing: fine lines, loss of bounce, a duller surface reflection, and eventually true laxity. But the visible result is downstream. The biological event is the change in tissue quality.
Why this matters for treatment
If the underlying problem is biological, the most durable response is biological. Treatments that stimulate fibroblasts, recruit growth factors, or rebuild the extracellular matrix address the cause rather than masking the symptom. Treatments that add volume on top can produce a pleasing photograph but do not improve the skin itself.
Healthy skin is the foundation. Everything else is decoration.
What the patient can control
- · Daily broad-spectrum SPF. UV is the single largest accelerator of dermal collagen breakdown.
- · Topical vitamin A derivatives, used consistently under medical guidance.
- · Antioxidants, particularly vitamin C, to limit oxidative damage.
- · Sleep, hydration, and not smoking. Boring, and the most powerful inputs available.
In-clinic regenerative protocols layer on top of these basics. They do not replace them.