Creative Touch Permanent Makeup and Aesthetics

Microneedling – also known as percutaneous collagen induction therapy – is a minimally invasive treatment in which fine needles create thousands of controlled micro-injuries in the epidermis and dermis, initiating the body’s intrinsic wound repair cascade. The resulting release of TGF-β, PDGF, and VEGF activates fibroblast migration and stimulates new Type I and III collagen, elastin, and glycosaminoglycan synthesis. The collagen formed integrates as an organised basket-weave lattice that persists for five to seven years. A distinct and clinically significant secondary function is transient dermal microporation – the open microchannels substantially increase skin permeability, enabling direct dermal delivery of topical actives such as polynucleotides, HA preparations, and vitamin C. Microneedling carries an excellent safety profile across all Fitzpatrick skin types and is the most versatile platform treatment in the portfolio for skin quality improvement, scar management, and combination delivery protocols.

Microneedling – formally termed percutaneous collagen induction therapy – is a minimally invasive procedure in which multiple fine needles create controlled micro-injuries to the epidermis and dermis. The treatment does not ablate tissue; it preserves the epidermis whilst creating micro-wounds that initiate the skin’s natural healing cascade, producing new structural proteins and improving skin quality through entirely endogenous biological processes. ^[2] Device formats range from manual dermarollers (192+ needles in cylindrical arrays) to motorised automated pen devices such as the Dermapen, which allow precise depth control from 0.5mm at the superficial end to 3mm for scar and body applications. The pen format produces a stamping motion that minimises epidermal trauma between needle points compared to rolling – a clinically meaningful difference for safety across darker skin types.

The Wound Healing Cascade

The mechanism begins the moment a needle punctures tissue. The three-phase wound healing response is initiated:

Phase 1 – Inflammation (0–3 days): Micro-injury activates platelets and neutrophils, which release TGF-β (transforming growth factor beta), PDGF (platelet-derived growth factor), and CTAP (connective tissue activation protein) into the wound site. These signals recruit fibroblasts and keratinocytes and establish the initial growth factor environment that drives the subsequent phases. ^[2]

Phase 2 – Proliferation (3 days – 2 weeks): Fibroblasts migrate to the wounded area and begin producing Type III collagen (early repair collagen), elastin, glycosaminoglycans, and proteoglycans. VEGF drives angiogenesis simultaneously – new capillary formation improves nutrient and oxygen supply to the treated tissue, supporting the sustained synthesis activity that follows. At approximately five days, a fibronectin matrix forms from β-fibroblast arrangement. This fibronectin scaffold determines the spatial pattern of new collagen deposition, and it is this organised matrix that produces the basket-weave collagen architecture characteristic of successfully treated skin rather than the parallel-bundle arrangement of scar tissue. ^[2]

Phase 3 – Remodelling (2 weeks – 6 months): Type III collagen is progressively converted to structurally stronger Type I collagen via collagenases and matrix metalloproteinases in a controlled remodelling process. The TGF-β3 isoform predominance during this phase specifically suppresses the parallel-fibre arrangement associated with fibrosis, instead directing the organised basket-weave matrix that produces skin quality improvement. The resulting collagen network remains functionally integrated for five to seven years before natural degradation. ^[2]

The Collagen Timeline

Elastin: The Timeline That Requires Explanation

Elastin follows a distinctly different timeline to collagen, and one that is worth understanding for client consultation. A statistically significant decrease in total elastin is measurable at one month post-treatment – an initial degradation of existing disorganised elastic fibres that appears to be a precursor step to new synthesis. By three months, elastin formation has increased significantly above baseline. ^[2] A client reviewed at four weeks who asks whether their skin feels less elastic is not reporting an adverse event; they are describing the midpoint of a two-phase elastin remodelling process. This is worth communicating at consultation so it does not become an unnecessary concern.

Drug Delivery: The Microchannel Advantage

Beyond its structural collagen effects, microneedling has a second, clinically independent function that is as significant as the wound healing cascade in a treatment portfolio context: transient dermal microporation.

Each needle pass creates microchannels through the stratum corneum – the primary barrier to topical active penetration. These channels remain open for anywhere from a few minutes to several hours depending on needle depth and individual skin characteristics, during which time the skin’s permeability for hydrophilic water-soluble molecules is substantially increased. ^[2] Actives that would otherwise be blocked by the intact stratum corneum can reach the vascularised dermis directly, bypassing the absorption limitation that constrains topical-only application.

This mechanism is the basis for the microneedling delivery system used with Lumi-PN (topical PDRN applied through microchannels) and Kiara Reju (the device-compatible HA skin booster formulation), both of which are designed specifically for microneedling-assisted dermal delivery rather than standalone topical use. It also makes microneedling the natural platform treatment for vitamin C serum delivery in clients where stratum corneum penetration of ascorbic acid is otherwise limited by concentration and vehicle. The drug delivery function operates in addition to – not instead of – the wound healing cascade; both occur simultaneously within the same treatment session.

Barrier and Filaggrin Effects

A less widely discussed but clinically relevant outcome of microneedling is its positive effect on epidermal barrier function – not simply a downstream consequence of improved dermal structure but a directly measurable upstream change. Controlled micro-injury upregulates transglutaminase-1 (TGM-1), the key enzyme that cross-links filaggrin proteins to form the cornified envelope surrounding corneocytes. ^[2] Ki-67 (a proliferation marker) and filaggrin expression both increase significantly six days post-treatment in ex vivo models, indicating genuine barrier reconstruction rather than temporary surface improvement. Additionally, upregulation of SPTLC3 – the primary enzyme in ceramide synthesis – increases ceramide concentrations measurably, contributing to improved stratum corneum hydration and reduced TEWL over a treatment course. The initial microporation transiently increases TEWL; by 90 minutes this normalises, and over a treatment course, TEWL improves beyond baseline as dermal and epidermal density increase. ^[2]

Evidence Base

The evidence for microneedling is established rather than emerging, though quality is variable across indication areas. A 2025 narrative review drawing on 70 peer-reviewed studies (PubMed, Web of Science, Embase) confirmed the core mechanistic pathways – collagen and elastin production, angiogenesis, transient permeability increase, and post-treatment epidermal barrier enhancement – as the principal physiological mechanisms. ^[2]

Acne scarring carries the strongest evidence base. Eight RCTs comparing microneedling to fractional laser resurfacing, PRP, and TCA-CROSS found comparable clinical outcomes with a meaningfully lower risk of side effects – specifically, less post-inflammatory hyperpigmentation than ablative alternatives and safe use across FST I–VI. Icepick and boxcar scars respond more reliably than rolling scars; a multi-patient series found 80% of participants showed 50–75% scar improvement after an average of 2.5 sessions.

Photoaging shows consistent benefit across profilometry, elasticity measurement, and epidermal density assessment. Monthly sessions produce significant reductions in wrinkle depth and improvement in skin tightness; improvements accumulate with successive sessions and are measurable at three months post-treatment completion. ^[2]

Hair loss: Microneedling combined with minoxidil consistently outperforms minoxidil alone in evidence-based comparison, through two routes – enhanced transdermal minoxidil delivery through microchannels, and growth factor stimulation in the perifollicular environment. This is one of the few genuinely synergistic device-drug pairings in aesthetics practice with consistent controlled evidence.

Stretch marks show 55% moderate-to-excellent improvement after three to four sessions at four-week intervals, comparable to laser therapy with fewer adverse effects.

Microneedling vs RF Microneedling

Standard microneedling and RF microneedling share the wound healing cascade but diverge in every other clinically meaningful dimension. A 2025 Seoul National University split-face RCT (n=29, female, age ≥60) – the first large prospective head-to-head comparison – found that MNRF produced statistically significant improvements in wrinkle parameters, gross elasticity, hydration, and TEWL at both three and five months; standard microneedling reached significance in most parameters only at five months, and improvements were consistently less pronounced. ^[1] Critically, MNRF significantly reduced the proportion of p16^INK4A^-positive senescent fibroblasts in the dermis – replacing them with newly proliferating non-senescent fibroblasts – whilst standard microneedling did not produce this effect. The correlation between senescent fibroblast reduction and collagen density improvement in MNRF responders suggests this is a mechanism difference with direct outcome consequences, not just an incremental improvement. Standard microneedling’s advantage remains its drug delivery function, its excellent FST I–VI safety profile, and its appropriate positioning for skin quality maintenance, scarring, and combination delivery – with RF microneedling as the escalation pathway when structural laxity, more significant photoageing, or senescent fibroblast burden becomes the primary clinical concern.