The acne cleared. The reminder did not.
The acne cleared. The reminder did not.
There is a particular frustration in this that people rarely say out loud. You did the work. You got the breakouts under control, sometimes after years. And what you are left with is a face that still tells the story in raking light, across video calls, and in the bathroom mirror at the wrong angle.
This page is for that.
It is also for anyone whose concern is texture more generally. Roughness, enlarged pores, unevenness, the sense that your skin is not smooth in the way it used to be, whether or not acne was ever involved.
The first thing to say is that scarring is treatable. Not erasable, and anyone promising that is misleading you, but genuinely and substantially improvable. The second thing is that it is only treatable if the right tool is matched to the right problem, and this is an area where the wrong plan produces years of expensive disappointment.
This matters enormously, because two of these three improve on their own with the right support and one does not.
Post-inflammatory erythema. Flat pink or red marks where a lesion used to be. These are vascular, meaning dilated capillaries near the surface, not pigment and not scar tissue. Very common in fair skin. They fade over months, and light-based treatment accelerates that dramatically.
Post-inflammatory hyperpigmentation. Flat brown, grey or deeper marks. This is pigment, produced by melanocytes responding to inflammation. More common and considerably more persistent in olive and deeper skin tones. It fades slowly, and it responds well to targeted actives and resurfacing.
True atrophic scarring. Genuine textural loss, where inflammation destroyed collagen in the dermis and the body did not fully replace it. Run a finger over it and you feel a dip. Change the angle of the light and it becomes more obvious rather than less.
Only the third is scarring. It does not fade with time, it does not respond to brightening products, and it requires something that rebuilds collagen.
Why this distinction is worth your money. People spend a great deal on scar treatments for marks that would have faded anyway, and considerably less than they should on actual scars because they have been told to be patient. We assess this under magnification at consultation and tell you which you have.
If it is flat, it is a mark. If it has depth, it is a scar.
This is the most important section on the page. Three scar types sit on most faces, they look broadly similar to a patient, and they respond to completely different interventions.
Narrow, deep, steep-sided. They look like small punctures and they often extend surprisingly far into the dermis relative to their width.
These are the most difficult category. Because they are narrow and deep, general resurfacing and needling reach the surrounding skin far more effectively than they reach the base of the scar itself. A course of needling frequently improves the skin around an ice pick scar while leaving the scar looking much the same, which is why people feel their treatment did nothing.
Focal techniques exist that treat these specifically rather than treating the whole face and hoping. If ice pick scarring is the dominant part of your picture, we will tell you that honestly at consultation and discuss what is appropriate, including where that sits outside what we offer.
Wider than ice pick, with defined edges and a flat floor. Shallow or deep, round or oval.
These respond well to collagen stimulation, because there is a floor to lift and enough width for treatment to reach it. Skin needling, resurfacing and medium-depth peels all do useful work here, and shallow boxcars often improve substantially.
Soft, sloping edges, giving the skin an undulating quality. Frequently the most visible in raking light and the most responsive to the right treatment, once you understand them.
The critical point is that a rolling scar is not a hole. The surface is largely intact. Fibrous bands have formed underneath, anchoring the base of the scar to deeper tissue and pulling it downward.
If the problem is a tether beneath, nothing applied to the top will fix it. You can needle that skin, peel it and resurface it and the band will still be pulling. This is the single most common reason someone tells us they have had six needling sessions with very little change.
Rolling scars need releasing first.
Raised rather than depressed, firm, sometimes itchy or tender. More common on the jawline, chest, shoulders and back.
This is a different problem entirely, involving too much collagen rather than too little, and it is managed medically. We will assess it and refer you rather than treating it, and everything on this page about collagen stimulation is actively unsuitable.
Texture is the concern people find hardest to describe and clinicians find easiest to treat badly, because "my skin feels rough" can mean at least five different things sitting at five different depths.
The useful question is not what your texture looks like. It is which layer the problem is in, because that determines what has any chance of reaching it.
The stratum corneum is a wall of dead cells that should shed continuously and evenly. When that shedding slows, which it does with age, with dehydration, in winter, and after barrier damage, cells accumulate unevenly at the surface.
The result is roughness you can feel, dullness because an uneven surface scatters light rather than reflecting it cleanly, flaking, and makeup that clings and separates.
This is the most superficial and the most quickly improved. Enzyme treatments, gentle acids and a retinoid at home usually resolve it within weeks. If your texture concern is genuinely surface-level, you should expect visible change fast and you should be suspicious of anyone selling you a long course.
This is texture you feel more than you see, and it is one of the most common presentations we assess.
Closed comedones. Small, flesh-coloured, slightly raised bumps that give the skin a pebbled or sandpaper quality, most often across the forehead, cheeks and jawline. They are follicles blocked below an intact surface, and they will not extract until something has softened the plug.
Sebaceous filaments. The greyish dots across the nose that people mistake for blackheads and try to remove permanently. They are a normal structure, not a blockage, and they refill because the follicle is doing its job. They can be managed. They cannot be eliminated, and anyone promising otherwise is selling you something.
Milia. Tiny firm white cysts sitting just under the surface, most commonly around the eyes and cheeks. Keratin trapped in a closed pocket. They do not respond to skincare and they need physical extraction, which is quick and simple in clinic.
Sebaceous hyperplasia. Small, soft, yellowish bumps with a slight central dimple, usually on the forehead and cheeks and often mistaken for milia. These are enlarged oil glands rather than blockages, they are entirely benign, and they need a different approach again.
Congestion needs decongesting rather than exfoliating harder. Salicylic acid, which is oil-soluble and can travel into the follicle, does considerably more here than any surface scrub.
Pore size is largely genetic and it is influenced by three things you can actually affect.
Sebum output, because a follicle full of oil is a follicle held open.
Congestion, because a plug of compacted cells and oil physically widens the opening.
The collagen surrounding it, because a pore is a hole in a supporting structure. As dermal collagen weakens the opening loses its scaffolding and appears larger and more oval, which is why pores become more noticeable with age and with sun damage even in people whose oil production has fallen.
That third mechanism is the one nobody mentions and it is the reason collagen-stimulating treatment genuinely helps pore appearance.
What we will not tell you is that we can permanently shrink a pore. We can reduce congestion, help regulate oil, and improve the collagen support around it, and the visible result of that is meaningful. Closing pores is not a thing that happens.
This is where texture becomes structural rather than superficial, and where it stops responding to anything applied to the surface.
Atrophic scarring, covered in detail above.
Solar elastosis. Long-term UV exposure damages elastic fibres, which accumulate as abnormal, disorganised material in the dermis. The clinical result is thickened, coarse, yellowish skin with deep etched lines, most obvious on the neck, chest and the back of the neck in anyone who worked or played outdoors.
Collagen disorganisation. Even without discrete scarring, historical inflammation and cumulative UV leave the dermal matrix less orderly than it was. Skin looks and feels less refined without any single identifiable fault.
Crepiness. Fine, closely spaced lines with a papery quality, most obvious under the eyes, on the neck and on the décolletage. This is thinning combined with elastin loss, and it is a different problem to wrinkles.
Dermal texture needs treatment that reaches the dermis. Collagen stimulation through needling, medium-depth resurfacing, and biostimulatory infusions. Nothing topical remodels this, and a great deal of money is spent pretending otherwise.
This is worth a section of its own, because it explains a specific and frustrating presentation: skin that is doing everything right, being treated appropriately, and responding less than it should.
Glycation is a non-enzymatic reaction between sugars and proteins. No enzyme controls it, which means it happens whenever sugar and protein are in contact for long enough. It is the same chemistry that browns a piece of toast, which is a genuinely useful thing to picture.
In skin, the proteins involved are collagen and elastin. The end results are called advanced glycation end products, or AGEs.
Glycation accumulates preferentially in long-lived proteins with slow turnover, and skin collagen is among the slowest in the body. Estimates put the half-life of skin collagen at around fifteen years.
That is the crux of it. A protein that hangs around for fifteen years has fifteen years of exposure to accumulate damage, and it does not get replaced quickly enough to clear it.
It cross-links your collagen. AGEs form bridges between adjacent fibres. The dermal matrix becomes stiffer, less elastic and less able to move, which is the difference between skin that springs back and skin that does not.
It impairs remodelling, and this is the part that matters most on this page. Glycated collagen is less susceptible to the enzymes that normally break down and replace old fibres. That interferes with the removal of old collagen and, downstream, with the formation of new collagen, including the conversion of the type III collagen laid down during healing into the mature type I collagen that provides lasting structure.
Read that again in the context of everything above. Skin needling, subcision and resurfacing all work by triggering a wound-healing cascade that lays down type III collagen and remodels it into type I over the following months. Heavily glycated skin runs that process less efficiently.
It is a plausible explanation for why two people with apparently similar scarring, treated identically, get meaningfully different results.
It drives inflammation. AGEs bind a receptor called RAGE, which is expressed on fibroblasts, keratinocytes and immune cells in the skin. That binding triggers inflammatory signalling and generates reactive oxygen species. Inflammation degrades collagen, which produces more of the problem.
It affects pigment. AGEs have been shown to promote melanin production through the same RAGE receptor, which links glycation to the pigmentary side of ageing as well as the structural one.
It slows healing. Research on wound healing in high-AGE populations, including people with diabetes, shows longer closure times and altered scar formation.
Blood sugar. The internal source. Chronic high-glycaemic eating and insulin resistance drive it, and diabetes is the extreme model of what glycation does to tissue.
Diet directly. Foods cooked at high dry heat, meaning grilled, fried, roasted and browned, contain AGEs that are absorbed. This is the Maillard reaction on your plate rather than in your dermis.
UV exposure. Ultraviolet radiation increases AGE production in the skin, which means photoageing and glycation are not separate processes running in parallel. They compound each other.
Smoking. Accelerates it substantially.
Time. Unavoidable, and the reason this becomes visible from the forties onward.
There is no single sign, but a recognisable pattern.
A sallow, slightly yellowed tone that brightening products do not shift. Loss of spring and elasticity rather than loss of volume. Skin that feels stiffer and less pliable. A resistant, leathery quality to the texture. Slower recovery from treatment and from injury.
If your skin has that quality and it is not responding to appropriate treatment as expected, glycation is worth considering as part of the reason.
We will be careful here, because this is an area where marketing has substantially outrun the evidence.
Prevention is where the real leverage is. Cross-links, once formed, are difficult to reverse. Managing blood sugar, moderating high-glycaemic and heavily browned foods, protecting from UV rigorously, and not smoking all reduce the rate of accumulation. That is unglamorous advice and it is the honest version.
Antioxidant support has a rationale. AGE formation involves oxidative processes, and topical and dietary antioxidants attenuate some of the associated changes in experimental and clinical studies. Vitamin C matters doubly here, both as an antioxidant and as an essential cofactor in collagen synthesis.
Anti-glycation actives exist and the evidence is developing. Compounds including carnosine and various glycation inhibitors have shown effects in laboratory and animal work, with some clinical data. It is a promising area rather than a solved one, and we are not going to sell you a cream on the strength of a cell culture study.
Stimulate new collagen. Since glycated collagen remodels poorly, the practical clinical response is to build new collagen that has not yet accumulated damage. That is exactly what needling with boosters and resurfacing do, and it is why these treatments remain worthwhile in glycated skin even though the process is less efficient.
Address it internally where relevant. This sits squarely in Alida's territory, and blood sugar regulation is one of the better-evidenced things in the whole naturopathic conversation.
Scarring occurs when inflammation ruptures the follicle wall deep in the dermis. The contents spill into surrounding tissue, the immune response spreads outward, and collagen is destroyed in the process. If the body's repair does not fully replace what was lost, you are left with a depression.
Several factors influence who this happens to.
Depth and duration of inflammation. Nodular and cystic acne scars far more readily than surface pustules, and acne left untreated for years scars more than acne treated promptly.
Picking. This is the one entirely within your control. Squeezing extends the rupture, drives the inflammation deeper, and reliably converts a mark that would have faded into a scar that will not.
Genetics. Some people simply lay down and remodel collagen differently.
Delay to treatment. The most consistent finding in this area, and the reason we say plainly on our acne page that waiting has a cost.
If you are reading this while still having active breakouts, please treat the acne. Every month of active inflammatory acne is scarring that will need treating later.
Most people assume a scar is a fixed thing. It formed, it settled, and it will look the same at fifty-five as it did at twenty-five.
That is not quite how it works, and understanding why changes how people think about the timing of treatment.
The scar stays the same. The skin around it does not.
An atrophic scar is a depression in the dermis. How visible it is depends almost entirely on the quality and thickness of the tissue surrounding it, and that tissue changes considerably across a life.
Collagen density falls. Elastin degrades and is not meaningfully replaced. The dermis thins. As the surrounding support weakens, the walls of the depression become less supported, the edges soften and spread, and the whole thing casts a longer shadow.
A scar that was barely noticeable in your twenties can be genuinely obvious in your fifties without ever having changed itself. What changed was everything around it.
Skin that reflects light less evenly shows scarring more.
Scarring is perceived almost entirely through shadow. Young skin reflects light relatively uniformly, which softens the appearance of small depressions. As texture becomes less even, as pigment becomes more mottled and as the surface loses clarity, light scatters unevenly and every contour becomes more pronounced.
There is a useful piece of research behind this. Studies examining facial perception have found that skin surface quality alone, holding facial shape and structure constant, measurably changes both how old a face is judged to be and how it is perceived more broadly. Scarring is a surface quality attribute. It is genuinely contributing to how your face reads, independent of lines or volume.
The capacity to repair declines.
This is the part that matters most for timing, and it is the honest reason we would rather see people sooner.
Every treatment on this page works by asking the skin to build new collagen. Fibroblasts become less numerous and less responsive with age. Collagen synthesis slows. Healing takes longer. And as we covered in the section on glycation, accumulated cross-linking makes the remodelling process itself less efficient.
The result is that the same treatment, performed identically, generally produces more at thirty-five than at sixty. Not nothing at sixty, and we treat scarring at every age with good results. But the raw material you are working with is better earlier, and that is simply true.
What this is not.
It is not an argument for panic, and we are not going to use it as one.
Nothing about this means you have missed your chance, and age of scarring makes remarkably little difference to whether it responds. Someone treating twenty-year-old scars in their forties will see real change, and we have that conversation regularly and enjoy it.
What it does mean is that indefinite postponement has a cost, and that the cost is quiet rather than dramatic. Skin does not suddenly become untreatable. It becomes gradually less efficient at the thing you will eventually ask it to do.
So if you have been telling yourself you will deal with this when things settle down, that is entirely your call to make and we will not pressure you. We would simply rather you made it knowing that the window is a sliding one rather than a fixed one.
We are a medical-dermal clinic. Caitlin is a Registered Nurse with ten years in cosmetic medicine, Belinda is our Senior Dermal Clinician with around ten years of industry experience, and the whole team works to a shared philosophy: assess first, treat conservatively, sequence with intent, and never do more to the skin than it can handle.
Scarring is the clearest illustration of why the clinic is structured this way.
Most scarring plans fail for a structural reason rather than a clinical one. The patient is treated by a Dermal Clinician who cannot access the medical layer, or by a prescriber who does not perform the resurfacing. Each does their part well. The patient stands in the gap between them, carrying the coordination.
Here it is one assessment and one plan. That matters at three specific points.
At assessment. Most faces carry three or four different problems at once. Rolling scars needing release, boxcars needing collagen, post-inflammatory erythema needing light, and pigment needing something else again. A plan has to address each with the appropriate tool, and that requires seeing all of them properly in the first place, under a Wood's lamp and a dermatoscope, at the same appointment.
At sequencing. Order changes the outcome more than technique does. Active acne is controlled before scar work begins, because treating inflamed skin creates more scarring and more pigment. Tethering is released before resurfacing, so the surface work is not fighting a band underneath. Vascular marking is treated separately from pigment.
At the boundary. Where something falls outside dermal scope, the medical side is already in the room, and where it falls outside both, we say so and refer.
Under local anaesthetic, a fine instrument is introduced beneath the scar and moved in a controlled fanning motion to release the fibrous bands holding it down. The base lifts. The space created then fills with new collagen as it heals, which lifts it further over the following weeks.
What it treats well. Rolling scars, and tethered boxcar scars with a clear anchoring component.
What it does not treat. Ice pick scars, which are too narrow and deep for this approach. Raised hypertrophic or keloid scarring, which needs medical management.
What to expect. Bruising, and we want to be upfront that it can be substantial. Plan for seven to fourteen days and do not book this the fortnight before an event. Swelling for a few days is normal. Most people need two to three sessions spaced four to eight weeks apart.
Risks include bruising and haematoma, temporary firmness or nodularity at treated sites, infection, and in a small number of people an incomplete response. All discussed in full beforehand.
How it fits. Subcision is very often the first step rather than a standalone treatment. Release the tethering, then use needling and resurfacing to refine the surface once the base has lifted. Sequenced that way, the needling afterwards works considerably harder than the same needling would have done first.
This is our primary collagen-building treatment and it works on two mechanisms simultaneously.
The mechanical mechanism. Controlled micro-channels trigger a genuine wound-healing cascade. Over the following weeks and months, fibroblasts lay down new collagen and elastin in the dermis. This is structural remodelling rather than surface improvement, and it is why the result continues developing for months after the final session. Nothing topical achieves this.
The delivery mechanism. Those same channels temporarily bypass the stratum corneum, the barrier that stops most actives reaching useful depth. An ingredient applied to intact skin and the same ingredient delivered through open channels are not the same treatment.
Level One pairs the needling with an LED or peel selected on the day, using a hyaluronic acid glide for comfort, plus post-care to take home.
Level Two adds a medical booster infusion formulated to your presenting concern.
We are careful here, because this is an area where marketing has run considerably ahead of the research.
Polynucleotides and PDRN. Derived from salmon or trout DNA, used both as a standalone infusion including Rejuran and within Byryzn Opuluxe V.
The mechanism is well described. PDRN acts on adenosine A2A receptors, reducing inflammatory signalling and promoting angiogenesis through upregulation of VEGF, while also supplying nucleotides that fibroblasts use directly. In experimental wound models PDRN produced significant increases in VEGF expression against control, at p less than 0.001. In atrophic scarring specifically, reduced inflammation combined with supported collagen remodelling is exactly the biology required.
Several clinical studies, predominantly from Korea, report better outcomes from PDRN combined with microneedling than from microneedling alone.
A 2026 narrative review of PDRN in aesthetic recovery was explicit about the limitations of this field: a shortage of randomised controlled trials in human aesthetic cohorts, small sample sizes, variability between formulations, and little long-term follow-up. The mechanistic case is strong and the clinical evidence is still developing. We think it is a reasonable, biologically sound addition. We are not going to tell you it is proven.
Byryzn Opuluxe V. A Korean-formulated booster brought into Australia by Hugel, combining PLLA, trout DNA PDRN, hyaluronic acid, glutathione, sphingomonas ferment extract, adenosine, an amino acid complex and a vitamin complex. Suited to post-acne skin needing several things at once rather than one concern in isolation.
PLLA. A biostimulator provoking a gradual fibroblast response that builds collagen over months. Useful where post-acne skin has lost general structural quality rather than developed discrete scars.
Tranexamic acid. The best-evidenced of the group, though most of that evidence sits in melasma. It acts on plasmin-driven inflammatory and pigment signalling, which makes it directly relevant to the brown marks acne leaves behind, particularly in deeper skin tones.
Peptides, growth factors, hyaluronic acid, amino acids and skin vitamins. Collagen signalling support, hydration and the raw materials for repair. The foundation of most infusions rather than the headline.
Each is selected and combined intentionally, never at random.
Expectations. Redness for one to three days. A course of three to six treatments spaced four to six weeks apart for meaningful textural change, and often more where scarring is significant.
Peels are the treatment people most often have done badly, because they are usually sold by name rather than selected by depth. A peel is only useful if it reaches the layer your problem is actually in, and everything above is a waste of downtime.
We stock professional ranges from PCA Skin, Dermaceutic, Toskani, Société, Cosmedix and Mesoestetic alongside compounded mono peels formulated to concentration. That inventory exists so we can select for depth rather than fit your skin to whatever is on the shelf.
Salicylic acid. A beta hydroxy acid, and the only one on this list that is oil-soluble. That single property is why it matters. It travels into the follicle rather than sitting on the surface, which makes it the most useful acid we have for the congestion layer, closed comedones and that pebbled, sandpaper texture. It is also anti-inflammatory in its own right.
Mandelic acid. The largest molecule of the alpha hydroxy acids, which means it penetrates most slowly and most evenly. That slowness is a feature rather than a limitation. Even penetration means less risk of provoking the inflammation that produces post-inflammatory pigmentation, which makes mandelic our default in olive and deeper skin tones and in anyone with a history of marking.
Lactic acid. An alpha hydroxy acid that is also a humectant, and a natural component of the skin's own moisturising factor. It exfoliates while drawing water in, which makes it one of the few acids appropriate for skin that is textured and dehydrated at the same time.
Glycolic acid. The smallest alpha hydroxy molecule, so it penetrates fastest and furthest of the AHAs. That makes it effective on surface and epidermal texture and it also makes it the one that most requires a properly prepared barrier underneath.
Retinoid and vitamin A peels. These work differently to everything above. Rather than dissolving bonds between cells, they act on cell signalling, driving turnover and collagen production from within. That makes them useful where the concern is dermal quality rather than surface build-up, and they suit people who cannot tolerate a strong retinoid at home.
Trichloroacetic acid. Not an AHA or a BHA. TCA works by denaturing protein, and the depth is controlled by concentration and the number of coats applied. This is the acid that does genuine textural work, and it is the backbone of our advanced level.
Level One. Very superficial. Working at the stratum corneum.
Enzyme treatments including the PCA Enzymatic and No Peel Peel and the Cosmedix Blueberry Smoothie, the Dermaceutic Milk Peel, the Société Açaí Berry lactic peel, Toskani's Radiance and Mandesome Duosome peels, and mandelic and lactic mono peels.
For texture, this level addresses surface roughness, dullness and light congestion. Little to no downtime. If your concern is layer-one texture, this is where you will get your result, and you should see it within a few treatments.
Level Two. Superficial. Working through the epidermis toward the basal layer.
The PCA Pigment Correcting peel, Dermaceutic's Crystal Peel and Cosmo Peel, the Toskani Clarifying Booster, Cosmedix Timeless, glycolic formulations, dedicated photo-ageing peels, and retinol-based peels.
This is where established congestion, post-inflammatory pigmentation and epidermal texture are properly addressed. Expect some flaking for a few days. Most people doing texture work spend the majority of their course here.
Level Three. Medium depth. Reaching the papillary and upper reticular dermis.
Modified and enhanced Jessner formulations including the Mesoestetic Meso Jessner and PCA's hydroquinone-free Enhanced Jessner's, the Toskani Rejuvenating peel, Dermaceutic Cosmo Peel Forte and Exo Peel, and TCA at twenty percent and above.
Jessner formulations are combination peels, traditionally layering salicylic and lactic acids together. Because they are applied in coats, the depth is controllable, which is why they suit skin that needs more than superficial work but is not ready for full TCA.
TCA is the one that reaches genuine textural change. Shallow atrophic scarring, dermal texture, enlarged pore appearance and photodamage all sit at a depth that nothing lighter will touch.
Expect five to seven days of visible peeling, a period where the skin looks worse before it looks better, and strict sun avoidance afterwards. It is not a treatment you book the week of an event.
Level Three always requires proper preparation beforehand, usually several weeks of appropriate home care and often a course through the lower levels first. That is not a formality. Treating unprepared, sun-exposed or barrier-compromised skin at depth is the most reliable way to generate post-inflammatory pigmentation in someone who did not previously have it.
We progress a level only when your skin has demonstrated it can handle the one below. In olive and deeper skin tones we progress more slowly and we prepare for longer, because the cost of getting it wrong is higher.
We generally run the corrective phase through cooler months and hold summer for protection and maintenance.
We do not perform Level Two or Level Three over active inflammatory acne, or on a compromised barrier.
Honestly, peels do the surface and epidermal work. They contribute meaningfully to dermal texture at Level Three and they are excellent for the pigment that accompanies scarring.
They do not replace collagen stimulation. If your concern is genuine atrophic scarring, a peel course alone will improve the skin around your scars and leave the scars themselves largely unchanged. The two work together and neither substitutes for the other.
We use the Lumenis M22 Stella with XPL, one of the first of these systems in Australia.
Post-inflammatory erythema, those flat pink and red marks that linger for months after the acne has gone, is vascular. Dilated capillaries near the surface. No cream, no acid and no amount of patience clears them efficiently, because they are not pigment and they are not scar tissue.
IPL targets the haemoglobin inside those vessels directly.
For someone whose skin has genuinely cleared but who still looks like they are breaking out, this is very often the missing piece, and it is the single most under-recognised treatment in post-acne care.
Typically three to four sessions spaced three to four weeks apart. A patch test and full consultation are required, and recent sun exposure rules it out.
Fractional CO2 resurfacing is joining the clinic, and for acne scarring it is the most significant addition we have made.
CO2 remains the most capable resurfacing technology available for textural change, working at depths and with a precision that neither peels nor needling reach. Historically the trade-off was results against considerable downtime. The CoolPeel protocol delivers energy in very short pulses so the surface is resurfaced without heat accumulating in surrounding tissue, which narrows that trade-off substantially.
The Tetra Pro platform also works across a genuine range of depths, so treatment can be matched to the scarring in front of it rather than delivered at one setting.
It does not change the sequencing described on this page. Active acne is controlled first, tethering is released first, and skin still needs preparation. If it is right for you, we will raise it at consultation, and we would rather you waited a few weeks for the appropriate treatment than paid for the wrong one now.
Home care does not remove a scar. It does three genuinely useful things around one.
It clears the marks. Post-inflammatory pigment responds well to consistent topical work. Vitamin C, niacinamide, azelaic acid and a retinoid all contribute, and iS Clinical Super Serum Advance+, which pairs fifteen percent L-ascorbic acid with a bioidentical copper tripeptide growth factor plus arbutin and kojic acid, is a clinic staple for exactly this.
Retinoids are the most evidence-supported topical in this entire category, and they are the one product where the science genuinely justifies the reputation.
How they actually work. Retinoic acid binds nuclear receptors inside the cell and alters gene transcription directly. It is not exfoliating the surface, it is changing what the cell is instructed to produce.
Four of those changes matter here.
It normalises the way the follicle sheds its lining, which addresses congestion at its origin rather than at the surface. It accelerates epidermal turnover, which improves surface texture and clarity. It increases synthesis of type I and type III collagen in the dermis, which is structural rather than cosmetic. And it inhibits the matrix metalloproteinases that degrade existing collagen, so it both builds and protects.
That combination is why a retinoid is the only topical with a legitimate claim on scarring and texture at the dermal level. Research published in the New England Journal of Medicine in 1993 demonstrated restoration of collagen formation in photodamaged human skin with topical retinoic acid, and the evidence has accumulated since.
Why strength is not the same as potency. Retinol is not retinoic acid. It has to be converted in the skin, retinol to retinaldehyde to retinoic acid, and every conversion step loses some. This is why a retinol percentage cannot be compared directly to a prescription strength, and why formulation and delivery matter as much as the number on the bottle.
The adjustment period is real. Four to twelve weeks of dryness, flaking, and sometimes a period where existing congestion is pushed to the surface faster than usual. This is expected. It is also the exact point at which most people abandon the single most useful product they own.
We work with this range specifically, and the reason is the delivery system and the graduated strengths.
Encapsulation. The retinol is encapsulated in bio-identical lipids, which releases it gradually into the skin rather than delivering it all at once. That controlled release is what separates a tolerable retinol from one people give up on, and it is the difference between a product that works because you keep using it and one that does not because you cannot.
The supporting formulation. These are not retinol in a basic base. Ectoin, a stress-protective molecule with anti-inflammatory and barrier-supportive properties. Squalane, glycerin, sodium hyaluronate and shea butter for the hydration that retinised skin needs. Panthenol for soothing. Tocopherol, ascorbic acid and glutathione as antioxidants. Bakuchiol and botanical boosters alongside the retinol itself, and the brand's Extremozyme technology for environmental protection.
The point of all of that is tolerability. A retinoid you can actually stay on is worth considerably more than a stronger one you use for six weeks and abandon.
Three strengths, and why the range is the whole point.
0.3 is where almost everyone begins. Enough to produce genuine change, gentle enough to build a habit on. For sensitive or reactive skin, and for anyone who has previously failed a retinoid, this is the sensible entry.
0.6 is the middle level, for skin that has demonstrated it tolerates 0.3 comfortably and is ready for more.
1.0 is the maximum strength, genuinely keratolytic, for well-conditioned skin working on established texture, congestion and photodamage.
How we introduce it. Every third night for the first three weeks. If that is comfortable, every second night. Progress upward only when the current strength has been tolerated for a sustained period, not because a month has passed.
Some people stay at 0.3 permanently and get excellent results. Escalating strength is not a marker of progress and there is no prize for reaching 1.0.
Retinoids before procedures. Worth knowing. Conditioning skin with a retinoid before peels and needling improves the outcome, accelerates healing, and reduces the risk of post-inflammatory pigmentation. This is part of why we insist on preparation before Level Three peels rather than treating on request.
We pause retinoids for a period before and after certain treatments, and we will tell you exactly when.
This is our most-used serum in scarring and post-acne skin, and the formulation earns it on three separate mechanisms rather than one.
Vitamin C as a collagen cofactor. Fifteen percent L-ascorbic acid. Beyond antioxidant protection, vitamin C is an essential cofactor for the enzymes that hydroxylate proline and lysine during collagen synthesis. Without adequate vitamin C, the collagen your skin produces is structurally weaker. In someone actively building collagen through needling or resurfacing, that is not a peripheral detail.
Copper tripeptide growth factor. A bioidentical copper tripeptide, which has among the better evidence bases of any cosmetic ingredient for supporting wound healing, collagen synthesis and tissue repair. In post-acne skin where the whole objective is repair, this is the ingredient doing the most specific work.
Pigment inhibition. Arbutin and kojic acid, both tyrosinase inhibitors, addressing the post-inflammatory hyperpigmentation that accompanies scarring in most people and dominates it in deeper skin tones.
So a single product is supporting the collagen synthesis you are paying for in clinic, supplying the cofactor that synthesis requires, and clearing the marks sitting alongside the scars.
That is why it is on nearly every plan we write for this concern.
It protects the work. Sunscreen, daily, without exception. UV worsens post-inflammatory pigmentation and undoes the results of nearly every resurfacing treatment we perform. Treating scarring without protecting it is money spent standing still.
And it stops you making more. If there is any active acne remaining, treating it is more important than any scar treatment. So is not picking.
We would rather set this expectation now than at your final appointment.
A good outcome in acne scarring is substantial improvement, not erasure. Skin that no longer catches the light in the same way, that photographs better, that you stop noticing. Not skin that looks like it never had acne.
Improvement is gradual, it is measured across months rather than weeks, and it continues developing after your last treatment because collagen remodelling does not stop when you leave.
Multiple scar types usually need multiple modalities, often in a specific order, and that takes time.
We photograph under standardised conditions with consistent lighting, because scarring is exactly the concern where memory is least reliable and where patients consistently underestimate their own progress. Raking light photography in particular shows change that a bathroom mirror will not.
Collagen synthesis is a nutritional process as much as a biological one. It requires adequate protein, vitamin C as an essential cofactor, zinc and other micronutrients, and it is impaired by chronic inflammation and poor sleep.
Where these are worth investigating, Alida looks at them, alongside practitioner-grade collagen where appropriate, where form and bioavailability matter far more than the number on the label.
This supports the work rather than replacing it. Nobody remodels a scar through diet.
Supports recovery after needling, subcision and resurfacing, and has a measurable effect on stress physiology. A single-blind randomised controlled trial found salivary cortisol significantly reduced after manual lymphatic drainage.
Infrared sauna, cold plunge and private shower. Worth noting that heat and sweat are avoided during recovery from needling, subcision and resurfacing, so timing around your treatment schedule needs discussing rather than assuming.
Consultation. Full assessment under Wood's lamp and dermatoscope. Scar types identified and mapped. Marks separated from scars. Standardised photography including raking light. Any active acne addressed first.
Phase one, release. Where rolling or tethered scarring is present, subcision comes first. Two to three sessions, four to eight weeks apart.
Phase two, build. Skin needling with boosters. Three to six sessions, four to six weeks apart. Medium-depth peels where appropriate.
Phase three, refine. Resurfacing for remaining texture. IPL for vascular marking. Pigment work where needed.
Maintenance. Home care indefinitely, with periodic treatment as required.
Realistically, a meaningful scarring plan runs across nine to eighteen months. We would rather tell you that at the beginning.
We will not quote before we have seen your skin, because a few shallow boxcars and widespread mixed scarring with tethering are not comparable.
At consultation you get a clear, itemised plan covering the full sequence, roughly how long it runs, and what it will cost across the phases rather than one appointment at a time.
Scarring is one of the more significant investments we ask people to make, and we would rather you saw the whole picture before you start than discover it incrementally.
If your budget is limited, tell us. We will tell you which single intervention gives you the most for your money, and it is often not the one people expect.
Cosmetic and dermal treatments do not attract a Medicare rebate.
If you have active moderate or severe acne requiring prescription management. If your scarring is hypertrophic or keloid. If ice pick scarring dominates and a focal or surgical technique would serve you better. And if you have not had a skin check.
We are a medical-dermal clinic, not a prescribing practice, and part of good practice is knowing where our scope ends.
Marks fade. Scars do not. If it has depth, time will not change it, and the years spent waiting are years the surrounding skin also ages.
It will fix some of it. Rolling scars tethered from below need releasing first or needling will underperform badly. Ice pick scars are too narrow and deep for it to reach. Boxcars and general texture respond well.
Needling is an excellent tool. It is not the only one, and a plan built entirely around it will only ever partly work.
No topical rebuilds lost dermal collagen. Topicals clear marks, improve surrounding skin and protect results, which is genuinely worth doing. They do not fill a scar.
Until it is controlled, yes. Until you are certain it will never return, no, or you will wait indefinitely. Stable and well managed is the threshold, not permanently cured.
Aggressive treatment on unprepared skin produces inflammation, and inflammation in scarring-prone skin produces more pigment and sometimes more scarring. This is a concern where patience genuinely outperforms intensity.
Age of scarring makes remarkably little difference. Atrophic scars are a structural deficit, and that deficit responds to collagen stimulation whether it formed last year or in 2003.
If it is flat, it is a mark and it will improve. If you can feel a dip, or it becomes more obvious when light hits your face from the side, it is a scar.
Most people have both. We assess under magnification and tell you the proportions, which usually turns out to be more encouraging than people expect.
Substantial, not complete. We avoid quoting percentages because scarring varies so widely, but the honest framing is that we aim for skin you stop noticing rather than skin that looks untouched.
A meaningful plan runs nine to eighteen months across several modalities. Collagen remodelling continues for months after the final treatment, so the result at your last appointment is not your final result.
It is performed under local anaesthetic so the procedure itself is comfortable. The bruising afterwards is the part to plan around, and it can be significant for seven to fourteen days.
Yes, with the caveat that body skin heals more slowly, scars there are frequently hypertrophic rather than atrophic, and results are generally less dramatic than on the face. We will be honest about what is achievable.
Yes, with adjusted protocols. Deeper skin tones carry a higher risk of post-inflammatory pigmentation from treatment itself, so preparation is longer, settings are more conservative, progression is slower, and some options are avoided. Careful treatment produces excellent results. Standardised treatment is what causes problems.
That is normal and it is not a barrier. What we need is control, not perfection. Occasional lesions are manageable alongside a scarring plan.
Every scarring plan at Plump begins with a full consultation. We assess your skin under Wood's lamp and dermatoscope, identify and map your scar types, separate marks from genuine scarring, photograph properly including raking light, and build a sequenced plan with realistic expectations and honest timelines.
There is no cost and no obligation.
Book online, or call or text us on 0478 844 048
Plump Aesthetic Clinic
525 Chapel Street, South Yarra
www.plumpaestheticclinic.com.au
We see patients from South Yarra, Prahran, Windsor, Toorak, Armadale, Richmond, Malvern, St Kilda, and across inner Melbourne.
Reviewed by the clinical team at Plump Aesthetic Clinic
Caitlin King, Registered Nurse, Founder and Clinical Director. Ten years in cosmetic medicine.
Belinda, Senior Dermal Clinician. Approximately ten years of industry experience.
Last reviewed: [month, year]
We treat skin, not trends. Where we make a claim about what a treatment does, we want it to be traceable to something better than marketing.
Acne scarring is an area where mechanistic reasoning is strong and high-quality clinical trial data is thinner than the marketing suggests. We will tell you which is which.
Key sources informing this page:
Reynolds RV, Yeung H, Cheng CE, et al. Guidelines of care for the management of acne vulgaris. Journal of the American Academy of Dermatology. 2024;90(5):1006.e1-1006.e30.
Polydeoxyribonucleotide (PDRN) in post-procedure recovery in aesthetic medicine: a narrative review. 2026.
Microneedling for non-cosmetic dermatologic conditions: a systematic review of efficacy and safety. 2025.
Wang Y, et al. The effects of advanced glycation end-products on skin and potential anti-glycation strategies. Experimental Dermatology. 2024;33:e15065.
Van Putte L, De Schrijver S, Moortgat P. The effects of advanced glycation end products (AGEs) on dermal wound healing and scar formation: a systematic review. Scars, Burns and Healing. 2016.
Ikeda H, Saheki Y, Sakano Y, Wada A, Ando H, Tagai K. Facial radiance influences facial attractiveness and affective impressions of faces. International Journal of Cosmetic Science. 2021;43(2):144-157.
Spring LK, Krakowski AC, Alam M, et al. Isotretinoin and timing of procedural interventions: a systematic review with consensus recommendations. JAMA Dermatology. 2017;153(8):802-809.
Important information: All treatments described on this page require an individual consultation with a qualified practitioner to determine suitability. Results vary between individuals and depend on scar type, depth, age, skin type and adherence to the treatment plan. Scarring is improved rather than eliminated and no result is guaranteed. All treatments carry risks and potential side effects, including bruising, swelling, infection and pigmentary change, which will be explained to you in full before you proceed. This information is general in nature and is not a substitute for individual medical advice.
