One thing before everything else
Skin after years of sun exposure is not just an aesthetic problem. Foci of actinic keratosis and pigmented lesions with an atypical appearance first require a dermatological assessment, not a brightening treatment.
We support the assessment of lesions with digital dermatoscopy, but this supports the decision, it is not a diagnosis. For lesions that raise doubt, we refer to cooperating dermatologists before we start anything.
On this page
What photoageing is
Photoageing, referred to in the literature as dermatoheliosis, is the process of skin ageing caused by chronic exposure to ultraviolet radiation, from the sun or from artificial sources such as sunbed lamps. The changes affect both the epidermis and the dermis.
The mechanism rests on two pillars. The first is reactive oxygen species, which form under the influence of UV and damage DNA, proteins and lipids in the skin. The second is the activation of matrix metalloproteinases, enzymes that break down collagen and elastin. The result is simultaneous degradation of fibres and reduced synthesis of new ones, and from this a loss of tension and elasticity.
This distinction has a practical meaning. We cannot stop chronological ageing, because it is genetically programmed. Photoageing can be prevented and its effects can be limited, and most of this work is done outside the practice.
Three UV ranges and how far they reach
Ultraviolet radiation is invisible to the eye, and its three ranges act on the skin in completely different ways. The difference comes down to wavelength: the longer it is, the deeper it reaches.
Ranges of ultraviolet radiation
100 nm
200
280
320
400 nm
UVC, from 100 to 280 nm
The most harmful range, but under natural conditions we are not exposed to it: it is almost completely absorbed by the Earth's atmosphere.
UVB, from 280 to 320 nm
Does not penetrate beyond the epidermis. Responsible for sunburn and for the synthesis of vitamin D. Most intense around midday and in summer, dependent on latitude.
UVA, from 320 to 400 nm
Reaches the deeper layers of the skin and the subcutaneous tissue. Present all year round, passes through clouds and window glass. The main cause of photoageing.
Schematic overview. Range boundaries as given in the clinic's source text.
Why UVA is most important here
UVA has the longest wavelength of the three ranges, so it reaches the deeper layers of the skin and the subcutaneous tissue. It is present all year round and passes through clouds and window glass. It is the main cause of photoageing, even though it does not cause sunburn that would make it noticeable.
Photoageing versus chronological ageing
Two processes that overlap in the same skin, but differ at the molecular, histological and clinical level.
Photoageing
Pathological, induced process
Induced by UV radiation, in the UVA and UVB ranges.
Accelerated degradation of collagen and elastin by matrix metalloproteinases.
Increased production of reactive oxygen species and DNA damage.
Characteristic pigmentation changes: freckles, solar lentigines, poikiloderma.
Damage to skin structure: roughness, telangiectasia, keratosis foci.
Possible prevention: sunscreens and antioxidants.
Chronological ageing
Natural, endogenous process
Genetically programmed, inevitable process.
Gradual thinning of the epidermis and dermis.
Gradual loss of skin function and regenerative capacity.
Pigmentation changes less pronounced than in photoageing.
Loss of elasticity and firmness, a decrease in fibroblast numbers.
Management focused on lifestyle, diet and skin regeneration.
Four degrees of post-sun damage
The classification describes the severity of changes, not chronological age. The age ranges given are typical, not obligatory: skin consistently protected from a young age can be one grade lower, and skin after years of sunbed use one grade higher.
I
Mild damage
Barely visible imperfections, with no pigmentation disorders or only minor ones. Usually do not require correction with make-up.
Typical age
28 to 35 years
II
Moderate damage
First wrinkles, slight pigmentation disorders, pale yellow clusters of actinic keratosis. Easy to camouflage with light make-up.
Typical age
35 to 50 years
III
Advanced damage
Established wrinkles, vascular changes: patches and telangiectasia, plus keratosis and discolouration. To be concealed with heavy make-up.
Typical age
50 to 60 years
IV
Severe damage
Deep gravitational and expression wrinkles, foci of actinic keratosis, with or without neoplastic features, pigmentation disorders that respond poorly to camouflage.
Typical age
65 years and over
This way of describing damage corresponds to the Glogau scale commonly used in dermatology. At the fourth grade, an issue arises that goes beyond aesthetics: foci of actinic keratosis may present with neoplastic features. In that case, the first step is a dermatologist.
How to recognise it
Photoageing rarely looks like a single change. It is usually a set of several, each with a different approach to management.
Freckles and solar lentigines
Pigmentation changes resulting from excessive melanin accumulation. The most common visible effect of photoageing and usually the first reason for a visit.
Poikiloderma
Pigmentation disorder accompanied by telangiectasia, most often on the neck and decolletage, that is, in areas that are exposed and rarely protected with sunscreen.
Telangiectasia, or spider veins
Permanently dilated vessels visible through the epidermis. They do not disappear on their own and may deepen over time.
Roughness and dryness
Skin becomes thinner and rough, in advanced form described as parchment like. The dry surface results from barrier damage, not from insufficient water intake.
Wrinkles and loss of firmness
The result of collagen and elastin degradation and fibre reorganisation. In photoageing they appear earlier than age alone would suggest.
Actinic keratosis lesions
Rough, pale yellow clusters in the most exposed areas. They require dermatological assessment, not an aesthetic treatment.
Photoprotection, or what works
Photoprotection is not just sunscreen. Sunscreen is one of five elements and none of them replaces the others. The order below reflects how much difference each actually makes.
Avoiding the sun
Limiting exposure during the hours of strongest sunlight, usually 10:00 to 16:00, and seeking shade. A free and the most effective element.
Clothing and eyewear
Fabrics with a high UV protection factor, a hat, sunglasses, clothing covering as much skin surface as possible.
Sunscreens
Broad spectrum preparations, matched to skin phototype and conditions. Used all year round, not only in summer.
Antioxidants
Topically or orally: vitamin C, vitamin E, polyphenols. They neutralise reactive oxygen species produced under UV exposure. The diet also matters, including vitamin A, zinc, rutin and coenzyme Q10.
Supplementation
Beta carotene, green tea extracts, lycopene, vitamin D. They provide additional protection but do not replace sunscreen.
Sunscreens fall into two types and it is worth knowing how they differ, as this changes how they are used.
Chemical filters
They absorb UV radiation and convert it into heat.
Physical filters
They reflect UV radiation. These include titanium dioxide and zinc oxide.
Sunscreen is chosen to match skin phototype and the conditions a person is in, not the season. A cosmetologist can help with setting a skincare plan. Self tanner, whose active ingredient is dihydroxyacetone reacting with amino acids in the stratum corneum, is an alternative to tanning but does not protect against UV.
What we do not take away from the sun
Moderate sun exposure has documented benefits and there is no reason to leave them unmentioned. It is a matter of proportion, not of avoiding light altogether.
Vitamin D
UVB radiation is necessary for its synthesis in the skin. Vitamin D supports calcium and phosphorus absorption, bone health and the work of the immune system. It can be supplemented.
Mood
Light affects serotonin production, which can help with seasonal affective disorder. Specialist lamps are an alternative.
Biological clock
Natural light helps regulate the circadian rhythm, which affects sleep quality.
Anti inflammatory effect
Moderate sun exposure brings relief in some skin conditions, for example psoriasis. This course of treatment is led by a dermatologist, not a cosmetology practice.
Hypotheses that call for caution
Research suggests that moderate exposure may reduce the risk of some cancers, type 1 diabetes and autoimmune diseases, likely through vitamin D. This is a lead, not a recommendation.
The largest amount of UVB radiation, responsible both for vitamin D synthesis and for sunburn, falls around midday. In the morning and late afternoon there is much less of it, which lowers the risk but also the efficiency of vitamin D synthesis. Vitamin D can be supplemented, skin after photodamage cannot.
Treatments for changes that are already there
Once changes have become established, photoprotection stops being enough, but it does not stop applying: without it every treatment works against the next dose of UV. Below are the methods used most often, along with what they are chosen for.
Working on skin tone and surface roughness. Exfoliating the epidermis speeds up cell turnover and evens out skin tone.
Pigment changes with clear borders. Energy targets the melanin, and the skin's natural processes remove the broken down pigment.
Diffuse changes: uneven tone together with redness and vessels, where a wider treatment field matters.
Hydration and skin density. The preparation is delivered intradermally, without needing to cross the epidermal barrier.
Tension and structure of the skin, with the epidermis preserved. Considered when the problem is skin laxity, not colour.
The deepest method on this list, for established changes: remodelling of the dermis along with a reduction in wrinkles and roughness.
Retinoids and antioxidants in home skincare
The foundation all the other methods build on. The skincare plan is set by the cosmetologist at the consultation.
Treatments for photoageing attract the most interest in autumn, and there is a reason for that: consistent photoprotection is easier to maintain then. We carry them out all year round, however, with appropriately stricter recommendations.
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Responsible for the content
NL Clinic, Katowice
How the content is created
Last updated
15 August 2026
Data confirmed by clinic materials: definition of dermatoheliosis, mechanism involving reactive oxygen species and metalloproteinases, the boundaries of the UVA, UVB and UVC ranges, four degrees of post-sun damage with age brackets, a comparison of the features of photoageing and chronological ageing, the elements of photoprotection, the classification of filters, the mechanism of self-tanners, the benefits of moderate exposure. The material is for information purposes and does not replace a consultation or qualification.
The questions we are asked most often
How does photoageing differ from ordinary skin ageing?
Chronological ageing is a natural, genetically programmed process: the skin gradually thins and loses its regenerative capacity. Photoageing is a pathological process caused by UV radiation, which speeds up this path and adds its own features, above all pronounced pigmentation changes, roughness and telangiectasia.
Do I age through window glass too?
UVA radiation passes through clouds and through window glass and is present all year round. It is mainly responsible for photoageing. That is why photoprotection also makes sense in winter and in rooms with plenty of natural light.
Is sunscreen enough?
Sunscreen is one element of photoprotection, not the whole of it. The others are avoiding the sun during the hours of strongest sunlight, clothing and sunglasses, antioxidants used topically or orally, and supplementation. Supplements do not replace sunscreen.
Is self-tanner safer than the sun?
The main ingredient in self-tanners is dihydroxyacetone, which reacts with amino acids in the stratum corneum of the epidermis and changes its colour. It is regarded as a safe substance and does not cause skin damage. Self-tanner does not, however, protect against UV radiation and does not replace sunscreen.
Are treatments for photoageing only carried out in autumn?
Autumn and winter are more convenient, because consistent photoprotection and lower UV exposure are easier to maintain then. Treatment in summer is possible, but it requires rigorous sun protection and giving up sunbathing.
Does the sun have any benefits for the skin?
Moderate exposure supports vitamin D synthesis, serotonin production and the regulation of the body clock, and it has an anti-inflammatory effect in some skin conditions. In the context of aesthetics, however, excessive exposure does more harm than good, and vitamin D can be supplemented.
Is a sunbed safer than the sun?
No. Sunbed lamps are an artificial source of ultraviolet radiation that causes photoageing just as the sun does. The changes we describe on this page apply to both sources.
Where to start if I notice changes on my skin?
From a skin assessment, not from choosing a treatment. At the consultation we establish which changes are pigmentation related, which are vascular, and which require a dermatological assessment first. We support the assessment of pigmentation changes with digital dermatoscopy, but this supports the decision, it is not a diagnosis.
The content is for information. It does not replace a consultation, an examination or an individual assessment.