“Actinic” Conditions in Dermatology

Introduction

The term ‘actinic’ originates from the Greek word ‘aktinos’, signifying ‘ray’ or ‘beam’. It is often used interchangeably with ‘solar’ to denote morphological changes resulting from prolonged sunlight exposure. While ‘solar’ specifically pertains to sunlight exposure, ‘actinic’ encompasses any radiation capable of inducing tissue changes.[1] We aim to encapsulate dermatological conditions under the term ‘actinic’.

Actinic Keratosis

Actinic keratosis (AK), also known as solar or senile keratosis, is a precancerous skin lesion resulting from chronic exposure to ultraviolet (UV) rays, leading to abnormal proliferation of epidermal keratinocytes. The main contributing factor in the pathogenesis of AK is excessive UV radiation exposure, known to act as a carcinogen, thereby activating molecular signalling cascades and resulting in abnormal regulatory cytokine levels, immunosuppressive effects, abnormal cell differentiation, and impaired apoptosis Clinically, AK presents as rough, skin-coloured to reddish-brown papules, macules, or plaques with adherent yellowish-brown scales, primarily observed on sun-exposed areas such as the face, scalp, neck sides, vermilion border of the lower lip, forearms, and hands [Figure 1]. Symptoms such as itching, pain, or minor trauma-induced bleeding may indicate a higher risk of squamous cell carcinoma progression. Histopathologically, AK exhibits atypical keratinocytes at varying depths of the epidermis, with six recognised variants: hypertrophic, atrophic, Bowenoid, acantholytic, pigmented, and lichenoid.[2]

Figure 1.

Actinic keratosis: Well-defined, hyperpigmented, and yellowish-crusted adherent plaques with irregular borders seen over the vertex region of the scalp

Actinic keratosis may display fluctuating behaviour over time. It may spontaneously regress, remain stable, or progress to invasive squamous cell carcinoma, with most SCCs arising from preexisting lesions. The rate of malignant conversion of actinic keratosis to squamous cell carcinoma ranges from 0.1% to 10%.[2,3]

Actinic Prurigo

Also known as Hutchison’s summer prurigo or hereditary polymorphous light eruption, this is a rare immunologically mediated photodermatosis that results from abnormal photosensitivity to the UVB and UVA spectra. The pathogenesis of actinic prurigo is thought to be due to delayed type-IV hypersensitive response to UVA and UVB radiation mediated by both TH1 and TH2 response in genetically predisposed individuals. HLA-DR4 (specifically DRB1*0407 subtype) is seen in 90% of cases. Clinically, the lesions are characterised by intensely itchy papules or papulovesicles, nodules that typically become excoriated and may develop eczematisation in the sun-exposed areas such as the face and extremities.

A skin biopsy reveals hyperkeratosis, spongiosis, and acanthosis in the epidermis, along with dermal lymphocytic perivascular infiltration. Studies have shown that eosinophil and mast cell infiltration in the affected dermal areas, coupled with elevated IgE levels, correlate with a delayed type IVb hypersensitivity response.[3,4,5]

Chronic Actinic Dermatitis (Actinic reticuloid)

Chronic actinic dermatitis (CAD) is an uncommon, immunologically mediated photodermatosis characterised by infiltrated papules and plaques that predominantly affect sun-exposed skin in response to UV rays [Figure 2]. The pathomechanism involves a delayed-type hypersensitivity reaction to an endogenous antigen generated by UV radiation. This antigen is a byproduct of molecular changes in DNA caused by UV exposure. Under normal circumstances, UV radiation induces localised immunosuppression, preventing the development of clinical lesions even in the presence of such photo-induced antigens. However, in patients with CAD, this immunosuppressive effect is impaired, allowing clinical lesions to form.

Figure 2.

Chronic actinic dermatitis: Diffuse erythematous to hyperpigmented plaques and nodules with areas of erosion seen over the forehead, bilateral periorbital and malar regions, and nose

CAD encompasses a spectrum of conditions, including persistent light reactivity, photosensitive eczema, and actinic reticuloid. Typical clinical presentations include pruritic papules, eczematous and lichenified nodules, and plaques on sun-exposed areas. Histopathology of CAD shows spongiosis and acanthosis, along with superficial and deep dermal perivascular lymphohistiocytic infiltrates. In severe cases, more prominent infiltrates and marked focal lymphocytic exocytosis with irregular nuclear outlines often mimic cutaneous T-cell lymphoma (CTCL).[6]

Disseminated Superficial Actinic Porokeratosis

Disseminated superficial actinic porokeratosis (DSAP) is the most prevalent variant of porokeratosis, typically appearing in the third or fourth decade of life, with a slight female predominance. The etiopathological factors associated with DSAP include genetics, ultraviolet radiation, trauma, infection, and immunosuppression. Mutations in the mevalonate pathway (MVK gene), which confers protection against UV-induced cell death, have been found to be associated with both familial and sporadic forms of DSAP. Clinically, the lesions manifest as asymptomatic, disseminated reddish to brown annular keratotic patches with an atrophic centre and an elevated hyperkeratotic rim at the periphery [Figure 3]. These lesions primarily occur on sun-exposed areas such as the forearms and distal legs. The typical histologic feature of DSAP is the cornoid lamella, a parakeratotic column of cells with an underlying granular layer that is either thin or absent, and with dyskeratotic cells [Figure 4].[7,8]

Figure 3.

Disseminated superficial actinic porokeratosis: Multiple well-defined annular hyperpigmented patches with an atrophic centre and an elevated hyperkeratotic rim at the periphery; multiple healed lesions with post-inflammatory hyperpigmentation and scars seen over the left flexor aspect of the forearm

Figure 4.

Disseminated superficial actinic porokeratosis: Basket weave orthokeratosis with spongiosis, and a keratin-filled invagination with underlying parakeratotic column representing the cornoid lamella. There is hypogranulosis corresponding to the parakeratotic area (H and E × 40)

Actinic Cheilitis

Actinic cheilitis, also known as sailor’s lip, solar cheilosis, or actinic keratosis of the lip, is a premalignant condition caused by chronic sun exposure, primarily affecting the lower lip. The major contributory factors of actinic cheilitis include the physical characteristics of the lips, such as their shape, a thin transitional zone between the oral mucosa and skin, fewer sebaceous glands, and reduced melanin content, all of which increase the likelihood of UV radiation exposure and provide less protection. The pathomechanism involves damage to the tumour suppressor p53 gene due to chronic UV exposure, resulting in the uncontrolled replication of abnormal cells. Initially, the lips may appear red and oedematous, progressing to dry, flaky keratotic patches over time. The characteristic lesions of actinic cheilitis include solitary to multiple greyish-white plaques or nodules with a ‘sandpapery’ texture upon palpation, often blurring the vermillion border of the lips [Figure 5]. Histopathological features include hyperkeratosis, solar elastosis, and epithelial dysplasia, which may vary from mild to severe (dyskeratosis, mitoses, pleomorphism, keratin pearls, and drop-shaped projections), along with perivascular inflammation [Figure 6].[9,10]

Figure 5.

Actinic cheilitis: Erythematous and yellowish-crusted plaques with blurring of the vermillion border seen over the left lower lip mucosa

Figure 6.

Actinic cheilitis: Stratified squamous epithelium with hyperkeratosis a focal parakeratosis. The basal layer exhibits mild-to-moderate nuclear atypia with disordered maturation. The dermis shows solar elastosis, chronic inflammatory infiltrates composed predominantly of lymphocytes. The deep dermis shows perivascular inflammatory infiltrates (H and E × 10)

Actinic Lichen Planus

Actinic lichen planus, also known as lichen planus subtropicus or lichen planus actinicus, is a rare variant of lichen planus that primarily affects children and young adults with darker skin living in tropical or subtropical regions. Although the precise aetiology is uncertain, sun exposure is invariably a significant contributing factor. Various other factors that are likely to predispose individuals to this subtype of lichen planus include genetics, infections, and environmental and hormonal influences. Actinic lichen planus (LP) can manifest clinically in three distinct forms: annular (most common), pigmented, or dyschromic. The characteristic lesions of this variant include well-defined annular or discoid patches or plaques on sun-exposed sites. These lesions typically have a violaceous-to-hyperpigmented centre surrounded by a striking hypopigmented zone [Figure 7]. Both histopathological and dermoscopic findings in actinic lichen planus resemble those found in classical lichen planus [Figure 8]. Histopathological features include hyperkeratosis, wedge-shaped hypergranulosis with orthokeratosis, a linear band-like infiltrate (mostly lymphocytes), saw-toothed rete ridges, and Civatte bodies.[11,12]

Figure 7.

Actinic lichen planus: A single, well-defined violaceous plaque surrounded by a rim of halo seen on the left side of the temporal region

Figure 8.

Actinic lichen planus: Epidermis showing basket weave orthokeratosis, mild spongiosis, wedge-shaped hypergranulosis, basal vacuolar degeneration, saw-toothed rete ridges, and dense lymphocytic infiltrates in the upper dermis (H and E × 40)

Actinic Lichen Nitidus

Also known as lichen nitidus actinicus and Summer Time Actinic Lichenoid Eruption (SALE), this rare variant of lichen nitidus is distinguished by small, pinpoint to pinhead-sized discrete or grouped papules. These papules are typically asymptomatic, flesh-coloured, and have a flat, shiny surface. In actinic LN, photo-exposed regions such as the forehead, malar area of the face, ‘V’ area of the neck, and extremities are primarily affected. The characteristic histopathologic features include parakeratosis, an absent granular layer, basal cell degeneration, and a ‘ball-in-claw’ arrangement of lymphocytic infiltrate involving the papillary dermis [Figure 9].[13,14]

Figure 9.

Actinic lichen nitidus: Basket weave orthokeratosis, with thinned out epidermis with occasional basal cell vacuolar degeneration, and a well-circumscribed, lymphohistiocytic infiltrate present in the upper dermis encircled by elongated rete ridges in a claw-like fashion (H and E × 10)

Actinic Granuloma

Actinic granuloma, also known as O’Brien actinic granuloma, is an uncommon granulomatous condition affecting photo-damaged skin. It is a granulomatous response to photodamage, where histiocytes and multinucleated foreign-body type cells engulf elastotic fibres against a background of solar elastosis. Lesions manifest as solitary or multiple annular or polycyclic formations with an erythematous, elevated edge that may extend centrifugally, measuring up to 6 cm [Figure 10]. The centre typically displays hypopigmentation and atrophy. It predominantly affects photo-exposed regions such as the face, chest, neck, or upper limbs. Biopsy of the lesion, usually taken radially across the elevated edge and stained with van Gieson stain, reveals three distinct zones: normal skin with actinic elastosis, the thickened annulus showing a histiocytic and giant cell inflammatory reaction in relation to elastotic fibres, and the absence of elastic tissue in the centre of the lesion (within the annulus) [Figure 11].[15,16] Adequate sun protection can improve the condition, and no treatment is of proven benefit.

Figure 10.

Actinic granuloma: Multiple annular skin-coloured plaques with polycyclic and elevated edges seen on the right side of the neck and anterior trunk

Figure 11.

Actinic granuloma: Epidermis showing basket-weave orthokeratosis with flattened rete pegs. The dermis shows adnexal structures along with collection of lymphocytes, histiocytes, and foreign body giant cells engulfing the elastotic fibres (H and E × 10)

Actinic Purpura

Also known as Bateman’s purpura, senile purpura, traumatic purpura, and solar purpura, this condition primarily affects the elderly, with occasional occurrences in younger individuals. UV exposure damages connective tissue, compromising the structure and support of the microvasculature. In elderly patients, the weakened connective tissue in the dermis makes blood vessels prone to rupture, even from minor trauma, leading to blood extravasation. Clinically, it is characterised by unsightly ecchymoses and dark purple macules, typically found on the arms or legs [Figure 12].[17]

Figure 12.

Actinic purpura: Multiple well-defined violaceous macules and patches seen over the extensor aspect of the left lower leg

Actinic Elastosis

Actinic elastosis, also known as solar elastosis, is a manifestation of hypertrophic skin photodamage resulting from cumulative lifetime exposure to ultraviolet radiation. Clinically, it presents with yellowish discoloration and thickening of the skin, particularly on the forehead, bald scalp, and posterior aspect of the neck [Figure 13]. Histologically, it is characterised by diminished collagen and the accumulation of amorphous masses containing degenerated elastic fibres in the papillary and upper reticular dermis.[18,19]

Figure 13.

Actinic elastosis: Wrinkling and sagging of the skin with exaggerated skin texture seen on the face

Actinic Comedonal Plaque

Also referred to as an ectopic variant of Favre-Racouchot syndrome or nodular actinic elastosis with cysts and comedones, this condition is a clinical variant of actinic elastosis. It is primarily reported in Caucasian men over the 5^th decade (with a 6% prevalence), but rare cases have also been seen in dark-skinned individuals, including Indians. Males are more commonly affected, likely due to increased sun exposure and smoking.[20] Clinically, it features yellowish confluent plaques studded with comedones with symmetrical involvement, typically located on the neck, thorax, dorsal nose, helix of the ears, and forearms [Figure 14]. The histopathology shows solar elastosis, dermal fibrosis, perifollicular lymphocytic infiltrate, and keratin-plugged hair follicles [Figure 15].[20]

Figure 14.

Actinic comedonal plaque: Multiple well-defined confluent papules studded with comedones seen on the left cheek

Figure 15.

Actinic comedonal plaque: Epidermis with hyperkeratosis, parakeratosis, and focal acanthosis, mild dilated follicular infundibula, some containing keratinous plugs, consistent with comedonal change. The underlying dermis shows mild perivascular lymphocytic infiltrate (H and E X40)

Actinic Folliculitis

Also known as actinic superficial folliculitis, acne aestivalis, or Mallorca acne, this is an uncommon, recurrent seasonal photodermatosis. UV radiation-induced epidermal thickening and follicular infundibular occlusion trigger inflammation. Clinically, it presents as non-pruritic, monomorphic pustules and papules that appear 4–24 hours after sunlight exposure, predominantly on the face, upper chest, and arms. The key histological feature is dilated keratin-filled follicles within a matrix of amorphous degraded collagen.[19,21]

Actinic Lentiginosis

Actinic lentigines, also known as solar lentigines, lentigo senilis, or liver spots, predominantly affect elderly individuals and typically appear after the fifth decade of life due to UV exposure. This condition represents chronically photodamaged skin with signs of aging. Mutations in FGFR3 and PIK3CA have been identified in both solar lentigo and seborrheic keratosis, suggesting a shared genetic origin. They are macular, tan, and can be large with irregular borders. Actinic lentigines are well-defined, hyperpigmented macules that do not fade during winter. Clinically, they must be differentiated from ephelides (freckles), as ephelides may fade with age and during winter. The histological hallmark of actinic lentigines is elongated rete ridges with club-shaped projections into the dermis. Histopathologically, ephelides are characterised by larger melanocytes with more dendrites and larger melanosomes, whereas in actinic lentigines, melanocytes and melanosomes are of normal size, but elongated rete ridges are present.[19,22]

Actinic Telangiectasia

Also known as solar telangiectasia, this condition is often caused by chronic sun exposure. It is clinically characterised by small telangiectatic macules in areas frequently exposed to sunlight, such as the face, neck, and chest.[19] Table 1 summarises the key features of the actinic conditions in dermatology.

Table 1.

Summary of features of actinic conditions in dermatology

Conditions	Age of presentation	Gender	Most common site	Clinical features	Histopathology	Differential diagnosis
Actinic keratosis	Elderly individuals	Male > Female	Sun-exposed areas, especially the face, scalp, neck sides, vermilion border of the lower lip, forearms, and hands	Rough, skin-coloured to reddish-brown papules, macules, or plaques with adherent yellowish-brown scales	• Hypertrophic: parakeratosis, orthokeratosis & prominent irregular acanthosis • Atrophic: thin epidermis • Lichenoid: band-like lymphocytic infiltrates in DEJ, scattered apoptosis, and vacuolar changes in the basal layer • Acantholytic: suprabasal clefting between atypical keratinocytes • Pigmented: increased melanin in the basal keratinocytes and melanocytes; melanophages- papillary dermis • Proliferative: dermal projections of nested atypical keratinocytes; dense dermal inflammation • Bowenoid: near full thickness atypia, usually focal Pagetoid: pale cells	• Seborrheic keratosis, verruca vulgaris, benign lichenoid keratosis, stucco keratosis, porokeratosis, discoid lupus erythematosus, Bowen’s disease, and squamous cell carcinoma
Actinic prurigo	Prepubescent individuals (mean onset- before 10 years)	Females	Face (especially over the zygomatic arches, nasal bridge &lower lip) Extremities	Intensely itchy, erythematous papules, papulovesicles & nodules May get excoriated, resulting in eczematisation, scarring, and hyper- or hypopigmentation	Epidermis: Hyperkeratosis, spongiosis, and acanthosis Dermal lymphocytic perivascular infiltration	• Polymorphous light eruption (PMLE) • Atopic eczema, • Insect bite reactions • Prurigo nodularis
Chronic actinic dermatitis (Actinic reticuloid)	Elderly in 5th to 6th decade	Predominantly males	Face, neck, upper chest in a V distribution, and backs of hands	• Pruritic papules, eczematous and lichenified nodules, and plaques on sun-exposed areas	• Spongiosis, acanthosis, & exocytosis • Perivascular lymphocytic infiltrate with eosinophils • Increased dermal dendrocytes & increased T-lymphocyte infiltration	• Air-borne contact dermatitis (ABCD), photo-aggravated allergic contact dermatitis, atopic eczema, or photosensitivity secondary to drugs, and cutaneous T-cell lymphoma
Disseminated superficial actinic porokeratosis	Third or fourth decade of life	Slight female predominance	• Sun-exposed areas such as the forearms and distal legs	• Asymptomatic, disseminated reddish to brown annular keratotic patches with an atrophic centre and an elevated hyperkeratotic rim at the periphery	• Cornoid lamella- a parakeratotic column of cells with an underlying granular layer that is either thin or absent, and with dyskeratotic cells	• Actinic keratoses, granuloma annulare, lichen planus, seborrheic keratoses, tinea corporis, and flat warts
Actinic cheilitis	Increased age-especially over 60 years	Male > Female	Lower lip including vermillion border	• Solitary to multiple greyish-white plaques or nodules with a ‘sandpapery’ texture upon palpation	• Hyperkeratosis, solar elastosis, and epithelial dysplasia, which may vary from mild to severe (dyskeratosis, mitoses, pleomorphism, keratin pearls, and drop-shaped projections), along with perivascular inflammation	• Squamous cell carcinoma, basal cell carcinoma, malignant melanoma, herpes, leucoplakia, and various forms of cheilitis
Actinic lichen planus	Children and young adults	May affect females than males	• Face (especially the forehead, cheeks, and lips) • Upper chest, the extensor surface of the distal forearms, and the dorsal surface of the hands	• Clinically in three distinct forms: annular (most common), pigmented, or dyschromic • Well-defined annular or discoid patches or plaques on sun-exposed sites • Lesions typically have a violaceous to hyperpigmented centre surrounded by a striking hypopigmented zone	• Hyperkeratosis, wedge-shaped hypergranulosis with orthokeratosis, a linear band-like infiltrate (mostly lymphocytes), saw-toothed rete ridges, and Civatte bodies	• Discoid lupus erythematosus, PMLE, granuloma annulare, and lichen planus pigmentosus
Actinic lichen nitidus	Children and young adults	No gender predilection reported	• Photo-exposed regions such as the forehead, malar area of the face, ‘V’ area of the neck, and extremities	• Asymptomatic, flesh-coloured, and have a flat, shiny surface	• Parakeratosis, an absent granular layer, and basal cell degeneration • A ‘ball-in-claw’ arrangement of lymphocytic infiltrate involving the papillary dermis
Actinic granuloma	Middle-aged individuals in the 3rd decade or younger	Female > males	• Face, chest, neck, or upper limb	• Solitary or multiple annular or polycyclic formations with an erythematous, elevated edge that may extend centrifugally, measuring up to 6 cm • The centre typically displays hypopigmentation and atrophy	• Biopsy of the lesion, stained with van Gieson stain, reveals three distinct zones: • Normal skin with actinic elastosis • Thickened annulus- histiocytic and giant cell inflammatory reaction in relation to elastotic fibres Absence of elastic tissue in the centre of the lesion (within the annulus)	Granuloma annulare, Necrobiosis lipoidica, elastosis perforans serpiginosa, and sarcoidosis
Actinic purpura	Elderly	No sex predilection	• Typically found on the forearms, hands, legs, face & neck	• Ecchymoses and dark purple macules • Surrounding skin- thin, pigmented, and inelastic • Often accompanied by other photo-aging features such as wrinkles, lentigines, yellowish hue, actinic keratosis, and pseudo scars	• Lesion-thin epidermis with many abnormal keratinocytes in a disorderly pattern • Dermis shows extravasation of red blood cells and hemosiderin deposition with no inflammatory cells • Surrounding skin with solar elastosis appears as blue homogenised elastotic material at the base of the epidermis • Amount of collagen- markedly decreased	• Steroid-induced purpura • Physical trauma • Anticoagulant use, scurvy, vitamin C, and K deficiencies • Psychogenic purpura, palpable purpura Primary systemic amyloidosis
Actinic elastosis	After the fourth decade	-	Forehead, bald scalp, and posterior aspect of the neck	Yellowish discoloration and thickening of the skin	• Diminished collagen and the accumulation of amorphous masses containing degenerated elastic fibres in the papillary and upper reticular dermis	• Plane xanthoma • Pseudoxanthoma elasticum (PXE) • Colloid milium
Actinic comedonal plaque	Typically over the 5th decade	Predominantly men	• Arm, forearms, neck, chest, dorsum of the nose, and helix of the ears	• Solitary nodular plaques with a cribriform appearance and comedone-like structures • Confluent plaques are composed of erythematous to bluish papules and nodules	• Dilated keratin-filled follicles are present within areas of elastotic, amorphous material and degenerated collagen • The overlying epidermis is usually dyskeratotic and atrophic	• Acne comedones, milia, colloid milium, syringomas, trichoepitheliomas, and sebaceous hyperplasia • Basal cell carcinoma, amyloidosis, and nodular chondrodermatitis of the helix
Actinic folliculitis	Young to middle-aged adults	Affects both genders equally	Face, upper chest, and arms	• Non-pruritic, monomorphic pustules and papules that appear 4–24 hours after sunlight exposure	• Dilated keratin-filled follicles within a matrix of amorphous degraded collagen	• Polymorphic light eruption, miliaria, papulopustular rosacea, photo-aggravated rosacea, and photo-aggravated acne vulgaris
Actinic lentiginosis	Elderly individuals (typically appear after the 5th decade of life	-	• Face in both sexes and the shoulders in males	• Well-defined, tan to hyperpigmented macules with irregular borders; they do not fade during winter	• Elongated rete ridges with club-shaped projections into the dermis • Melanocytes and melanosomes- normal size	• Seborrheic keratosis, lentigo maligna, junctional nevus, freckles, lichenoid keratosis, pigmented BCC, and other types of lentigines

Conclusion

To conclude, numerous dermatological conditions stem from photo-induced (actinic) causes, exhibiting distinct pathomechanisms and morphologies yet sharing a common distribution pattern. This article compiles a variety of actinic conditions in dermatology, highlighting their unique characteristics that serve as diagnostic clues.

Conflicts of interest

There are no conflicts of interest.

Funding Statement

Nil.