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Melanoma

Skin Conditions
Melanoma
What is melanoma?

Melanoma is a malignant tumor that originates from melanocytes located at the dermoepidermal junction. It is most commonly found on the skin but can also appear in the eye (such as the conjunctiva and iris), the meninges, and the mucous membranes. Melanoma lesions are typically heavily pigmented, although amelanotic tumors (i.e., lacking dark coloration) also exist. It is considered the most aggressive form of skin cancer because it can metastasize and is potentially life-threatening.

Melanoma
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The epidemiology of melanoma

Melanoma accounts for approximately 4–5% of all cancers. It primarily affects individuals of white ethnicity and is rare among Black and Asian populations. The incidence of the disease is significantly higher in Northern European countries, particularly in the Scandinavian region. In Greece, the rates are lower compared to other European countries, with approximately 12–13 new cases per 100,000 inhabitants annually. The average age at diagnosis is estimated at around 55 years, and both sexes appear to be affected equally.

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Risk factors for the development of melanoma

Key risk factors for the development of melanoma include:

  • Personal history of melanoma
  • Family history of melanoma
  • Inherited mutations in the CDKN2A and MC1R genes
  • Xeroderma pigmentosum
  • Atypical mole syndrome
  • Immunosuppression
  • Exposure to ultraviolet radiation – sunburns and a history of tanning bed use, especially at a young age
  • Phenotypic characteristics (Fitzpatrick skin phototypes I and II)
  • A high number of melanocytic nevi (more than 100)
  • Presence of multiple dysplastic nevi
  • Large congenital nevi (greater than 20 cm in adults).
Molecular classification of melanoma

The molecular classification refers to alterations in the following major signaling pathways:

  • The RAS–RAF–MEK–ERK pathway
  • The p16^INK4A–CDK4–RB pathway
  • The ARF–p53 pathway
  • And, to a lesser extent, the PTEN–PI3K pathway.
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What are the warning signs of melanoma

Anything that appears on our body from the list below should prompt a visit to the dermatologist for clinical and dermoscopic evaluation:

  1. A new mole appearing after the onset of puberty, especially in adults or the elderly, that shows changes in shape, color, or size
  2. An existing mole that changes in shape, color, or size
  3. Any mole with more than three colors or loss of symmetry
  4. A mole that bleeds or itches without prior trauma
  5. Any new persistent lesion—pigmented or vascular—without a clear diagnosis
  6. A new longitudinal pigmented streak on a nail, especially if it involves the nail matrix
  7. An enlarging subungual lesion
The clinical types of melanoma

Melanoma is classified into the following most common clinical types:

  • Superficial Spreading Melanoma (approximately 70% of cases): Initially characterized by horizontal (radial) growth, later progressing to vertical growth with the formation of a nodule. It typically begins as a heavily pigmented macule that spreads superficially, showing shades of brown and black with areas of red, gray, and white. As it invades deeper, a nodule may develop.
    • Nodular Melanoma (10–15%): Characterized by the formation of a dark papule (a small, solid skin elevation ranging from a pinhead to 1 cm in diameter) that progresses into a nodule which may ulcerate.
    • Acral Lentiginous Melanoma (less than 5%): Occurs on the soles, palms, and beneath the nails. As it thickens, the nail may stop growing normally. Clinically, it resembles lentigo maligna and superficial spreading melanoma.
    • Lentigo Maligna Melanoma (5–8%): Seen mainly in older individuals in areas of chronic sun exposure (face, neck). It arises from a lentigo maligna lesion, part of which gradually thickens and may become nodular, indicating invasion through the basement membrane. It typically exhibits multiple colors within the lesion.
    • Amelanotic Melanoma (about 0.5%): A rare and often nodular melanoma subtype that lacks pigmentation, making it more difficult to recognize.
    • Desmoplastic Melanoma (less than 0.5%): Rare, observed in elderly individuals in chronically sun-exposed areas. It appears as a nodule or plaque and is a dermal tumor composed of spindle-shaped cells without melanin. It often extends into the subcutaneous fat and infiltrates nearby nerves.
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What are the dermoscopic criteria for melanoma?

A. General dermoscopic structure

Polymorphous pattern, characterized by:

  • Asymmetry
  • Four different colors
  • Three types of dermoscopic structures: reticular, globular, and homogeneous

B. Specific dermoscopic findings

Melanoma-specific criteria include:

  • Atypical pigment network
  • Irregular dots and globules
  • Irregular streaks, blue-white structures, irregular blotches
  • Polymorphous vessels
  • Areas of ulceration, regression structures, crusts

There are also specialized dermoscopic criteria for:

  • Facial melanoma
  • Acral (palmar and plantar) melanoma
  • Subungual melanoma
  • Amelanotic melanoma
  • Pediatric melanoma
Melanoma in childhood

It can be divided into preadolescent and adolescent categories. The preadolescent type is further classified into:

  • Congenital (present in utero or at birth)
  • Neonatal (within the first year of life)
  • Childhood melanoma (up to puberty)

Its annual incidence is estimated at 0.8 cases per million children. Recent studies show an increasing frequency, particularly in adolescent melanoma.

Due to the rarity of pediatric melanoma, clear clinical and dermoscopic criteria have not yet been established. Lesions are more commonly non-pigmented and nodular, often resembling pyogenic granulomas or non-pigmented Spitz nevi.

In clinical practice, melanoma is suspected in:

  • Congenital pigmented nevi larger than 4 cm in diameter
  • Spitz nevi appearing after the age of 12.
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What is the role of the dermatologist in melanoma?

Dermatologists are confronted daily with a large number and variety of pigmented skin lesions. It is estimated that the ratio of melanomas to benign skin lesions is approximately 1 in 200,000. The dermatologist’s responsibility is to identify the malignant lesion among thousands of nevi—early and at a curable stage.

Thus, the dermatologist’s role is fundamental and includes:

  • Early detection: through clinical examination, dermoscopic analysis, and annual preventive dermoscopic screening (total body scan)
  • Initial excision: confirmation of diagnosis and disease staging
  • Postoperative regular follow-up
Primary excision methods

The primary method of excision is surgical removal, most commonly through elliptical excision.

Surgical excision is the gold standard approach, performed with 2–3 mm of healthy peripheral margins and including subcutaneous tissue, when feasible depending on the lesion’s location.

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Although this is a common myth, it is not scientifically accurate. Removing a mole that does not show any signs of malignancy does not cause skin cancer.

In cases where cancer developed after mole removal, it means that the mole was already malignant and had not been completely excised from the beginning. Unfortunately, this misconception has led many patients to delay seeking medical attention—often resulting in diagnosis at a more advanced stage of the disease.

If you notice any changes in an existing lesion or the appearance of a new one on your skin, you should consult your dermatologist immediately.

As a general rule, according to the Hellenic Society of Dermatology and Venereology, melanoma is characterized by a set of clinical features known as the ABCDE rule, which stands for:

  • A – Asymmetry: one half of the lesion does not match the other
  • B – Border: irregular, notched, or blurred edges
  • C – Colour: uneven color or recent change in color; presence of multiple shades
  • D – Diameter: greater than 6 mm
  • E – Evolving: a lesion that is changing in size, shape, color, or behavior (such as bleeding or itching)

Any clinical change in a skin lesion that falls under one or more of these categories should be promptly evaluated by your dermatologist. Early diagnosis is your strongest ally in treatment!

Do you have any questions or concerns? We are here to help.

Basal cell carcinoma

Skin Conditions
Basal cell carcinoma
What is basal cell carcinoma (epithelioma)?

Basal cell carcinoma (BCC) is a malignant skin tumor that grows slowly and very rarely metastasizes, but it is locally invasive and destructive. It belongs to the group of non-melanocytic skin cancers. It arises from undifferentiated cells of the basal layer of the epidermis and skin appendages. BCC is the most common malignant skin tumor in the white population, accounting for 75% of all skin cancers.

BASAL CELL CARCINOMA
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The clinical presentation of basal cell carcinoma

Basal cell carcinoma may initially present as:

  1. A pink papule that gradually enlarges
  2. An erosion that shows no tendency to heal
  3. A pearly-colored nodule with a smooth, shiny surface and the characteristic presence of fine telangiectasias

The typical clinical appearance of basal cell carcinoma usually becomes clearer after a considerable period from its onset. Patients often mistake it for another skin condition, such as xerosis or eczema, before consulting a dermatologist.

 

Basal cell carcinomas typically appear (in 80% of cases) on the face and neck—especially on the eyelids, zygomatic area, cheeks, forehead, upper lip, and nose—and less frequently in other areas of the body. In most cases, they develop in sun-exposed areas and usually appear as solitary lesions. The occurrence of two or more basal cell carcinomas in the same individual is much rarer.

 

The differential diagnosis is broad and includes both benign and malignant skin conditions and tumors. On one hand, basal cell carcinoma may mimic benign conditions such as intradermal nevi, sebaceous hyperplasia, molluscum contagiosum, psoriasis, and eczema, potentially delaying diagnosis. On the other hand, it may clinically resemble malignant tumors such as squamous cell carcinoma, keratoacanthoma, Bowen’s disease, or even melanoma.

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The clinical types of basal cell carcinoma
  • According to Lever, there is a wide variety of clinical types of BCC. More specifically, it is classified into:

    • Nodular–ulcerative (the most common type)
    • Pigmented
    • Sclerodermiform (morpheaform)
    • Superficial or pagetoid
    • Fibroepithelioma of Pinkus
    • Multiple basal cell carcinoma syndrome
    • Linear and generalized follicular basal cell nevus
    • Basex-Rombo syndrome
    • BCC arising on sebaceous nevus of Jadassohn
    • Basosquamous carcinoma (metatypical carcinoma).
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The epidemiology of basal cell carcinoma

The incidence of basal cell carcinoma (BCC) in the United States is approximately 900,000 cases per year. It occurs more frequently in men than in women, although a rising trend in female cases has been observed in recent years.

The annual incidence rate of BCC is 146 per 100,000 inhabitants in the U.S., 132 per 100,000 in Europe, and between 1,000–2,000 per 100,000 in Australia. Although no official global statistics are available, a yearly increase in incidence of around 10% is estimated worldwide.

In Greece, there are no official data; however, an increasing number of cases are being recorded in patients presenting to dermatology clinics. Basal cell carcinoma is extremely rare among individuals of Black ethnicity.

It typically appears after the age of 40, with incidence increasing with age. About 80% of cases occur in patients over 60 years old. Nevertheless, it can develop at any age, even in children (e.g., in Gorlin syndrome or in immunosuppressed individuals). Notably, the highest rate of increase in BCC cases is observed in the 30–49 age group.

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What are the predisposing factors for the development of BCC?
  1. Ultraviolet (UV) radiation
    Prolonged and long-term sun exposure during childhood and adolescence, especially when associated with frequent sunburns, is considered the most important risk factor.
  2. Individual phenotypic characteristics
    Fair skin, blond or red hair, freckles, combined with sunburns in childhood, are associated with an increased risk of developing BCC.
  3. Radiodermatitis
    Caused by therapeutic use of Roentgen rays.
  4. Heredity
    Conditions such as the basal cell nevus syndrome (Gorlin syndrome), xeroderma pigmentosum, and other rare genetic syndromes.
  5. Post-burn scars, chronic non-healing ulcers, sebaceous nevi, and adnexal hamartomas.
  6. Chronic occupational or recreational outdoor activities.
  7. Occupational exposure to arsenic.
  8. History of photochemotherapy (PUVA), phototherapy (UVB), or radiotherapy.
  9. Immunosuppression
    Due to medications, non-Hodgkin lymphoma, or HIV infection.
  10. Personal history of basal cell carcinoma It is estimated that 40–50% of patients with BCC will develop a new neoplasm within the next five years.
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The treatment and management of basal cell carcinoma

The treatment options for BCC are individualized based on the clinical presentation and the patient’s medical history, and include the following:

  • Surgical excision with histopathological examination
  • Microscopically controlled surgery (MOHS)
  • Electrocautery, dermabrasion, and CO₂ laser treatment
  • Cryosurgery
  • Radiotherapy
  • Photodynamic therapy
  • Retinoids
  • Topical chemotherapeutic agents (podophyllin, 5-fluorouracil, imiquimod)
  • Interferon (intralesional injections)
  • Vismodegib – an orally available small-molecule inhibitor of the Hedgehog signaling pathway.
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The prognosis of basal cell carcinoma

The prognosis is excellent when BCC is diagnosed and treated promptly, appropriately, and thoroughly. It rarely metastasizes. According to studies, the likelihood of metastasis ranges from 0.0028% to 0.1%. Metastasis primarily occurs in extensive, ulcerated, and especially neglected BCCs. The most common sites of metastasis include regional lymph nodes, lungs, bones, and others.

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What is Gorlin syndrome (multiple basal cell carcinoma syndrome)?

It is a rare syndrome inherited in an autosomal dominant manner, with an estimated frequency of 1 in 56,000 individuals. It is characterized by the development of basal cell carcinomas beginning in childhood, and even infancy, which continue to appear throughout life.

Lesions primarily occur in sun-exposed areas, with characteristic involvement of the palms. Associated manifestations include palmar pits, odontogenic cysts of the lower jaw, hypertelorism, and other tumors (such as ovarian fibromas and medulloblastoma).

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Here comes the good news: BCC very rarely causes metastases and primarily has a locally destructive effect on the skin and underlying tissues. Furthermore, early diagnosis and treatment lead to cure without resulting in disfigurement or aesthetic alterations caused by extensive surgical procedures.

There are certain specific subtypes of BCC (such as superficial BCC) that may be treated with local destructive methods (e.g., cryotherapy). However, surgical excision of BCC has a significantly lower recurrence rate compared to these methods.

BCCs have a tendency to recur, especially those located on the head and nose. For this reason, regular and systematic follow-up is recommended after treatment—not just in the short term.

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Squamous Cell Carcinoma

Skin Conditions
Squamous Cell Carcinoma
What is it?

Squamous cell carcinoma (SCC), also known as squamous cell epithelioma, is a malignant tumor originating from the keratinocytes of the epidermis. It is the second most common type of skin cancer. The earlier SCC is diagnosed, the easier it is to treat. Early diagnosis leads to cure in the majority of cases.

SQUAMOUS CELL CARCINOMA- SCC
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Which areas of the body are most commonly affected

SCC is found both on the skin and on mucous membranes, where it represents the most common type of cancer. It develops either de novo (from the beginning),

or more commonly, on pre-existing cutaneous or mucosal epithelial precancerous lesions.

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Clinical presentation of the lesion

Squamous cell carcinoma usually presents as an ulcerated nodule with an irregular, reddish, exophytic surface that is slightly painful and easily bleeds. The base of the tumor is indurated due to infiltration, and this “board-like” hardness often extends beyond the visible margins of the tumor. The floor appears dirty and contains either easily bleeding papillomatous outgrowths or, more commonly, white spots corresponding to areas of keratinization. Often, the ulceration is covered by a crust. In other cases, SCC may present as a raised exophytic mass without a tendency to ulcerate.

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The epidemiology of SCC

The incidence varies across different geographic regions. The highest rates are observed in Australia, with an annual incidence of 250 cases per 100,000 inhabitants. In the United States, the annual incidence is 146 cases per 100,000 white men, 100 per 100,000 white women, and 3 per 100,000 individuals of Black ethnicity.

These data highlight the significant protective role of melanin in the epidermal keratinocytes against the harmful effects of ultraviolet radiation. The incidence of squamous cell carcinoma increases with age, due to the cumulative effect of UV exposure.

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The etiopathogenesis of squamous cell carcinoma

Ultraviolet radiation plays a prominent role in the development of squamous cell carcinoma, with its effects being cumulative. Additionally, skin pigmentation is a significant factor, as individuals with fair skin phototypes are more susceptible to skin cancer.

Other factors with carcinogenic potential for the skin include:

  • Human papillomavirus (HPV) types (6, 11, 16, etc.)
  • Ionizing radiation
  • Infrared radiation
  • Photochemotherapy (PUVA)
  • Arsenic
  • Polycyclic aromatic hydrocarbons
  • Therapeutic use of nitrogen mustard (in cutaneous lymphomas)
  • Chronic non-healing ulcers
  • Scars and chronic inflammatory conditions
  • Immunosuppression (e.g., HIV infection, organ transplant recipients)
  • Heredity
  • Genodermatoses
  • Precancerous lesions
  • Chronic dermatoses
  • Smoking (especially in cases of lip squamous cell carcinoma)
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Which precancerous dermatoses are associated with the development of squamous cell carcinoma

a. Hyperkeratoses, such as actinic keratoses, solar keratoses, cutaneous horn, and arsenical keratosis
b. Porokeratoses (Mibelli type and disseminated superficial actinic porokeratosis)
c. Epidermal sebaceous nevus of Jadassohn
d. Bowenoid papulosis
e. Actinic cheilitis
f. Leukoplakia

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Which non-precancerous dermatoses predispose to the possible development of squamous cell carcinoma

Non-precancerous dermatoses with a potential risk of developing squamous cell carcinoma include discoid lupus erythematosus, chronic non-healing ulcers, erosive lichen planus of the mucous membranes, lichen sclerosus et atrophicus, deep fungal infections, hidradenitis suppurativa, tertiary syphilis, epidermolysis bullosa, lymphogranuloma venereum, granuloma inguinale, and others.

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The clinical types of squamous cell carcinoma

The clinical types of squamous cell carcinoma include:

1. In situ forms: Bowen’s disease, Paget’s disease, Queyrat’s erythroplasia, and leukoplakia
2. De novo SCC
3. SCC arising from precancerous lesions
4. SCC of the extremities

5. SCC of the lower lip
6. SCC of the oral cavity
7. SCC of the genitalia: vulva, penis, scrotum
8. Verrucous carcinoma (a rarer form of squamous cell carcinoma).

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Treatment of squamous cell carcinoma

a. Surgical excision with safety margins of 0.5–1 cm, when feasible, followed by histopathological examination
b. MOHS micrographic surgery (the ideal method of removal)
c. In cases of lymph node involvement, MOHS surgery combined with lymph node dissection is recommended
d. In the presence of metastases, initial chemotherapy is advised, followed by surgical excision and then radiotherapy.

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Individuals considered to be at higher risk for developing squamous cell carcinoma include:

  • Older adults
  • Individuals with a hereditary predisposition
  • People with fair skin and light-colored eyes who burn easily in the sun and do not tan
  • Individuals with blond or red hair
  • Males
  • People with occupational or recreational outdoor exposure and chronic ultraviolet radiation exposure
  • Individuals exposed to ionizing radiation
  • People with long-term exposure to substances such as arsenic
  • Patients with HPV infection
  • Immunosuppressed individuals (e.g., those with HIV)

The removal of a squamous cell carcinoma does not eliminate the possibility of developing a new cancerous lesion in the same or another area of the body. For this reason, follow-up examinations with a dermatologist every six months are recommended. In the event of any clinical change in a pre-existing lesion or the appearance of a new one, it is important to inform your dermatologist immediately.

Do you have any questions or concerns? We are here to help.

Actinic keratoses

Skin Conditions
Actinic keratoses
What are they?

Actinic keratoses are common, persistent, scaly lesions found on the sun-exposed areas of the skin in elderly individuals with fair skin. They represent intraepithelial dysplasias of the skin and are the most frequent precancerous lesions in humans. Their size can range from a few millimeters to large confluent plaques measuring several centimeters, especially in patients with significant photoaging.

Actinic keratoses
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1)What causes actinic keratoses?

Actinic keratoses are caused by the long-term harmful effects of ultraviolet radiation on the keratinocytes of the epidermis. They are the most common precancerous lesions of human skin and are now considered intraepithelial neoplasms (in situ squamous cell carcinoma) of the skin. They occur more frequently in men, which is usually related to the shorter hair length on the male scalp.

High-risk groups for developing actinic keratoses include individuals with prolonged sun exposure due to occupational reasons (farmers, fishermen, etc.) or recreational activities (outdoor athletes, mountaineers, etc.), transplant recipients, and patients under chronic immunosuppression. The risk of developing squamous cell carcinoma in patients with actinic keratosis is estimated at 10 to 20%, especially in cases with multiple lesions and duration longer than 10 years.

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How do actinic keratoses present clinically

Actinic keratoses clinically present as erythematous macules or plaques that sometimes coalesce, with adherent yellowish-white scales on their surface. When palpated, they have a sandpaper-like texture. Attempting to remove the scales causes pain and leaves slight bleeding, which is a characteristic clinical diagnostic sign.
The clinical spectrum includes, besides typical actinic keratosis, the expanding pigmented actinic keratosis, hypertrophic actinic keratosis, lichenoid actinic keratosis, Bowen’s type actinic keratosis, and actinic cheilitis. Actinic keratoses are also considered precursor lesions to the formation of cutaneous horns.

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Dermoscopy findings of actinic keratoses

A. In non-pigmented actinic keratoses, the following are observed:

  • “Strawberry pattern” on a red background
  • Non-focused vessels around open hair follicles
  • White rosettes (whitish dots resembling a “rosette” or four-dot sign)

B. In pigmented actinic keratoses, the following are observed:

  • Gray-brown granules and globules around follicular openings
  • Mixed ring-like and granular pattern
  • Rhomboid structures
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Treatment options for actinic keratoses

There are several therapeutic options for managing actinic keratoses. Depending on the specifics of each case, the dermatologist’s experience, and the equipment available, each dermatologist can choose among the following:

  1. CO₂ – Er:YAG laser
  2. Cryotherapy
  3. Electrocoagulation
  4. Topical application of 5‑FU
  5. Topical application of imiquimod cream
  6. Topical application of diclofenac cream
  7. Topical application of ingenol mebutate
  8. Topical photodynamic therapy
  9. Surgical excision – histological examination if invasion to squamous cell carcinoma is suspected
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To prevent the appearance of actinic keratoses, the individual must practice photoprotection. It is recommended to avoid solar radiation, especially between 10 a.m. and 4 p.m., seek shade, and avoid sunburns. Complementary sun‑protection measures include choosing appropriate clothing (e.g., hat, sunglasses) and using an umbrella at the beach. Let us not forget that the use of sunscreens with a high protection factor against UVB and UVA radiation should be a daily practice during sunny months on sun‑exposed areas of the body. Regular dermatological examinations, dermoscopy, and mapping by a dermatologist, particularly in high‑risk individuals, constitute an important measure for timely prevention and treatment.

Finally, self‑examination for any changes in the clinical features of one’s body helps in the early detection of recurrences or new lesions.

Actinic keratoses are precancerous lesions, because over time they are likely to evolve into a type of cancer, squamous cell carcinoma. However, only a dermatologist can diagnose the lesion and recommend the appropriate method of management.

Skin with extensive photoaging and actinic keratoses requires, in addition to regular dermatological examinations, periodic self‐examination. Any change in a preexisting lesion, particularly in sun‐exposed areas (such as the onset of pain, bleeding, or morphological changes in shape, size, color, etc.), as well as the appearance of new lesions, should prompt the patient to seek immediate dermatological assessment.

Absolutely YES! Mapping and dermoscopy constitute our most important weapon for the prevention and timely diagnosis–treatment, NOT ONLY of melanocytic (melanoma) but also of non‑melanocytic cancerous and precancerous skin lesions, such as actinic keratoses.

Additionally, the presence of actinic keratoses and the chronic, cumulative exposure to ultraviolet radiation that preceded their appearance constitute a predisposing factor for the potential development of other malignant skin tumors.

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SeborrHeic keratoses

Skin Conditions
SeborrHeic keratoses
What are seborrheic keratoses?

Seborrheic keratoses are very common benign lesions of the epidermis, exhibiting a wide variety of clinical appearances and arising from the proliferation of epidermal cells. Specifically, there is an increase in the thickness of the stratum corneum, the outermost layer of the skin. They usually appear in individuals over the age of 30. The majority of people develop at least one lesion during their lifetime, with an incidence of about 35% in the general population.

They cause primarily cosmetic concerns and, in some cases, due to their location, they may become irritated and inflamed.

Seborrheic Keratosis
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What causes seborrheic keratoses and what symptoms do they have

Dermatology has not yet determined the exact pathogenic mechanism leading to the development of seborrheic keratoses. They are generally considered part of the natural aging process, with some hereditary predisposition recognized, but no racial predilection. Chronic exposure to ultraviolet radiation is also an important factor in their appearance.

Seborrheic keratoses usually do not cause symptoms but can sometimes cause discomfort. The lesions may occasionally itch. In other cases, due to their location, irritation or injury can occur because they rub against or get caught on clothing.

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Clinical presentation of seborrheic keratoses

Clinically, seborrheic keratoses show great variability and different degrees of pigmentation. They appear as solitary or multiple well-demarcated lesions, with colors ranging from white, pink, black, or a combination of colors. Their surface may be smooth, scaly, or verrucous, and they can be found anywhere on the body except the palms and soles. Their shape varies from oval, round, to irregular. The term dermatosis papulosa nigra refers to seborrheic keratoses occurring in individuals of African descent, while stucco keratosis describes seborrheic keratoses commonly found on the shins of elderly Caucasian individuals.

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Prognosis and differential diagnosis

They are generally benign lesions. Differential diagnosis, depending on the type of seborrheic keratoses, should be made from melanocytic nevi, pigmented actinic keratoses, melanoma, pigmented basal cell carcinoma, and others.

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Dermoscopy approach to seborrheic keratoses

With dermoscopic examination, we exclude the possibility of a melanocytic lesion.

We identify specific features of seborrheic keratoses, which include:

  • Comedo-like openings
  • Fissures (cerebriform or verrucous appearance)
  • Milia-like cysts
  • Fingerprint-like pattern
  • Forked (branched) vessels
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Therapeutic management

Treatment of seborrheic keratoses is performed solely for cosmetic and practical reasons, unless there is doubt about their diagnosis during clinical examination and dermoscopic analysis.

The recommended treatment options include:

1. Curettage
2. Cryosurgery
3. CO2 LASER application (the most popular and commonly used method)
4. Surgical excision, suturing, and histological examination when there is diagnostic uncertainty.

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If you have previously been diagnosed by a dermatologist with seborrheic keratosis, it is advisable to visit them if you notice changes in the lesion’s color, size, or shape. Also, if it develops symptoms such as intense itching, swelling, ulceration, or bleeding. Finally, if you observe an increase in the number of lesions.

 

Complete removal of a seborrheic keratosis by an experienced dermatologist is usually accompanied by a very low chance of lesion recurrence. However, individuals predisposed to developing seborrheic keratoses may develop new, unrelated lesions over time.

Do you have a question or concern? We are here to help.

Moles

Skin Conditions
Moles
What are melanocytic nevi?

Melanocytic nevi are benign melanocytic formations of the skin, composed of melanocytes arranged in epidermal nests or clusters, each consisting of an aggregation of three or more melanocytes in close contact. Besides the epidermis, nevi may extend into the dermis. The melanocytes forming the nevi are classified according to their location as epithelioid (superficial), nevus cells (upper dermis), and spindle-shaped (deep dermis). Commonly, nevi are known as moles.

Nevi may be present at birth (congenital nevi) and continue to appear throughout life. However, new nevi most frequently emerge during the first three to four decades of life, with a particular increase during adolescence, followed by gradual regression that can lead to their complete disappearance.

Therefore, while the appearance of new nevi is common in young individuals, their appearance in older age groups is unusual and warrants examination by a dermatologist, especially for any new melanocytic lesion after age 60, to exclude malignancy.

Moles
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Pathogenesis and clinical presentation of melanocytic nevi

The origin of common nevi is largely unknown and remains an area of ongoing research. Both genetic and acquired factors appear to contribute to their development. Current data show that in the majority of melanocytic nevi (80%), mutations in the B-RAF gene are present, which likely play a central role in their pathogenesis. Additionally, predisposing factors for the appearance of nevi include chronic UV exposure, sunburns, blistering skin diseases (e.g., Stevens-Johnson syndrome, Epidermolysis Bullosa), immunosuppression (chemotherapy, solid organ or bone marrow transplantation, HIV), hormonal therapies and disorders (Addison’s disease, thyroid disorders), pregnancy, phototherapy, heredity, and others.

Furthermore, studies have shown that phenotypic characteristics such as skin and hair color significantly influence the total number of nevi in an individual. For example, research indicates that people of African descent tend to have fewer nevi, while individuals of Caucasian descent, due to lower tolerance to ultraviolet radiation, tend to have a higher number of nevi.

Common melanocytic nevi exhibit great variability in appearance. Most normal nevi are round or oval in shape, and may be either raised or flat with clear borders and homogeneous coloration. Their color is usually some shade of brown.

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Classification of nevi

Melanocytic nevi consist of congenital (or present at birth) nevi and acquired melanocytic nevi (which appear during childhood and adolescence). The family of congenital nevi includes the cellular nevus, while the acquired group includes common melanocytic nevi, blue nevi, Spitz nevus, Reed nevus, as well as a special group called dysplastic nevi.

Sutton nevus
A melanocytic nevus surrounded by a white halo (depigmented zone), often unnoticed in individuals with lighter skin except during summer when the skin is tanned. Common in children and young adults, it results from an immune reaction against the nevus. They are often multiple and commonly appear on the back. This phenomenon may occur on more than one nevus simultaneously. Over time, the central nevus disappears, leaving a depigmented patch. According to literature, individuals with Sutton nevi have a relatively increased risk (18-26%) of developing vitiligo compared to the general population.

Meyerson nevus
A melanocytic nevus surrounded by an inflammatory zone resembling eczema and may be itchy. Meyerson nevi may coexist with Sutton nevi, but the central nevus does not disappear in Meyerson nevus. In most cases, the Meyerson nevus is benign.

Blue nevus
Characterized by a bluish or blue-black color. The blue color results from the Tyndall effect of light scattering in the dermis, where melanin is located deeper than usual in the dermoepidermal junction. Blue nevi are acquired and appear during childhood and adolescence. They should remain stable in size and be regularly examined for changes. Sudden appearance in certain areas, such as the buttocks (cellular blue nevi), warrants excision and histological examination. They are usually found all over the body, with more than half occurring on the backs of the hands and feet, followed by the trunk and face.

Spitz nevus
A heterogeneous group of acquired melanocytic lesions composed of epithelioid or spindle-shaped cells with abundant cytoplasm and large nuclei. It usually appears in childhood as a red, raised nodule that grows rapidly and then stabilizes with a characteristic dermoscopic pattern. Common sites are the face and legs but can appear anywhere on the body. In children, it is often red; in adults, it appears more pigmented, resembling blue nevus or melanoma. Spitz nevus requires regular monitoring in both children and adults, with removal recommended upon any atypia.

Reed nevus
Similar to Spitz nevus (dermoscopic star pattern) but with an average onset age of 25 and darker pigmentation. Usually benign, but excision may be recommended to exclude malignancy. More common in females.

Dysplastic or atypical nevus
Observed in 10% of Caucasians, often on sun-exposed areas like the back, and is a risk factor for melanoma. Criteria for dysplastic nevus include:

  • Diameter over 5 mm
  • Entirely or partially flat
  • Two of the following: asymmetry, irregular shape, indistinct borders, color heterogeneity

Dermatologists evaluate dysplastic nevi and classify cellular atypia as mild, moderate, or severe. Management ranges from observation to treatment depending on individual assessment.

Ota nevus
Congenital, usually unilateral, affecting the first and second branches of the trigeminal nerve. Typical locations include the forehead, periorbital area, conjunctiva, and tympanic membrane. Laser treatment can address the cosmetic concerns.

Ito nevus
Clinically similar to Ota nevus but affects the acromioclavicular nerve area, appearing on the deltoid, supraclavicular, and scapular regions.

Becker nevus
Appears in childhood or adolescence anywhere on the body as a slightly brown, hairy hyperpigmented patch measuring 2–40 cm.

Congenital melanocytic nevi
Present at birth or within the first two years of life, classified by size:

  • Small (up to 1.5 cm)
  • Medium (1.5–20 cm)
  • Large (>20 cm)

They may show hair growth, nodules, or ulcerations and sometimes resemble melanoma. Congenital nevi grow with the child, including hair growth. Small and medium nevi require regular dermatologic monitoring for atypia, while large nevi, due to increased melanoma risk (which develops subepidermally), should be removed.

 

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Methods of nevus removal

Removal of nevi and sending them for histological examination is necessary when there is suspicion of malignancy. This is the only way to definitively exclude or confirm its presence. However, a nevus may also need to be removed for cosmetic reasons or when it causes discomfort in daily life, for example, if it is irritated by clothing, jewelry, or shaving due to its location. Depending on the individual case, the nevus’s location, its classification, and the patient's medical history, the treating dermatologist will recommend the most appropriate removal method. Removal of a nevus can be performed by:

  • Surgical excision: Suspicious nevi should always be surgically removed with healthy margins to avoid altering the microscopic appearance of the excision margins. The resulting wound is closed with sutures.
  • CO2 laser removal: This technique is used only when there is no suspicion of malignancy and the nevus is removed for cosmetic reasons or due to frequent trauma. Laser excision usually leaves no scar.
  • Shave excision: The nevus is removed precisely at its margin to minimize trauma and achieve the best cosmetic outcome. Hemostasis can be achieved with electrocautery or CO2 laser.
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The best method for prevention and monitoring, especially for individuals with a large number of moles who cannot self-monitor for clinical changes, as well as for those with fewer moles, is mole mapping performed by a dermatologist.

During this procedure, full-body photographs of the moles are taken, followed by dermoscopy using specialized equipment by the treating dermatologist. The frequency of this examination, typically every six months or annually, is individualized and recommended by Dr. Theocharis S. Preventive mole mapping enables periodic evaluation of mole size and microscopic structure, comparison of past and new images at each visit, analysis and grading of malignancy risk, detection of changes in existing moles, and identification of new moles. After all, the best prevention starts with proper patient education from the doctor.

The ABCDE method is a recognized dermatological approach that helps identify suspicious lesions with the naked eye. If we observe any of the following clinical changes in a mole:

  • Asymmetry
  • Borders (Irregular, scalloped, or poorly defined edges clearly distinct from the surrounding skin)
  • Color (Uneven color ranging from light brown to dark brown)
  • Diameter (Larger than 6 millimeters)
  • Evolution (Changes in size, color, or shape)

We must immediately inform the treating dermatologist for further investigation and examination.

 

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Melasma

Skin Conditions
Melasma
What is melasma?

The term “melasma” originates from the ancient Greek word melas, meaning “black.”

Melasma is a fairly common pigmentation disorder of the skin, characterized by an excess of melanin in the epidermis and the upper dermis (within macrophages). It is an acquired skin discoloration affecting the tone of the skin.

MELASMA
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Clinical presentation of melasma

Clinically, it presents as macules or patchy plaques with irregular borders, ranging in color from light to dark brown.

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Sites of melasma appearance

The most common site of melasma is the face, but it can also appear on sun-exposed areas such as the neck and hands. Melasma occurs more frequently in women with darker skin tones and tends to worsen during the summer months. Depending on the exact location, it is classified into three types:

  • Centrofacial (the most common type, affecting the forehead, cheeks, nose, upper lip, and chin)
  • Malar (cheeks and nose)
  • Mandibular (along the jawline)

Additionally, based on the depth of melanin deposition, melasma is classified into four types:

  • Epidermal (increased melanin in the epidermis; the melasma appears more prominent under Wood’s lamp examination)
  • Dermal (presence of many melanophages throughout the dermis; no enhancement of pigmentation under Wood’s lamp)
  • Mixed type (a combination of the above: increased melanin in the epidermis and many macrophages in the dermis; Wood’s lamp reveals areas with enhanced pigmentation, some with reduced pigment, and others with no change)

Indeterminate type (seen in Fitzpatrick skin types V–VI).

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What are the causes of melasma

The exact cause of melasma has not been fully clarified.

However, several factors appear to play a significant role, such as:

  • Exposure to ultraviolet radiation (sunlight or artificial UV radiation)
  • Dark skin tone
  • Heredity
  • Estrogen (pregnancy, contraceptive pills, or other hormonal treatments)
  • Thyroid disorders

Melasma tends to appear or worsen during the summer months and improve during the winter.

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Ways to manage melasma

It can be managed either conservatively with the topical application of appropriate products and formulations, or in combination with the use of laser devices. Treating melasma is a time-consuming process that often requires repetition and patience from the patient, as it frequently recurs.

Dr. Sotiris Theocharis selects the most suitable, individualized treatment plan, always tailored to the patient’s specific needs. This plan typically includes a combination of therapies for more effective melasma management, such as topical depigmenting agents (Kligman’s formula), the Fractional Erbium:YAG laser, antioxidant serums, mesotherapy with depigmenting agents (e.g., glutathione), and PRP.

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A patient with melasma must understand that proper use of sunscreen and other photoprotective measures not only helps prevent new lesions from forming but also prevents worsening of existing ones.

Therefore, the most important product to apply is a high-protection sunscreen, all year round. It must be applied correctly, with reapplication every two to four hours. Additionally, after completing treatment, the dermatologist recommends the use of special products to maintain the results long-term and prevent recurrence.

It is very important for patients with melasma to understand that some cases are very persistent, and in those, we achieve improvement but not complete elimination of the problem. This mainly occurs with older, diffuse discolorations where the pigmentation is located in the deeper layers of the skin.

Improvement in the clinical appearance of melasma results from a combination of treatments that require a long period, repetition, and consistent cooperation with the treating dermatologist. Unfortunately, melasma can often recur or even become more intense, which is why systematic use of sunscreen throughout the year is essential.

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Vitiligo

Skin Conditions
Vitiligo
What is vitiligo?

Vitiligo is an acquired, chronic, benign skin disorder of unknown cause, characterized by the inability to produce melanin due to the progressive loss of functional melanocytes in the affected skin, resulting in cosmetic concerns for patients. Vitiligo may also affect mucous membranes (e.g., the lining of the mouth) and the eyes.

Vitiligo
Everything You Need to Know
1
Cause of vitiligo

The exact mechanism by which melanocytes are destroyed or disappear from the affected areas of the skin has not been fully clarified. However, many theories have been proposed regarding the cause of this condition, with the most widely accepted being the classification of vitiligo—specifically the non-dermatomal form—as an autoimmune disease.

A condition is considered autoimmune when the immune system mistakenly identifies certain cells of the body as foreign and attacks them. The various theories developed do not exclude one another and often appear to coexist, contributing collectively to the onset of the disease.

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What are the epidemiological data of the disease

The prevalence of the disease in the general population is between 0.5% and 2%. Both sexes can be affected by vitiligo. The age of onset varies, ranging from childhood to old age. Several studies show that 25% of cases occur during childhood, often affecting the child’s psychological well-being.

In the majority of cases, the patient’s history reports disease onset following emotional stress, skin trauma (Koebner phenomenon), or another illness. In a large percentage of cases, vitiligo also tends to be hereditary. A positive family history is present in 10% to 50% of patients. Finally, it may coexist with other conditions, such as autoimmune thyroiditis.

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Therapeutic management of vitiligo

As simple as the diagnosis of the disease may be, its management is equally complex. For a patient with vitiligo, the following are recommended:

  1. General measures:
  • Photoprotection is essential, and sun exposure must be avoided
  • Avoid friction or trauma to the skin
  • Avoid stress-inducing factors and provide psychological support to the patient when necessary
  • Use of topical camouflage products (makeup) on exposed areas

2. Topical therapy, which includes:

  • Topical corticosteroids
  • Topical application of calcineurin inhibitors (tacrolimus – pimecrolimus), which can also be used on sensitive areas such as the eyelids and the face in general
  • Topical creams containing piperine, placenta, etc.

3. Phototherapy: UVB-nb or PUVA can be used (with either topical or oral administration of psoralens). The first-line treatment is UVB-nb phototherapy.

4. Depigmentation of the remaining skin in patients with universal stable vitiligo who only have a few patches of normal skin.

5. Surgical treatment (various techniques of autologous transplantation).

6. Laser: The 308 nm excimer laser is used.

7. Follicular unit transplantation using the FUE method (this treatment is under investigation).

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Clinical presentation of vitiligo

The disease clinically appears in the form of asymptomatic, depigmented (milk- or chalk-colored) macules and patches of varying size, with clearly defined borders separating them from healthy skin. They are selectively located around natural body orifices (around the mouth, eyes, navel, anus), in areas of increased friction (elbows, knees, armpits, inguinal folds, ankle joints), in areas with increased pigmentation (e.g., the nipple), and on the genital organs. White hair on the scalp is also common, occurring in approximately 10% to 60% of patients.

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Clinical types of vitiligo

According to medical science, vitiligo is classified into the following categories based on its clinical presentation:

Localized: The depigmented areas appear in one or a few specific parts of the body. This category includes:

    • Focal: One or more macules in a single area of the skin without dermatomal distribution
    • Segmental (dermatomal): One or more macules on one side of the body, where the patches stop at the midline; most commonly appears in children
    • Mucosal: Patches appear only on the mucous membranes

Generalized: This is the most common type of vitiligo (more than 90% of cases), where depigmented patches appear in multiple areas of the body and usually develop symmetrically on corresponding parts. This category includes:

  • Common (vulgaris): Macules scattered across the body
  • Acrofacial: Macules on the face and the distal extremities

Mixed: A combination of acrofacial or generalized vitiligo with segmental lesions

Universal: Depigmentation of the entire or nearly entire surface of the skin.

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From which other conditions should vitiligo be differentiated

Vitiligo should be differentiated from pityriasis versicolor, progressive macular hypomelanosis of the trunk, post-inflammatory hypopigmentation, and chemical leukoderma (depigmentation of the skin caused by chemical substances and medications). Solitary lesions should be differentiated from achromic nevus, nevus anemicus, and lichen sclerosus et atrophicus.

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Vitiligo is not a skin infection, nor is it a contagious disease. It cannot be transmitted through physical contact from a patient to a healthy individual.

Vitiligo usually progresses slowly once it appears. However, it may remain stable for a long period or, in some cases, suddenly worsen. In order to help prevent the spread of vitiligo as much as possible, patients must be particularly cautious about avoiding injuries, as trauma can lead to the appearance of new lesions.

Additionally, patients should consistently use sunscreen—both to protect the depigmented patches and to shield healthy skin from sunburn, which can also contribute to the development of new lesions (Koebner phenomenon).



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