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Resident Forum
2026
:6;
66
doi:
10.25259/CSDM_42_2026

Nasal lesions in dermatology: A comprehensive clinico-syndromic and morphological guide with emerging entities

Department of Dermatology, Venereology and Leprosy, Chitradurga Medical College and Research Institute, Chitradurga, Karnataka, India
Department of Community Medicine, Chitradurga Medical College and Research Institute, Chitradurga, Karnataka, India
Department of Medicine, Chitradurga Medical College and Research Institute, Chitradurga, Karnataka, India.
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Corresponding author: Spandana Devrahalli Krishnamurthy, Department of Dermatology, Venereology and Leprosy, Chitradurga Medical College and Research Institute, Chitradurga, Karnataka, India. drspandana0896@gmail.com
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This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-Share Alike 4.0 License, which allows others to remix, transform, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.

How to cite this article: Krishnamurthy SD, Yuvaraj BY, Thippeswamy V. Nasal lesions in dermatology: A comprehensive clinico-syndromic and morphological guide with emerging entities. CosmoDerma. 2026;6:66. doi: 10.25259/CSDM_42_2026

INTRODUCTION

The nose represents a unique and clinically significant cutaneous region where dermatological conditions frequently manifest with distinct patterns and diagnostic implications. Owing to its exposed position, specialized skin characteristics, and high density of sebaceous units, the nasal skin is prone to a broad spectrum of disorders ranging from inflammatory and vascular dermatoses to benign and malignant tumors, often challenging both diagnosis and management.[1,2] In addition, continuous exposure to ultraviolet radiation, environmental pollutants, and minor repetitive trauma further contributes to the susceptibility of this region to both acute and chronic dermatoses. Its central facial location further amplifies cosmetic visibility and psychosocial impact, making early recognition and appropriate intervention crucial.[2]

Specific conditions such as rhinophyma, a phymatous variant of rosacea, underscore the interplay between chronic inflammation, vascular dysregulation, and connective tissue remodeling in nasal skin pathology.[3,4] The progression from transient erythema to fixed tissue hypertrophy reflects a spectrum of disease severity that may be modified by early therapeutic intervention. The nose may also serve as an early sentinel site for systemic disease, including violaceous plaques in sarcoidosis and destructive midline lesions in granulomatosis with polyangiitis.[5,6] In many cases, nasal involvement precedes systemic manifestations, thereby offering a critical window for early diagnosis. Recognition of such findings often enables earlier systemic evaluation and improved prognostic outcomes.

This review adopts a structured, pattern-based approach to nasal dermatoses, integrating anatomical relevance, deformities, inflammatory and infectious disorders, neoplasms, syndromic associations, systemic diagnostic clues, procedural dermatology, psychosocial aspects, and recently emerging entities, thereby providing a comprehensive clinical framework for dermatologists.

ANATOMICAL LANDMARKS AND SURGICAL RELEVANCE

The nasal tip and alae contain thick sebaceous skin with dense pilosebaceous units, whereas the dorsum possesses relatively sparse subcutaneous tissue and thinner coverage over osteocartilaginous structures.[7] This anatomical variation explains the differential distribution of acneiform disorders, vascular lesions, and scarring tendencies across nasal subunits. Furthermore, variations in lymphatic drainage influence the spread of infections and neoplastic cells.

A rich superficial and deep vascular plexus contributes to prominent erythema, rapid wound healing, and increased intraoperative bleeding risk. Knowledge of angular and dorsal nasal arterial anatomy is critical during filler injections and flap reconstruction to prevent ischemic necrosis or visual compromise.[8,9] In addition, the presence of end-arterial circulation in certain zones increases vulnerability to vascular occlusion during cosmetic procedures.

Understanding nasal esthetic subunits and structural support zones, such as the keystone area, guides reconstructive planning and optimizes cosmetic outcomes [Table 1].[7] Consideration of relaxed skin tension lines and subunit replacement principles further enhances surgical precision and esthetic integration.

Table 1: Key facial and nasal anatomical landmarks with their clinical and surgical significance.
Anatomical landmark Clinical significance
Angular and dorsal nasal arteries Critical for fillers/flaps; occlusion→necrosis, blindness
Dangerous area of the face Retrograde spread→cavernous sinus thrombosis
Internal nasal valve Narrowest airway; key to airflow obstruction
K-area (Keystone area) Dorsal stability; disruption→saddle nose
Nasal tip End-arterial zone; high ischemic risk in procedures
Soft triangle of converse No cartilage; prone to notching/scarring
Nasal vestibule Common site for infections (furunculosis and vestibulitis)
Cosmetic subunits Guide reconstruction for optimal esthetic outcome
Sun terrace High UV exposure; prone to skin cancers
T-zone Sebaceous-rich: acne, rosacea, seborrheic dermatitis

UV: Ultraviolet

CONGENITAL AND ACQUIRED NASAL DEFORMITIES

Congenital nasal deformities often reflect embryologic disruption or genetic syndromes and may serve as early phenotypic markers of systemic disease.[10] Associated anomalies involving craniofacial structures, the central nervous system, or the airway may coexist and warrant comprehensive evaluation. Structural abnormalities such as saddle nose, bifid nose, or hypoplastic alae require multidisciplinary evaluation and long-term follow-up.

Acquired deformities commonly arise from trauma, infection, granulomatous inflammation, vasculitis, substance abuse, or neoplasia.[5,6] Chronic inflammatory destruction may lead to irreversible cartilage loss and functional impairment. Midline destruction should raise suspicion for autoimmune or infiltrative pathology. Early recognition facilitates timely intervention and improves reconstructive outcomes [Table 2].

Table 2: Summary of nasal deformities with characteristic features and their diagnostic association.
Deformity Key features Clinical association
Saddle nose Depressed bridge GPA, leprosy, syphilis, cocaine
Rhinophyma (potato nose) Bulbous fibrotic tip Chronic rosacea
Clown nose deformity Red nodular tip Cutaneous metastasis
Cocaine nose Septal perforation Cocaine abuse
Gummatous nose Ulcer+collapse Tertiary syphilis
Strawberry nose Granular erythema Sarcoidosis
Tapir nose Shrinking with crusting Leishmaniasis
Bulldog facies Depressed bridge Congenital syphilis
Binder syndrome Flat bridge, midface hypoplasia Congenital
Bifid nose Midline cleft Frontonasal dysplasia

GPA: Granulomatosis with polyangiitis

SEBACEOUS GLAND DISORDERS

The sebaceous richness of the nasal tip and alae predisposes to acne vulgaris, sebaceous hyperplasia, and phymatous change.[3] Increased sebaceous activity, altered keratinization, microbial colonization, and chronic inflammation contribute to the characteristic morphology of nasal lesions. Hormonal influences and environmental triggers may further modulate disease expression.

Rhinophyma represents advanced tissue hypertrophy with nodular thickening and fibrosis, typically developing in longstanding rosacea.[4] Progressive enlargement may lead to functional obstruction and significant cosmetic disfigurement. Early medical management may prevent irreversible deformity [Figure 1].

Bulbous enlargement of the nasal tip noted, suggestive of rhinophyma.
Figure 1: Bulbous enlargement of the nasal tip noted, suggestive of rhinophyma.

Sebaceous tumors occurring on the nose may act as cutaneous markers of Muir–Torre syndrome, prompting evaluation for internal malignancy.[11] Recognition of such lesions is crucial for initiating appropriate oncologic screening.

VASCULAR AND NEUROVASCULAR DISORDERS

Persistent centrofacial erythema and telangiectasia are hallmark features of rosacea and photodamage.[3,4] Flushing episodes may be triggered by thermal, dietary, or emotional stimuli, reflecting underlying neurovascular dysregulation. Differentiating vascular instability from inflammatory infiltration is essential for targeted therapy [Figure 2].

Steroid-induced telangiectasia involving the nasal and forehead regions.
Figure 2: Steroid-induced telangiectasia involving the nasal and forehead regions.

Nasal vascular changes may also indicate connective tissue diseases or vasculitic processes.[6] The presence of purpura, ulceration, or necrosis warrants urgent systemic evaluation. Early identification of vascular compromise can prevent tissue loss and systemic complications.

Dermoscopic and histopathologic correlation enhances diagnostic precision in ambiguous presentations.[12] Emerging imaging modalities such as high-frequency ultrasound may further aid in assessment.

INFECTIVE DERMATOSES

The nose frequently acts as a reservoir and sentinel site for cutaneous infections due to colonization of the anterior nares.[13] This colonization predisposes to recurrent infections and autoinoculation. Impetigo, folliculitis, and vestibulitis commonly arise in this region.

Chronic ulcerative or infiltrative lesions should raise suspicion for cutaneous leishmaniasis, lupus vulgaris, or leprosy.[14] Secondary bacterial infection may complicate these conditions, accelerating tissue destruction. Delay in diagnosis may result in cartilage destruction and disfigurement. Early microbiologic confirmation and targeted therapy are essential to prevent complications [Figures 3-6].

Residual facial scarring after smallpox, demonstrating classic varioliform pitting resulting from dermal destruction during acute infection.
Figure 3: Residual facial scarring after smallpox, demonstrating classic varioliform pitting resulting from dermal destruction during acute infection.
Erythematous, annular plaques with peripheral scaling over the face, consistent with tinea faciei.
Figure 4: Erythematous, annular plaques with peripheral scaling over the face, consistent with tinea faciei.
Filiform warts presenting as slender, finger-like projections over the nasal tip and philtrum of the nose.
Figure 5: Filiform warts presenting as slender, finger-like projections over the nasal tip and philtrum of the nose.
Saddle nose deformity with leonine facies in Hansen disease, showing nasal cartilage destruction and diffuse facial infiltration.
Figure 6: Saddle nose deformity with leonine facies in Hansen disease, showing nasal cartilage destruction and diffuse facial infiltration.

GRANULOMATOUS DISORDERS

Granulomatous plaques and nodules over the nose often represent early manifestations of systemic inflammatory disease. Lupus pernio is a classic cutaneous sign of sarcoidosis.[5] Such lesions are often chronic and resistant to therapy, reflecting underlying systemic involvement.

Saddle-nose deformity and destructive ulceration may indicate underlying vasculitis such as granulomatosis with polyangiitis.[6] Biopsy and serologic testing are essential for differentiation. Prompt recognition prevents progressive tissue loss and systemic morbidity.

NEOPLASTIC AND PREMALIGNANT CONDITIONS

The nose is a high-risk anatomical site for cutaneous malignancy due to cumulative ultraviolet exposure and thin dermal support. Basal cell carcinoma and squamous cell carcinoma frequently occur on the nasal dorsum and tip.[15,16] Delayed diagnosis may result in deeper invasion and complex reconstruction.

Actinic keratoses represent premalignant lesions that reflect field cancerization and require surveillance or intervention.[17] Dermoscopy aids early detection of subtle malignant changes.[12] Non-invasive imaging techniques are increasingly used for early diagnosis. Timely excision with tissue-sparing techniques preserves both function and cosmesis [Figures 7-9].[18]

Multiple small, firm, skin-colored papules over the nose and paranasal area, consistent with trichoepithelioma.
Figure 7: Multiple small, firm, skin-colored papules over the nose and paranasal area, consistent with trichoepithelioma.
Compound melanocytic nevus on the nose (1.5 mm) with symmetrical architecture and uniform pigmentation, without atypical features.
Figure 8: Compound melanocytic nevus on the nose (1.5 mm) with symmetrical architecture and uniform pigmentation, without atypical features.
Vitiligo patch involving the nasal and parasal areas, overlying which there are areas of rough, scaly changes suggestive of actinic keratosis.
Figure 9: Vitiligo patch involving the nasal and parasal areas, overlying which there are areas of rough, scaly changes suggestive of actinic keratosis.

GENODERMATOSES AND SYNDROMIC ASSOCIATIONS

Characteristic nasal lesions may provide early diagnostic clues to inherited disorders. Angiofibromas on the nasal tip may suggest tuberous sclerosis complex [Figure 10] while multiple basal cell carcinomas raise suspicion for Gorlin syndrome.[19] Additional cutaneous markers may coexist and assist in syndromic diagnosis.

Multiple tiny facial angiofibromas involving the nasal region, presenting as dome-shaped, pink-to-red papules, with an associated fibrous cephalic plaque on the forehead, characteristic of tuberous sclerosis complex.
Figure 10: Multiple tiny facial angiofibromas involving the nasal region, presenting as dome-shaped, pink-to-red papules, with an associated fibrous cephalic plaque on the forehead, characteristic of tuberous sclerosis complex.

Recognition of pigmentary or sebaceous abnormalities over the nose should prompt systemic screening and genetic counseling when appropriate [Table 3]. Early identification allows surveillance for associated neurologic, renal, or skeletal complications and improves long-term outcomes.

Table 3: Syndromic conditions presenting with characteristic nasal features that act as early diagnostic clues and guide systemic evaluation.
Syndrome Nasal feature Clinical significance
Tuberous sclerosis Angiofibromas Early diagnosis; CNS/renal screening
Basal cell nevus syndrome Multiple BCCs Requires surveillance
Muir–Torre syndrome Sebaceous tumors Internal malignancy marker
Leopard syndrome Pigmented macules Cardiac/systemic screening

CNS: Central nervous system, BCCs: Basal cell carcinomas

NOSE AS A DIAGNOSTIC CLUE IN SYSTEMIC DISEASE

The nose frequently reveals early markers of systemic illness through characteristic patterns such as malar erythema, ulceration, necrosis, or infiltrative plaques.[6,20] Subtle clinical signs may precede laboratory abnormalities, emphasizing the importance of careful inspection.

For example, butterfly rash over the nasal bridge is strongly associated with systemic lupus erythematosus [Figure 11], while destructive midline lesions warrant evaluation for vasculitis or malignancy. Recognition of classical named nasal signs enhances bedside diagnostic accuracy and guides focused systemic assessment [Table 4].

Table 4: Classical and named nasal signs with condensed clinical features, highlighting their diagnostic value in dermatological and systemic diseases.
Sign Key feature Association
Butterfly rash Malar erythema SLE
Lupus pernio Violaceous plaques Sarcoidosis
Hutchinson’s sign Vesicles on the tip Herpes zoster (ocular risk)
Saddle nose Depressed bridge GPA, infections
Nasal necrosis Black eschar Mucormycosis, vasculitis
Apple-jelly nodules Yellow-brown on diascopy Lupus vulgaris
Clown nose sign Red nodular lesion Metastasis
Nasal telangiectasia Dilated vessels Rosacea, CREST
Allergic salute Transverse crease Allergic rhinitis

SLE: Systemic lupus erythematosus, GPA: Granulomatosis with polyangiitis, CREST: Calcinosis cutis Raynaud’s phenomenon Esophageal dysmotility Sclerodactyly Telangiectasia

Malar rash involving the cheeks and nasal bridge, showing symmetrical erythema with sparing of the nasolabial folds, characteristic of systemic lupus erythematosus.
Figure 11: Malar rash involving the cheeks and nasal bridge, showing symmetrical erythema with sparing of the nasolabial folds, characteristic of systemic lupus erythematosus.

PROCEDURAL DERMATOLOGY

Procedures involving the nose require meticulous anatomical knowledge due to the complex vascular supply and esthetic prominence. Laser therapy for telangiectasia must be carefully titrated to minimize scarring and dyspigmentation.[3] Patient selection and parameter optimization are essential for safe outcomes.

Injectable fillers carry the risk of vascular occlusion and vision loss; therefore, slow injection techniques and awareness of arterial pathways are essential.[8,9] Use of cannulas and aspiration techniques may further reduce complications. Mohs micrographic surgery remains the gold standard for high-risk non-melanoma skin cancers, ensuring complete margin control with maximal tissue preservation.[18]

PSYCHOSOCIAL AND COSMETIC CONSIDERATIONS

Nasal dermatoses significantly influence self-esteem, interpersonal interactions, and overall quality of life.[2] Even minor lesions may produce disproportionate psychological distress because of facial centrality. Cultural perceptions of facial appearance may further influence patient concerns and treatment expectations.

Holistic management should address both medical treatment and cosmetic rehabilitation, including counseling and, when appropriate, camouflage techniques to optimize long-term outcomes.

EMERGING AND RECLASSIFIED NASAL DERMATOSES

Recent advances have expanded the spectrum of inflammatory, infectious, and autoinflammatory disorders affecting the nose. Improved molecular diagnostics have enabled the identification of novel genetic and immune-mediated conditions.[3] Advances in dermoscopy, imaging, and molecular pathology are refining diagnostic accuracy.

Ongoing research continues to refine classification and management strategies [Table 5], with increasing emphasis on personalized and targeted therapeutic approaches [Figure 12].

Table 5: The tables summarize newer and reclassified nasal dermatoses reported in dermatology and related specialties.
Entity Key nasal feature Pathomechanism Clinical significance
Lichenoid pseudovesicular papular eruption Tiny translucent papules Lichenoid interface dermatitis Mimics vesicular disorders; differentiates from LMDF/rosacea
Midline lethal granuloma (NK/T-cell lymphoma, nasal type – NKTCL) Progressive ulceration, destruction EBV-associated angiocentric lymphoma Aggressive; early biopsy essential
Neutrophilic dermatosis of the nasal tip Painful swollen nasal tip Neutrophilic infiltrate Steroid responsive
Lipin-1-associated inflammatory panniculitis (LPIN1 disease) Recurrent nasal/facial nodules Metabolic lobular panniculitis Systemic metabolic clue
Majeed syndrome (LPIN2-related disease) Sterile neutrophilic plaques IL-1-mediated autoinflammation Systemic autoinflammatory disorder
IgG4-related disease Rhinophyma-like induration Storiform fibrosis, IgG4 plasma cells Steroid-responsive systemic disease
COVID-associated pernio-like lesions Violaceous nasal plaques Interferon-mediated vascular injury Post-COVID-19 self-limited lesion
Pseudoacne of the nasal crease Acne-like papules Keratin granulomatous reaction Acne-resistant condition
Elastosis linearis rubra nasi Linear erythematous lesions Dermal elastosis Cosmetic relevance
Trigeminal trophic syndrome Unilateral nasal ulcer Neurogenic self-inflicted ulceration Neuropathic origin
VEXAS syndrome Neutrophilic nasal lesions UBA1 somatic mutation Severe adult autoinflammatory disease
Granulosis rubra nasi Nasal erythema, sweating Eccrine dysfunction Pediatric/adult variant described
Morbihan disease Solid facial/nasal edema Lymphatic obstruction Resistant rosacea variant
Trichodysplasia spinulosa Follicular spicules Polyomavirus infection Immunosuppression marker
Cocaine-induced nasal dermatosis Necrosis, crusting Vasculopathy, levamisole toxicity GPA/lymphoma mimic
CANDLE syndrome Perinasal nodules Proteasome dysfunction Pediatric autoinflammatory disease
Acquired dermal melanocytosis of the nose Blue-gray pigmentation Dermal melanocytes Laser responsive
Post-COVID nasal vasculopathy Ischemic necrosis Microthrombosis/endothelial injury Thrombotic complication
Mask/device-related nasal dermatosis Erosions, erythema Pressure+irritation Device-induced injury
Relapsing polychondritis Nasal cartilage inflammation Autoimmune chondritis Systemic cartilage disease
Primary cutaneous plasmacytosis Red-brown plaques Plasma cell infiltration Chronic benign course
Rosai–Dorfman disease Papules/plaques Histiocytosis (emperipolesis) Steroid responsive
Erdheim–Chester disease Xanthomatous plaques Non-Langerhans histiocytosis Multisystem involvement
Immune checkpoint inhibitor dermatitis Lichenoid nasal plaques Drug-induced interface dermatitis Cancer immunotherapy complication
Vaccine-associated chilblain-like lesions Violaceous nodules Lymphocytic vasculitis Post-vaccine self-limiting
Cutaneous small vessel vasculitis Purpura/ulcers Leukocytoclastic vasculitis Biopsy-proven vasculitis
Midface toddler excoriation syndrome Nasal/face excoriations PRDM12 mutation Rare genetic neuropathy

GPA: Granulomatosis with polyangiitis, NKTCL: NK/T-cell lymphoma, LMDF: Lupus miliaris disseminatus faciei, EBV: Epstein–Barr virus

Excoriated lesions over the midfacial region in a 2-year-old girl, consistent with toddler excoriation syndrome.
Figure 12: Excoriated lesions over the midfacial region in a 2-year-old girl, consistent with toddler excoriation syndrome.

APPROACH TO A PATIENT WITH NASAL LESIONS

Detailed history

  • Onset and duration: Acute versus chronic, progressive versus static

  • Symptoms: Pain, itching, burning, bleeding, discharge, nasal obstruction

  • Evolution: Papule → plaque → ulcer → deformity

  • Triggering factors: Sun exposure, heat, alcohol, trauma, cosmetics

  • Systemic symptoms: Fever, weight loss, joint pain, respiratory complaints

  • History: Acne, rosacea, autoimmune disease, infections (TB, leprosy)

  • Drug history: Steroids, immunosuppressants, antiretroviral therapy

  • Occupational/exposure history: Travel (leishmaniasis), infections

  • Family history: Genodermatoses (e.g., tuberous sclerosis and Gorlin syndrome).

Clinical examination

Inspection

  • Site: Tip, ala, dorsum, columella, vestibule

  • Number: Solitary versus multiple.

  • Morphology:

    • Macule/papule/nodule/plaque/ulcer

    • Verrucous, nodular, infiltrative, telangiectatic.

  • Color:

    • Erythematous → inflammatory

    • Violaceous → granulomatous (sarcoidosis)

    • Pearly → basal cell carcinoma

    • Pigmented → melanocytic lesion.

  • Surface changes: scaling, crusting, ulceration, scarring

  • Margins: well-defined versus ill-defined.

Palpation

  • Consistency: Soft, firm, indurated

  • Tenderness

  • Fixity to underlying structures

  • Local temperature

  • Bleeding on touch.

Pattern recognition (clinical clues)

  • Centrofacial erythema + telangiectasia → rosacea

  • Nodular thickening of the tip → rhinophyma

  • Ulcer with rolled border → basal cell carcinoma

  • Non-healing ulcer with induration → squamous cell carcinoma

  • Violaceous plaque → sarcoidosis (lupus pernio)

  • Saddle nose deformity → vasculitis/granulomatous disease

  • Crusted erosions → infections (impetigo, vestibulitis).

Look for systemic associations

  • Malar rash → systemic lupus erythematosus

  • Midline destructive lesions → granulomatosis with polyangiitis

  • Multiple angiofibromas → tuberous sclerosis

  • Sebaceous tumors → Muir–Torre syndrome

  • Chronic ulceration → infections (leprosy, leishmaniasis, and tuberculosis).

Dermoscopic evaluation

  • Helps differentiate:

    • Basal cell carcinoma → arborizing vessels

    • Squamous cell carcinoma/actinic keratosis → keratin scale, dotted vessels

    • Rosacea → linear vessels.

  • Improves early detection of malignancy.

Laboratory and diagnostic workup

  • Skin biopsy – Gold standard for unclear lesions

  • Microbiological tests:

    • Slit-skin smear (leprosy)

    • Culture/smear (bacterial/fungal infections).

  • Blood tests:

    • Anti-nuclear antibody (systemic lupus erythematosus)

    • Antineutrophil cytoplasmic antibodies (vasculitis)

    • Angiotensin converting enzyme levels (sarcoidosis).

  • Imaging:

    • Computed tomography/magnetic resonance imaging for deep or destructive lesions.

Red flag signs (urgent evaluation)

  • Rapidly enlarging lesion

  • Non-healing ulcer

  • Bleeding or crusting lesion

  • Tissue destruction or deformity

  • Associated systemic symptoms.

Management approach

  • Inflammatory → topical/systemic therapy (e.g., rosacea)

  • Infective → targeted antimicrobial therapy

  • Granulomatous/systemic → multidisciplinary management

  • Neoplastic → biopsy + surgical excision (Mohs if needed)

  • Cosmetic/procedural → lasers, fillers (with caution).

Psychosocial assessment

  • Assess impact on:

    • Self-esteem

    • Social interaction.

  • Offer:

    • Counseling

    • Cosmetic correction options.

Follow-up and monitoring

  • Regular follow-up for:

    • Malignancy recurrence

    • Chronic inflammatory diseases.

  • Patient education:

    • Sun protection

    • Early reporting of new lesions.

CONCLUSION

Nasal lesions encompass a broad spectrum of dermatological conditions ranging from benign inflammatory and infectious disorders to premalignant and malignant neoplasms. Given the anatomical prominence and sun-exposed nature of the nose, careful clinical evaluation, supported by dermoscopy and histopathology when indicated, is essential for accurate diagnosis. Early recognition of suspicious features—such as ulceration, induration, telangiectasia, or non-healing lesions—plays a crucial role in timely intervention and improved outcomes. A systematic approach not only aids in differentiating benign from malignant entities but also ensures appropriate management, thereby minimizing morbidity and cosmetic disfigurement.

Ethical approval:

Institutional Review Board approval is not required.

Declaration of patient consent:

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given consent for their images and other clinical information to be reported in the journal. The patient understands that the patient’s names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Conflicts of interest:

There are no conflicts of interest.

Use of artificial intelligence (AI)-assisted technology for manuscript preparation:

The authors confirm that there was no use of artificial intelligence (AI)-assisted technology for assisting in the writing or editing of the manuscript and no images were manipulated using AI.

Financial support and sponsorship: Nil.

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