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Quiz Case
2022
:19;
55
doi:
10.25259/Cytojournal_29_2021

Dumbbell-shaped swelling of the ear lobe: Cytomorphological clues

Department of Pathology, North Eastern Indira Gandhi Regional Institute of Health and Medical Sciences, Shillong, Meghalaya
Department of Pathology and Lab Medicine, All India Institute of Medical Sciences, Bibinagar, Telangana, India
Department of Pathology and Lab Medicine, All India Institute of Medical Sciences, Mangalagiri, Andhra Pradesh, India
Department of Pathology, Metropolis Healthcare Limited, Raipur, Chhattisgarh, India
Corresponding author: Jyotsna Naresh Bharti, Department of Pathology and Lab Medicine, All India Institute of Medical Sciences, Mangalagiri, Andhra Pradesh, India. jyotsnamamc@gmail.com
Licence
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: Dey B, Nigam JS, Bharti JN, Garg P. Dumbbell-shaped swelling of the ear lobe: Cytomorphological clues. CytoJournal 2022;19:55.

10 cm nodule (growing in size, firm, non-tender, dumbbell-shaped) on the left ear lobe in a 22-year-old male after ear-piercing 6 months ago. Fine-needle aspiration showed scant paucicellular material with a few spindle-shaped cells with scant to absent cytoplasm. Eosinophilic collagen-like material was seen in myxoid background [Figure 1].

Figure 1:
(a) Paucicellular smear with a few spindle cells (MGG, ×400). (b) with eosinophilic collagen-like material (MGG, ×400). (c) Gross: Skin-covered soft tissue with 10 cm nodule. (d) Hyperkeratotic stratified squamous epithelium with large dense bundles of glassy collagen in mid to deep dermis showed (H & E, ×100). Inset: Masson’s trichrome stain highlights the thick collagen bundles in the mid-dermis (×200).

Q1. What is your interpretation?

  1. Keloid

  2. Hypertrophic scar

  3. Nodular fasciitis

  4. Fibromatosis

Answer: Q1-A. Keloid.

Cytomorphological differential diagnosis of the present case includes keloid, hypertrophic scar, fibromatosis, and nodular fasciitis. On cytology, keloid shows sparse fibroblastic spindle to oval-shaped cells, either single or in clusters along with thick, hyalinized, glassy, and eosinophilic collagen bundles named “keloid collagen” in a mucinous ground substance.[1] Keloid should be differentiated from hypertrophic scar, which usually occurs within 4–8 weeks of injury, is limited to the site of injury, and can regress gradually over time.[2] Cytologically, the hypertrophic scar has similar features as that of keloid but tends to be more cellular than keloid.[3] Hypertrophic scar has fine fibrillary collagen and occasional foreign body type of giant cells.[3]

Nodular fasciitis occurs most commonly in young adults and is more common in the subcutaneous tissue of the upper extremities, trunk, head, and neck. It is a self-limiting fibrous neoplasm.[4] Nodular fasciitis is cellular and comprises dispersed cells mixed with a tight cluster of spindle-shaped cells showing marked pleomorphism with fusiform nuclei and cytoplasmic processes in a background of inflammatory cells and myxoid stroma.[1,5]

Fibromatosis occurs almost at every site of the body.[4] The exact cause is unknown.[4] Cytology of fibromatosis reveals variable cellular smear with the scattered spindle to fusiform cell clusters, stromal fragments, and collagen matrix material.[5]

Q2. Which of the following characteristic feature distinguishes keloid from the hypertrophic scar?

  1. Spindle- or oval-shaped fibroblastic cells

  2. Bland fibroblastic cells with bipolar cytoplasmic extension

  3. Mucinous ground substance

  4. Sparse chronic inflammatory background

Answer: Q2-C. Mucinous ground substance.

Both keloid and hypertrophic scars show similar cytomorphological features. Mucinous ground substance is scant or absent in hypertrophic scar as opposed to keloid.[3]

FURTHER FOLLOW-UP OF THE CASE

The mass was surgically excised. Grossly, it measured 10 cm in maximum dimension, and externally, it was skin-covered [Figure 1c]. On the cut section, it was solid and grayish-white. Histopathological sections showed hyperorthokeratotic stratified squamous epithelium. Superficial dermis showed fibroblastic cells arranged parallel to the epidermis. Mid to deep dermis showed large dense bundles of glassy collagen [Figure 1d]. Masson’s trichrome stain highlighted the thick collagen bundles in the mid-dermis (inset). A final diagnosis of keloid was made.

The patient was on regular follow-up. There was no recurrence after 6 months of follow-up.

Q3. Which type(s) of collagen is found in keloids?

  1. Type I

  2. Type II

  3. Type III

  4. Types I and III

Answer: Q3-D. Types I and III.

Keloid is characterized by haphazardly arranged large, thick, Types I and III hypocellular collagen bundles with no nodules, or excess myofibroblasts.[2] Hypertrophic scar has primarily fine, well-organized, and wavy Type III collagen bundles oriented parallel to epidermis surface with abundant nodules containing myofibroblasts.[2]

BRIEF REVIEW OF THE TOPIC

Keloid is a reactive condition resulting from excessive scar formation due to an aberrant healing process.[3] Various causes lead to the formation of excessive scars, including trauma, surgery, and burn.[3] Keloid usually occurs in the head-and-neck region, ear lobes, upper chest, and arms.[3] It presents as raised, well-circumscribed, firm nodule, often pruritic, and painful and most do not regress spontaneously.[3]

Keloids are most frequent among African population and less common in Caucasians.[6] Positive family history is not uncommon and probably reflects a genetic predisposition to keloid formation.[6] The genetic study for keloid showed susceptibility loci on chromosomes 2q23 and 7p11.[7] Different studies revealed that multiple genes are associated with keloid formation.[6,7] The role of Th2 inflammatory response with the production of interleukins (IL)-4, IL-5, IL-10, and IL-13 has been implicated in the pathogenesis of keloid.[8] Fibrogenic response to growth factors such as transforming growth factor-beta and platelet-derived growth factor (PDGF) also plays an integral role in the formation of keloids.[8]

Although histopathological features of keloid have been aptly described in the literature, cytomorphology of keloid is rarely reported in the literature.[1,5] As most of the cases of keloid are clinically evident, FNAC is rarely done in these lesions. FNAC may be done only in clinically uncertain cases. Hypertrophic scar, nodular fasciitis, and fibromatosis were the differential diagnoses considered in the present case. The cytomorphological features of keloid and its differential diagnoses are summarized in [Table 1].

Table 1: Cytomorphology of keloid and its differential diagnoses.
Cytomorphological features Keloid Hypertrophic scar Nodular fasciitis Fibromatosis
Cellularity Sparsely cellular Cellular Highly cellular Depending on age and location, the lesion may be cellular to acellular
Cell morphology Fibroblastic spindle to oval-shaped cells, either single or in clusters with bipolar cytoplasmic extensions Same as keloid Polymorphic cells have spindle, round, and oval to triangular-shaped cells. Cells have cytoplasmic processes and round to ovoid nuclei Fibroblastic oval to spindle-shaped cells in clusters with tapering cytoplasmic processes
Collagen Thick, hyalinized, eosinophilic “keloidal collagen” Fine fibrillar collagen Absent Densely eosinophilic collagen
Mucinous ground substance Present Scant or absent Myxoid background Absent
Chronic inflammatory cells Sparse Sparse Present Sparse
Giant cells Absent Occasional foreign body type giant cells Few binucleate/trinucleate cells Occasional multinucleated giant cells

Although hypertrophic scar and nodular fasciitis have traumatic etiology, they can regress without any surgical management. Keloid and fibromatosis require surgical excision and can recur if incompletely excised.[2,4] In addition to surgery, intralesional steroid injection, cryotherapy, laser removal, radiotherapy, and silicone gel sheeting are some of the most popular treatment modalities for keloid.[8] Less widely utilized therapies include topical imiquimod and antimetabolites such as 5-fluorouracil and bleomycin.[8]

In the present case, the cytological clues favoring keloid were paucicellular smears with the presence of eosinophilic collagen. The mass was surgically excised and there was no recurrence after 6 months of follow-up.

SUMMARY

Keloid is a common lesion with distinct cytological features. The characteristic cytological features include paucicellular spindle cells with eosinophilic collagen. The common cytomorphological differential diagnoses include a hypertrophic scar, nodular fasciitis, and fibromatosis.

COMPETING INTEREST STATEMENT BY ALL AUTHORS

The authors have no conflicts of interest.

AUTHORSHIP STATEMENT BY ALL AUTHORS

Concept: Biswajit Dey and Jitendra Singh Nigam. Design: Jyotsna Naresh Bharti, Biswajit Dey, Jitendra Singh Nigam, and Pooja Garg. Definition of Intellectual Content: Jyotsna Naresh Bharti and Biswajit Dey. Literature Search: Jyotsna Naresh Bharti, Biswajit Dey, Jitendra Singh Nigam, and Pooja Garg. Data Acquisition: Biswajit Dey and Pooja Garg. Data Analysis: Jyotsna Naresh Bharti, Biswajit Dey, Jitendra Singh Nigam, and Pooja Garg. Manuscript Preparation: Jyotsna Naresh Bharti, Biswajit Dey, Jitendra Singh Nigam, and Pooja Garg. Manuscript editing and Review: Jitendra Singh Nigam, Jyotsna Naresh Bharti, and Biswajit Dey.

ETHICS STATEMENT BY ALL AUTHORS

The informed and written consent was obtained from the patient. The case was submitted without identifiers.

LIST OF ABBREVIATIONS (In alphabetic order)

FNAC – Fine-needle aspiration cytology

PDGF – Platelet-derived growth factor

TGF-β – Transforming growth factor-beta

EDITORIAL/PEERREVIEW STATEMENT

To ensure the integrity and highest quality of CytoJournal publications, the review process of this manuscript was conducted under a double-blind model (authors are blinded for reviewers and vice versa) through an automatic online system.

References

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