Keloids are benign but locally aggressive fibroproliferative scars characterized by excessive extracellular matrix (ECM) deposition- initially rich in type III collagen, later replaced by collagen type I with persistent fibroblast activation and extension beyond the original wound boundaries. Keloid, meaning “crab’s claw,” derived from Greek to describe its characteristic clinical presentation.⁽¹⁾ They appear as elevated, firm bosselated papules and ill-defined plaques accompanied by variation in color, including erythematous, violaceous or brown hyperpigmentation. They frequently cause pain, pruritus, cosmetic disfigurement and occur more commonly in darker skin types and in certain anatomic sites like chest, shoulders, earlobes.

The pathogenesis is multifactorial - involving genetic susceptibility, dysregulated inflammation and immune responses, altered mechanotransduction and aberrant wound-healing cascades that favor persistent myofibroblast activity and collagen overproduction ^(1,2).

Therapeutic goals for keloids are reduction of bulk, symptom relief, functional and cosmetic improvement and prevention of recurrence. Management options include conservative measures such as silicone sheeting, pressure therapy, minimally invasive approaches like cryotherapy, intralesional injections, energy-based treatments (lasers), surgical excision  and intralesional radiotherapy in selected cases.

Among nonsurgical options, intralesional injections remain the cornerstone of treatment, particularly intralesional triamcinolone acetonide (ILTAC). TAC  gives a targeted antifibrotic, anti-inflammatory and antiproliferative effects.

 Intralesional therapy in keloids have key limitations:

1. Dense, fibrotic ECM and altered tissue architecture can impede uniform drug diffusion, producing areas of undertreatment.

2. Uneven distribution of injected agent may contribute to partial response and recurrence.

3. Repeated injections are often painful and may lead to local side effects (skin atrophy, telangiectasia, pigmentary changes).

These limitations motivate strategies that improve delivery and homogeneity of drug distribution within keloid tissue ^(3,4).

Reported response rates greatly vary in keloids and combination therapies like adding a surgical procedure can show improved outcomes than monotherapy alone ^(5,6).

Coring technology : Micro-coring and Macro-coring is a newer, minimally invasive mechanical modality that removes full-thickness skin cores of varying diameters to induce controlled dermal remodeling, collagen contraction and neocollagenesis. Clinically, micro-coring has been evaluated primarily for skin laxity, wrinkles, and scar improvement and has demonstrated safety and measurable tissue remodeling on histology. Because it creates true tissue channels (rather than mere punctures), coring is a plausible pre-treatment for enhancing intralesional drug access into dense scar tissue ^(7,8).

Rationale for combination: Mechanically creating controlled channels in keloid tissue prior to intralesional therapy could :

1. Increase permeability of drug

2. Allow more uniform and deeper dispersion of therapeutic agents

3. Potentially reduce the number and volume of painful injections

Synergize mechanical remodeling with pharmacologic antifibrotic effects to improve efficacy and reduce recurrence.

However till date, the direct application of laser micro or macro-coring immediately before intralesional drug injection in keloid treatment has not been established in the published clinical literature, thus this gap further justifies the proposed study.^(7,9)