Residerm Digital January'2026 issue

R.N.I No. MAHENG/2017/ 71390

Navigating Life’s Journey with Cockayne Syndrome: A Tale of Resilience and Hope

Total Pages : 20 January 2026 Vol 6* Issue 10

Enhancing Healing Outcomes in Chronic Non-Healing Leg Ulcers: The Role of Antibiotics, Mupirocin, and CollagenBased Dressings

ENTERING THE NEW YEAR WITH INSIGHTFUL CLINICAL PERSPECTIVES

EXECUTIVE EDITOR & PUBLISHER Dom Daniel

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Warm greetings to our readers as we welcome you to the New Year edition of Residerm. As we step into another year of learning and growth, we remain committed to our vision of providing a meaningful platform for indepth exploration of dermatology clinical cases relevant to daily practice. Residerm continues to support young and upcoming dermatologists by bridging textbook knowledge with real-world clinical decision-making through carefully curated, practice-oriented case discussions.

This edition presents two compelling clinical narratives.

The first, “Navigating Life’s Journey with Cockayne Syndrome: A Tale of Resilience and Hope,” highlights the importance of early recognition, multidisciplinary care, and empathetic patient management in rare genodermatoses. Beyond its scientific relevance, the case underscores the human aspect of dermatology— resilience, adaptability, and hope in the face of chronic disease.

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The second case, “Enhancing Healing Outcomes in Chronic Non-Healing Leg Ulcers: The Role of Antibiotics, Mupirocin, and Collagen-Based Dressings,” addresses a challenge commonly encountered in clinical practice. It provides valuable insights into infection control, wound care strategies, and the judicious use of topical and systemic therapies to optimize healing outcomes.

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We hope this New Year edition stimulates clinical thinking, encourages reflective practice, and inspires confidence in managing both rare and routine dermatological conditions. We thank our contributors and readers for being an integral part of the Residerm journey and look forward to another year of shared learning and excellence in dermatology.

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- Dom Daniel

Executive Editor & Publisher

CONTENT

04

Navigating Life’s Journey with Cockayne Syndrome: A Tale of Resilience and Hope Dr. Bhargavi Chitturi

3rd Year Resident Department of Dermatology, Venereology & Leprosy The Oxford Medical College, Hospital & Research Centre Bangalore

Dr. Anila Sara Thampi

MD (Dermatology) Assistant Professor Department of Dermatology, Venereology & Leprosy The Oxford Medical College, Hospital & Research Centre Bangalore

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Enhancing Healing Outcomes in Chronic NonHealing Leg Ulcers: The Role of Antibiotics, Mupirocin and Collagen-Based Dressings Dr. Sarish Kaur Walia

MD (DVL) Consultant Dermatologist Dr S.K Walia Skin Clinic Mohali, Punjab

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Navigating Life’s Journey with Cockayne Syndrome: A Tale of Resilience and Hope

Navigating Life’s Journey with Cockayne Syndrome: A Tale of Resilience and Hope Dr. Bhargavi Chitturi

3rd Year Resident Department of Dermatology, Venereology & Leprosy The Oxford Medical College, Hospital & Research Centre Bangalore

Dr. Anila Sara Thampi

MD (Dermatology) Assistant Professor Department of Dermatology, Venereology & Leprosy The Oxford Medical College, Hospital & Research Centre Bangalore

Introduction

Cockayne syndrome is a genetically inherited disorder with autosomal recessive transmission, first documented in 1936.

The condition arises due to pathogenic variants in the ERCC8 (commonly referred to as CSA) and ERCC6 (CSB) genes, which are located on chromosomes 5 and 10, respectively.

These genetic mutations lead to the development of two primary subtypes: CS4

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A, resulting from mutations in the ERCC8 gene and CS-B, associated with mutations in the ERCC6 gene, the latter subtype is distinguished by an increased sensitivity to ultraviolet radiation, resulting from a deficiency in the DNA repair mechanism.

Characterized by multisystem involvement, Cockayne syndrome presents a broad clinical spectrum including cachectic dwarfism,

Navigating Life’s Journey with Cockayne Syndrome: A Tale of Resilience and Hope

progressive neurological degeneration, cutaneous photosensitivity,............. microcephaly,............... developmental and growth retardation, sensorineural hearing loss, retinal degeneration, and premature aging. Clinically, the syndrome is categorized into four distinct subtypes, differentiated by the age at symptom onset and the degree of clinical severity.

Type I, the classical form, typically manifests after one year of age with progressive symptoms, including growth failure, neurodevelopmental and neurological dysfunction and photosensitivity. Type II, the congenital form, presents at birth with severe and rapidly progressing manifestations, often leading to early mortality.

Type III, a milder form, presents later in childhood and is characterized by slower disease progression.

The fourth variant, Xeroderma PigmentosaCockayne.....

Syndrome (XP-CS), is a hybrid syndrome that combines the clinical features of both CS and xeroderma pigmentosum, including cutaneous photosensitivity and a predisposition to

skin malignancies. Rare adult-onset cases may exhibit gait disturbances, cognitive impairment, chorea, and neuropathy, with neuroimaging often demonstrating diffuse cerebral and cerebellar atrophy.1, 2 The pathophysiology of Cockayne syndrome (CS) is primarily attributed to defects in the transcriptioncoupled nucleotide excision repair (TC-NER) pathway, caused by mutations in the ERCC6 (CSB) and ERCC8 (CSA) genes. TCNER is a critical DNA repair mechanism responsible for removing lesions that obstruct transcription, most commonly induced by ultraviolet (UV) radiation and oxidative stress.

Defective TC-NER results in stalled transcription, persistent DNA damage, and subsequent apoptosis, leading to progressive cellular dysfunction.

In contrast, the global genome nucleotide excision repair (GG-NER) pathway remains intact, explaining why CS patients do not exhibit a significantly elevated risk of malignancy. Nevertheless, the continuous accumulation of DNA

damage, particularly in metabolically active and post-mitotic cells such as neurons, drives neurodegeneration and impairs developmental progression. Beyond TCNER, the CSB protein plays a central role in base excision repair (BER), a pathway essential for repairing oxidative DNA lesions.

Cells lacking functional CSB demonstrate heightened sensitivity to oxidative agents such as hydrogen peroxide, gamma radiation, and alkylating compounds. This vulnerability contributes to persistent DNA damage, mitochondrial dysfunction, and elevated oxidative stress, thereby accelerating disease progression and premature aging. Additional molecular mechanisms include cell-cycle dysregulation mediated by upregulation of p21, a cyclin-dependent kinase inhibitor. Following DNA damage, p21 binds to proliferating cell nuclear antigen (PCNA), inhibiting DNA replication and causing G1/S arrest. While this response prevents malignant transformation, it also promotes apoptosis, contributing to growth January 2026

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Navigating Life’s Journey with Cockayne Syndrome: A Tale of Resilience and Hope

failure, cachexia, and tissue atrophy.

The hallmark neurodegeneration of CS is driven by unresolved endogenous DNA lesions within neurons, leading to transcriptional stalling and apoptosis. This mechanism underlies the profound neurodevelopmental........ impairment seen in patients, even in the absence of external genotoxic stress. Cockayne syndrome (CS) exerts a profoundly detrimental impact on a child's daily life, with early onset and rapid progression leading to severe cognitive and physical impairments.

Children with CS experience progressive neurodegeneration,........ rendering them unable to participate in education or social activities as intellectual and motor functions deteriorate. The disease often results in complete dependency on caregivers for basic tasks, severely limiting quality of life. Type I CS, presenting in early childhood, is particularly devastating, with most children succumbing to the disorder by early adolescence.

Given the progressive nature of the disease, 6

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early involvement of a multidisciplinary healthcare team is crucial in managing morbidity, providing therapeutic interventions, and enhancing the overall quality of life for affected children.1, 2 Case Report -1 We present the case of a 9-year-old patient with a cachectic habitus and microcephaly. The child exhibited characteristic craniofacial features, including an oval face, sunken eyes, a thin beaklike nose, absence of subcutaneous facial fat (particularly over the midface), and large ears, collectively imparting a bird-like appearance.

Photosensitivity was evident over all sunexposed areas of the skin.

Developmental assessment revealed delayed psychomotor milestones and intellectual disability. Oral examination demonstrated poor hygiene, gingivitis, and multiple dental caries.

Clinical evaluation together with laboratory investigations was consistent with a diagnosis of Cockayne syndrome (CS).

Figure 1: Characteristic craniofacial features of the patient with an oval face, sunken eyes, thin beak-like nose, midfacial fat loss and large ears, giving a bird-like appearance.

Case Report -2 A 9-year-old child with cachectic habitus and microcephaly, presenting with characteristic craniofacial features such as an oval face, sunken eyes, a thin beak-like nose, midfacial fat loss, and large ears, producing a bird-like appearance.

Photosensitivity was observed on sun-exposed skin. Developmental delay with impaired psychomotor skills and intellectual disability was noted. Oral examination revealed poor hygiene, gingivitis, and multiple dental caries.

Clinical and laboratory findings were consistent with Cockayne syndrome

Navigating Life’s Journey with Cockayne Syndrome: A Tale of Resilience and Hope

(CS).

Figure 2: Craniofacial features showing oval face, sunken eyes, beak-like nose, midfacial fat loss and large ears, giving a bird-like appearance.

Case Report -3 In this report, we present a 4-yearold child with clinical features suggestive of Cockayne syndrome (CS), a rare autosomal recessive disorder.

The patient exhibited a cachectic habitus and microcephaly, with distinctive craniofacial characteristics including

an oval face, sunken eyes, a thin beak-like nose, loss of subcutaneous fat over the midface and large, prominent ears, collectively giving a birdlike appearance. Cutaneous findings were notable for marked photosensitivity involving all sun-exposed areas.

Developmental assessment revealed global delay, with impaired psychomotor skills and intellectual disability. Oral examination demonstrated poor hygiene, gingivitis, and multiple dental caries, further contributing to systemic morbidity.

Clinical evaluation, together with relevant laboratory investigations, supported the diagnosis of CS, highlighting its multisystem involvement and characteristic diagnostic phenotype.

syndrome.

Diagnosis The diagnosis of Cockayne syndrome (CS) relies on a comprehensive clinical evaluation, supported by molecular genetic testing to identify pathogenic variants in DNA repair genes. Genetic confirmation is typically achieved through next-generation sequencing, which detects mutations in ERCC6 (CSB) and ERCC8 (CSA), both critical for transcriptioncoupled nucleotide excision repair.

This approach not only establishes the diagnosis but also aids in prognostication and genetic counseling. Neuroimaging plays an important role in diagnosis.

Magnetic resonance imaging (MRI) commonly demonstrates supratentorial white matter loss, ventricular dilation, cerebellar atrophy, and thinning of midline structures. Hypomyelination with preserved infratentorial myelination is a characteristic finding.

Computed tomography (CT) may reveal basal ganglia and cortical calcifications, while MR Figure 3: Facial features spectroscopy often shows of a child with Cockayne reduced N-acetylaspartate January 2026

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Navigating Life’s Journey with Cockayne Syndrome: A Tale of Resilience and Hope

(NAA) and choline, reflecting neurodegeneration and white matter disruption.3,4 Functional fibroblast assays provide additional diagnostic support.

Reduced recovery of RNA synthesis (RRS) following ultraviolet (UV) irradiation confirms impaired transcriptioncoupled repair, while unscheduled DNA synthesis (UDS) remains intact, distinguishing CS from other DNA repair disorders.5 Ophthalmologic evaluation is essential to assess disease involvement and progression.

Examination may reveal cataracts, pigmentary retinopathy, optic atrophy, or elevated intraocular pressure.6 Similarly, audiological testing—including puretone audiometry and brainstem auditory evoked responses (BAER)—helps identify sensorineural hearing loss and assess auditory pathway integrity.7 Developmental and neurological assessments contribute further by documenting psychomotor delay, cognitive decline, motor dysfunction, and growth retardation.

In selected cases, muscle biopsy may provide 8

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histopathological evidence of mitochondrial pathology, including ragged-red fibers or cytochrome c oxidase deficiency, particularly when molecular findings are inconclusive.8 Accurate diagnosis of CS integrates clinical, radiological, genetic, and functional evidence.

This comprehensive approach not only facilitates early recognition and tailored multidisciplinary management but also provides critical insights for prognosis and family counseling.

Treatment The management of Cockayne syndrome (CS) is primarily supportive, with a focus on preventing complications and optimizing the quality of life through a multidisciplinary approach.

Essential components of care include stringent photoprotection, nutritional support, rehabilitation therapies, and routine multisystem monitoring.

Photoprotection is vital due to UV hypersensitivity, necessitating the avoidance of direct sunlight and artificial UV sources, with the use of broad-spectrum sunscreens (SPF ≥50), UV-

protective clothing, and UVfiltering eyewear or masks.

Nutritional management is crucial, particularly in infancy, where feeding difficulties may require nasogastric or gastrostomy tube placement to ensure adequate caloric intake.

Ophthalmologic care is tailored to specific anomalies, such as cataracts and strabismus, with interventions including surgical removal, occlusion therapy, and corrective surgery. Dental care involves regular monitoring for dental caries, while audiological evaluations are essential to address sensorineural hearing loss, with hearing aids or prostheses and auditory-verbal therapy as needed. Physiotherapy and psychomotor rehabilitation are necessary to address motor deficits, and assistive devices like wheelchairs, walkers and orthotic supports may be required for mobility and independence.

Neurodevelopmental and psychological support, including individualized educational interventions and psychological care, are critical for addressing cognitive, emotional and adaptive

Navigating Life’s Journey with Cockayne Syndrome: A Tale of Resilience and Hope

challenges. Pharmacologic management is tailored, with carbidopa-levodopa for extrapyramidal symptoms and antiepileptic medications for seizures.

Regular monitoring of renal, hepatic, cardiovascular and metabolic parameters is essential to detect and address systemic complications early.5 Overall, the care of CS requires a coordinated, longitudinal approach by a multidisciplinary team to manage the disease's complex and progressive nature effectively.

Discussion Cockayne syndrome (CS) is a rare autosomal recessive neurodegenerative........... disorder caused by biallelic mutations, with an estimated incidence of 1 in 250,000 live births.

Accurate differentiation from other phenotypically overlapping conditions is crucial for prognosis and management.

Xeroderma pigmentosum (XP) also presents with photosensitivity but is distinguished by a markedly increased risk of cutaneous malignancies and absence of progressive neurodegeneration...........

Hutchinson-Gilford........... progeria resembles CS in its progeroid features yet lacks photosensitivity and ocular abnormalities.

Bloom syndrome presents with growth retardation and erythema but typically spares neurological function.

Werner syndrome manifests with premature aging during adolescence but does not cause severe cognitive decline.

RothmundThomson syndrome can be identified by characteristic poikiloderma, especially over the buttocks and limbs, which is uncommon in CS. Metabolic disorders such as Hartnup disease may mimic neurological features but lack the hallmark photosensitivity and craniofacial abnormalities of CS, helping to distinguish these conditions 9,10 Complications clinically. of this disorder encompass a broad spectrum of multisystem involvement, including dental anomalies such as caries, enamel hypoplasia, and abnormal tooth morphology or number.

Cardiovascular sequelae involve hypertension and premature atherosclerosis, while renal impairment may progress to

renal failure. Gastrointestinal manifestations include gastroesophageal reflux, and hepatic vulnerability is exemplified by acute liver failure secondary to metronidazole toxicity.

Progressive peripheral motor and sensory neuropathies contribute to gait difficulties, accompanied by bladder and bowel dysfunction.

Neurological complications are extensive, featuring intellectual disability, developmental delays, ataxia, tremor, seizures, spasticity, and sensorineural hearing loss.

A hallmark phenotypic feature is the cachectic “birdlike” facies, characterized by micrognathia and loss of facial subcutaneous fat.

Cutaneous photosensitivity precipitates skin atrophy, pigmentary changes, and telangiectasia. The presence of musculoskeletal complications, including joint stiffness, spinal curvature, and reduced bone density, further contributes to the deterioration of physical function.

Autonomic dysfunction may present as thermoregulatory instability and gastrointestinal dysmotility.

These diverse and progressive January 2026

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Navigating Life’s Journey with Cockayne Syndrome: A Tale of Resilience and Hope

manifestations underscore the disorder’s complexity and the critical need for a multidisciplinary, comprehensive approach to management.5, 11 Early and precise diagnosis of Cockayne syndrome, distinguishing it from other congenital disorders, is imperative due to the significant variability in prognosis and therapeutic interventions.

Diagnostic confirmation is achieved through molecular genetic analysis of pathogenic variants in the ERCC6 and ERCC8 (formerly CKN1) genes, supplemented

by DNA repair functional assays. However, these tests are still not widely available and so the prompt identification of the clinical syndrome is crucial for a proper diagnosis. Treatment for Cockayne syndrome is largely supportive, aiming to minimize complications and improve the quality of life for affected individuals.

Life expectancy is significantly reduced, typically to around 12 years, especially in early-onset cases, due to progressive neurodegeneration and multisystem involvement, making regular assessments 10

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crucial to monitor disease progression and identify emerging health issues.

Ongoing, individualized care is necessary, with a focus on managing multisystemic manifestations, such as neurological and metabolic disturbances.

Timely interventions are essential to mitigate systemic complications and improve overall patient outcomes.1, 5 Conclusion Cockayne syndrome is an uncommon inherited disorder arising from mutations impairing DNA repair mechanisms, presenting with considerable phenotypic variability that challenges clinical diagnosis and requires molecular genetic confirmation.

Optimal management demands a multidisciplinary approach, comprehensive perioperative evaluation, and customized anesthetic strategies to minimize perioperative risks.

Ongoing elucidation of its molecular mechanisms is vital to enhance diagnostic precision and guide the development of targeted therapeutic interventions.

Reference 1. Karikkineth AC, ScheibyeKnudsen M, Fivenson E,

Croteau DL, Bohr VA. Cockayne syndrome: Clinical features, model systems and pathways.

Ageing Res Rev. 2017; 33:3-17. doi:10.1016/j.arr.2016.08.002.

2. Hafsi W, Saleh HM. Cockayne Syndrome.

In: StatPearls.

Treasure Island (FL): StatPearls Publishing; January 11, 2024.

3. Koob M, Laugel V, Durand M, et al. Neuroimaging in Cockayne syndrome. AJNR Am J Neuroradiol. 2010; 31(9):16231630. doi:10.3174/ajnr.A2135.

4. He X, Zhang Y, Huang X, et al. preimplantation genetic testing for Cockayne syndrome with a novel ERCC6 variant in a Chinese family. Front Genet.

2024; 15:1435622. Published 2024 Oct 15. doi:10.3389/ fgene.2024.1435622.

5. Spitz MA, Severac F, Obringer C, et al. Diagnostic and severity scores for Cockayne syndrome.

Orphanet J Rare Dis. 2021; 16(1):63. Published 2021 Feb 3. Doi: 10.1186/s13023-02101686-8.

6. Wu Y, Zheng Y, Yan X, Huang Y, Jiang Y, Li H. Ocular findings in a patient with Cockayne syndrome with two mutations in the ERCC6 gene. Ophthalmic Genet. 2017; 38(2):175-177. doi :10.3109/13816810.2016.11718 81.

7. Shemen

LJ,

Mitchell

DP,

Navigating Life’s Journey with Cockayne Syndrome: A Tale of Resilience and Hope Farkashidy J. Cockayne syndrome--an audiologic and temporal bone analysis. Am J Otol. 1984; 5(4):300-307.

8. Rapin I, Weidenheim K, Lindenbaum Y, et al. Cockayne syndrome in adults: review with clinical and pathologic study of a new case. J Child Neurol. 2006; 21(11):991-1006. Doi: 10.1177/ 08830738060210110101.

9. Narayanan, Dhanya L; Tuteja, Moni; McIntyre, Adam D1; Hegele, Robert A1; Calmels,; Mandal, Kausik; Phadke, Shubha R. Clinical and Mutation Spectra of Cockayne Syndrome in India.

Neurology India 69(2): p 362366, Mar–Apr 2021. | DOI: 10.4103/0028-3886.314579.

10. Bhupathi, M., Vittal, C.S.N., Mediboina, A., Rachakonda, S.T. and Aijaz, A. 2023. Cockayne syndrome: an uncommon clinical entity.

International Journal of Contemporary Pediatrics. 10, 9 (Aug. 2023), 1472–1474.

DOI:https://doi. org/10.18203/2349-3291. ijcp20232599.

11. Rajamani G, Stafki SA, Daugherty AL, et al. Cognitive Decline and Other Late-Stage Neurologic Complications in Cockayne Syndrome.

Neurol Clin Pract.

2024; 14(4):e200309. doi:10.1212/ CPJ.0000000000200309.

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Enhancing Healing Outcomes in Chronic Non-Healing Leg Ulcers: The Role of Antibiotics, Mupirocin, and Collagen-Based Dressings

Enhancing Healing Outcomes in Chronic Non-Healing Leg Ulcers: The Role of Antibiotics, Mupirocin, and Collagen-Based Dressings Dr. Sarish Kaur Walia MD (DVL) Consultant Dermatologist Dr S.K Walia Skin Clinic Mohali, Punjab

Introduction

Wound healing is a complex, tightly regulated biological process that restores tissue integrity and function following disruption of the skin barrier. As the body’s largest organ, the skin provides essential protection against physical, chemical, and microbial insults and prevents water loss; therefore, any injury compromises homeostasis and increases susceptibility to infection and fluid imbalance. Tissue repair relies on a coordinated interplay of cellular and molecular events, and impaired healing—as seen in diabetic ulcers, pressure injuries and other chronic wounds—poses significant 12

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clinical and economic challenges.

Healing outcomes are influenced by local factors such as tissue oxygenation, perfusion and infection, as well as systemic factors that regulate cellular proliferation, extracellular matrix deposition, angiogenesis, and tissue remodeling.

Adequate oxygenation is critical throughout the healing cascade. Oxygen supports ATP production, fibroblast proliferation, collagen synthesis, keratinocyte migration, angiogenesis and wound contraction. Hypoxia disrupts these processes and prolongs inflammation, while oxygen also facilitates reactive oxygen species– mediated microbial killing

Enhancing Healing Outcomes in Chronic Non-Healing Leg Ulcers: The Role of Antibiotics, Mupirocin, and Collagen-Based Dressings

and functions as a signaling molecule for immune and reparative pathways.

However, excessive oxygen exposure can induce oxidative tissue damage.1,2 Wound repair progresses through overlapping yet distinct phases: hemostasis and inflammation, proliferation, and remodeling.

Hemostasis begins with vasoconstriction, platelet aggregation, and formation of a fibrin scaffold, mediated by growth factors including transforming growth factor-beta, plateletderived growth factor, and vascular endothelial growth factor.

This transitions into the inflammatory phase, where neutrophils remove pathogens and debris, and macrophages secrete cytokines that promote fibroblast activation, angiogenesis, and keratinocyte migration.

During the proliferative phase, fibroblasts multiply and produce extracellular matrix components, granulation tissue forms, type III collagen is deposited, and myofibroblasts drive wound contraction.

Concurrent neovascularization supports nutrient and oxygen delivery essential for resurfacing by migrating keratinocytes.1,2

The remodeling phase is characterized by replacement of type III collagen with type I collagen through matrix metalloproteinase-regulated turnover, gradually increasing tensile strength, though repaired tissue typically regains only about 80% of its original strength. Infection prolongs inflammation, increases matrix metalloproteinase activity, degrades growth factors, and can foster biofilm formation, making timely debridement and antimicrobial therapy crucial.

Systemic factors—including age, sex hormones, stress, comorbidities, nutrition, and medications—also affect healing. Aging delays inflammation, reduces macrophage function, impairs angiogenesis, and diminishes collagen deposition.

Estrogens enhance repair and matrix synthesis, whereas androgens and glucocorticoids impair fibroblast activity and angiogenesis. Psychological stress alters hypothalamicpituitary-adrenal axis function and suppresses immune responses.

Diabetes mellitus contributes to chronic tissue hypoxia, dysregulated angiogenesis, excess reactive oxygen species and advanced

glycation end-products, and fibroblast and keratinocyte dysfunction. Obesity reduces perfusion, increases wound tension, and predisposes to infection, while medications such as glucocorticoids, NSAIDs, chemotherapeutic agents, and angiogenesis inhibitors further hinder tissue repair.1,2 Effective wound management therefore requires optimization of tissue oxygenation, meticulous infection control, management of comorbidities and metabolic disorders, modulation of physiological stress, consideration of ageand sex-related differences, judicious use of pharmacologic agents, and support of tissue perfusion, all aimed at promoting timely, high-quality tissue restoration and functional recovery of the skin.

Case Report A 30-year-old female presented with a chronic, non-healing ulcer over the anterior aspect of the right lower leg, persisting for several weeks. The ulcer had shown slow progression, accompanied by episodes of increased discharge, pain, and surrounding pigmentation.

Clinical examination revealed a deep ulcer with January 2026

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Enhancing Healing Outcomes in Chronic Non-Healing Leg Ulcers: The Role of Antibiotics, Mupirocin, and Collagen-Based Dressings

irregular margins located just above the ankle, with a base covered by yellow necrotic slough and areas of granulation tissue. Purulent discharge was evident, indicating secondary bacterial infection, while the periwound skin exhibited post-inflammatory hyperpigmentation,...... dryness, and signs of chronic inflammation. The wound edges were mildly undermined, suggestive of delayed epithelialization, although the surrounding tissues showed no signs of compartment syndrome or significant edema, and peripheral pulses remained intact.

These findings pointed toward a chronic wound state driven by persistent infection and prolonged inflammation.

Management included systemic antibiotics to reduce microbial load and inflammation, along with topical mupirocin to target gram-positive colonization and maintain a cleaner wound environment. Gentle debridement was performed to remove necrotic slough and encourage healthy granulation, supported by maintaining optimal moisture balance.

To further enhance healing, collagen-based dressings were applied to promote extracellular matrix 14

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regeneration, support fibroblast migration, accelerate granulation tissue formation, and reduce elevated protease activity commonly associated with chronic wounds.

Before treatment

After treatment Figure 1: Chronic, non-healing ulcer over the anterior aspect of the right lower leg

Enhancing Healing Outcomes in Chronic Non-Healing Leg Ulcers: The Role of Antibiotics, Mupirocin, and Collagen-Based Dressings

Diagnosis Diagnosis of wound involves a comprehensive clinical and instrumental evaluation to determine its type, severity, and healing potential. Clinical assessment through visual inspection and palpation is fundamental for evaluating wound size, depth, exudate, and tissue quality. Digital planimetry provides precise measurement of wound area and perimeter, enabling accurate monitoring of healing progression.3 Serial photographic documentation tracks morphological and temporal changes in the wound.4 Ultrasound imaging assesses soft tissue integrity, wound depth, and the presence of fluid collections.5 Thermography detects local temperature variations indicative of inflammation or infection.6 Laser Doppler flowmetry quantifies microvascular perfusion within the wound bed, while near-infrared spectroscopy evaluates tissue oxygenation and blood flow.7 Biochemical analysis of wound exudate for inflammatory mediators, proteases, and growth factors further informs healing status, supporting a

comprehensive, multimodal assessment of wound progression and response to therapy.3 Treatment Antibiotics are essential in wound management because they reduce bacterial load, prevent local infection from progressing to systemic involvement, and help restore a microbial balance that supports the normal phases of healing— namely inflammation, proliferation, and remodeling. They function by selectively targeting key bacterial processes, such as inhibiting cell wall synthesis with betalactams and glycopeptides, blocking protein synthesis with aminoglycosides, macrolides, and tetracyclines, interfering with nucleic acid synthesis through fluoroquinolones and rifamycins, or disrupting metabolic pathways with sulfonamides and trimethoprim.

These mechanisms exhibit minimal toxicity to human cells due to the absence of these pathways in host tissues. Antibiotics may be administered systemically for spreading infections or applied topically with wound dressings to lower

bioburden. However, their efficacy can be significantly reduced by biofilms, which shield microorganisms by limiting penetration, slowing metabolic activity, and promoting resistance.

Effective management requires biofilm disruption through debridement or adjunctive agents, careful antibiotic stewardship, and integration with nonantibiotic strategies such as antiseptics and advanced wound therapies.8,9 Topical Mupirocin, a secondary metabolite of the Gram negative bacterium Pseudomonas fluorescens, is a topical antibiotic that inhibits bacterial protein synthesis by binding to isoleucyl tRNA synthetase.

It is highly effective against Staphylococcus aureus and Streptococcus species, including methicillin resistant strains, making it a key agent in MRSA management. It preserves normal skin microbiota such as Propionibacterium, supporting the skin barrier.

Mupirocin is bacteriostatic at low concentrations and becomes bactericidal with sustained use of the 2 percent formulation, achieving effective activity within 24 hours.

Its January 2026

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Enhancing Healing Outcomes in Chronic Non-Healing Leg Ulcers: The Role of Antibiotics, Mupirocin, and Collagen-Based Dressings

efficacy increases in acidic environments, and the naturally low pH of the skin enhances its antimicrobial performance, supporting its role as a well-tolerated and effective topical treatment for wound related 10 infections.

Collagen-based wound dressings play a pivotal role in modern wound management by harnessing the structural and bioactive properties of collagen to support tissue repair.

Wound healing progresses through hemostasis, inflammation, proliferation, and remodeling, with collagen—constituting...... nearly 25% of total human protein—serving as the key extracellular matrix component.

Its triplehelical fibrillar structure promotes fibroblast chemotaxis, cell adhesion, proliferation, angiogenesis, keratinocyte migration, re-epithelialization, and controlled moisture balance while regulating protease activity. Collagen biomaterials such as hydrogels, films, sponges, nanofibers, and denatured derivatives emulate the ECM but often require reinforcement through crosslinking or incorporation 16

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of hydroxyapatite, bioglass, carbon nanotubes, glycosaminoglycans,....... elastin-like polypeptides, or chitosan to improve mechanical stability.

Collagen degradation generates bioactive fragments that modulate inflammation, angiogenesis, and remodeling, guiding the transition from type III to type I collagen to restore tensile strength.11 Advanced wound management combines targeted therapies to optimize tissue repair.

Growth factors such as platelet-derived growth factor stimulate fibroblast activity, matrix deposition, and angiogenesis, while stem cell therapies enhance neovascularization,........ modulate inflammation, and support regeneration.

Bioengineered skin substitutes provide structural scaffolding for keratinocyte and fibroblast adhesion, promoting reepithelialization. Mechanical support—such as offloading devices and splints— reduces tissue stress and ischemia. Nutritional optimization with adequate protein, vitamins A, C, D, zinc, and iron, along with control of diabetes

and vascular disease, improves healing. Effective pain management and continuous monitoring of wound progression enable timely adjustments and prevent complications.12 Discussion The skin, the largest organ by surface area, serves as a vital protective barrier shielding internal tissues from mechanical trauma, microbial invasion, ultraviolet radiation, and extreme temperatures. Its constant exposure to environmental stressors makes it particularly vulnerable to injury, and damage to this barrier has significant clinical, functional, and economic repercussions.

Nonhealing wounds, surgical and traumatic scars, and burns impose a considerable healthcare burden, especially among individuals with diabetes, advanced age, or genetic disorders such as sickle cell disease, all of whom are predisposed to impaired wound repair and longterm complications. Despite numerous therapeutic modalities, clinical outcomes often remain suboptimal, underscoring the need for more effective regenerative strategies. Normal skin

Enhancing Healing Outcomes in Chronic Non-Healing Leg Ulcers: The Role of Antibiotics, Mupirocin, and Collagen-Based Dressings

repair is a highly coordinated, multistep process involving diverse cell types across the epidermis, dermis, and subcutaneous layers.

Healing progresses through overlapping phases that include rapid clot formation, inflammation, proliferation, re-epithelialization, and remodeling to restore tensile strength. The epidermis provides an impermeable external barrier and houses appendages such as sebaceous glands, sweat glands, and hair follicles. Beneath it, the dermis offers structural support, vascular networks, mechanoreceptors, and immune surveillance, while the subcutaneous adipose tissue supplies metabolic energy and growth factors essential for dermal regeneration. Injury initiates vasoconstriction and platelet aggregation, forming a fibrin-rich scaffold that halts bleeding and supports early inflammatory cells. Neutrophils arrive first to counter microbial invasion, followed by monocytes that differentiate into macrophages. Adaptive immune cells—including Langerhans cells, dermal dendritic cells, and T lymphocytes—modulate

outcomes, with conditions such as connective tissue disorders or hyperhomocysteinemia.... highlighting the importance of individualized care and targeted interventions.

Wound repair is a highly coordinated process involving vascular, cellular, and molecular mechanisms, guided by local and systemic factors including nutrition, medications, environmental conditions, and genetic Effective predisposition.13 management begins with meticulous cleansing and debridement to remove necrotic tissue, foreign material, and contaminants, optimizing the wound bed for repair. Infection control is critical, with systemic antibiotics preventing or treating infection, lowering complication rates, and supporting timely healing, while topical agents such as mupirocin provide localized protection against common pathogens, including MRSA, with minimal systemic effects.

Collagen-based dressings enhance tissue regeneration, accelerate closure, maintain a moist healing environment, and improve functional Advances recovery.8,9,10,11 factors can in wound care, including wound healing

antigen clearance and direct immune signaling.

As inflammation subsides, endothelial cells proliferate to form new blood vessels, supported by pericytes and circulating progenitor cells. Fibroblasts infiltrate the wound, depositing extracellular matrix and differentiating into myofibroblasts to contract wound edges and generate granulation tissue.

Reepithelialization occurs through proliferation of epidermal stem cells and dedifferentiation of mature keratinocytes, aided by the plasticity of appendageal stem cells. Subcutaneous stromal cells further enhance repair through cytokine and growth factor release, though inflammatory dysfunction in this layer contributes to poor healing in conditions like diabetes and obesity.

Ultimately, adult wound healing typically results in fibrosis rather than true regeneration, predisposing to hypertrophic or keloid scarring, while impaired repair may lead to chronic wounds with risks of recurrence, infection, and limb loss.1,2,3 Genetic influence

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Enhancing Healing Outcomes in Chronic Non-Healing Leg Ulcers: The Role of Antibiotics, Mupirocin, and Collagen-Based Dressings

tissue engineering, cellular reprogramming, and biomimetic scaffolds, are creating personalized, biologically informed approaches that promote efficient tissue regeneration, restore barrier function, minimize complications, and ultimately improve patient outcomes.12 Conclusion Wound healing is a complex, coordinated process influenced by local, systemic and genetic factors, yet it can be effectively optimized through modern interventions.

Meticulous cleansing and debridement, along with systemic antibiotics and topical mupirocin, control infection and prepare the wound for repair. Collagenbased dressings accelerate healing, support tissue regeneration, maintain moisture, and improve recovery.

Advances in tissue engineering, cellular therapies, and biomimetic scaffolds offer personalized, biologically informed approaches that restore barrier function, enhance regeneration, and minimize complications, underscoring the potential for faster, safer, and more effective wound management.

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Reference 1. Wilkinson HN, Hardman MJ. Wound healing: cellular mechanisms and pathological outcomes. Open Biol. 2020; 10(9):200223. doi:10.1098/ rsob.200223 2. Tottoli EM, Dorati R, Genta I, Chiesa E, Pisani S, Conti B. Skin Wound Healing Process and New Emerging Technologies for Skin Wound Care and Regeneration.

Pharmaceutics. 2020; 12(8):735. https://doi.org/10.3390/ pharmaceutics12080735 3. Sharun K, Banu SA, Mamachan M, et al. Comparative assessment of smartphonebased digital planimetry for wound area measurement. Narra J. 2025; 5(2):e1987. doi:10.52225/ narra.v5i2.1987.

4. Li KC, Lee YH, Lin YH. Automated Image-Based Wound Area Assessment in Outpatient Clinics Using Computer-Aided Methods: A Development and Validation Study.

Medicina (Kaunas). 2025; 61(6):1099.

Published 2025 Jun 17. Doi: 10.3390/medicina61061099 5. Li S, Mohamedi AH, Senkowsky J, Nair A, Tang L. Imaging in Chronic Wound Diagnostics. Adv Wound Care (New Rochelle).

2020; 9(5):245-263. doi:10.1089/ wound.2019.0967.

6. Ramirez-GarciaLuna JL,........

Bartlett R, Arriaga-Caballero JE,

Fraser RDJ, Saiko G. Infrared Thermography in Wound Care, Surgery, and Sports Medicine: A Review.

Front Physiol.

2022; 13:838528. Published 2022 Mar 3. doi:10.3389/ fphys.2022.838528.

7. Khatib M, Jabir S, Fitzgerald O'Connor E, Philp B. A systematic review of the evolution of laser Doppler techniques in burn depth assessment. Plast Surg Int. 2014; 2014:621792. doi:10.1155/2014/621792 8. Kaiser P, Wächter J, Windbergs M. Therapy of infected wounds: overcoming clinical challenges by advanced drug delivery systems. Drug Deliv Transl Res. 2021; 11(4):15451567. doi:10.1007/s13346-02100932-7 9. Oluwole DO, Coleman L, Buchanan W, Chen T, La Ragione RM, Liu LX. AntibioticsFree Compounds for Chronic Wound Healing. Pharmaceutics.

2022; 14(5):1021. Published 2022 May 9. doi:10.3390/ pharmaceutics14051021 10. Rivera P, Bello MB, Brito G, Pichardo G, Cruz E, Blanco D. Therapeutic Efficacy of 2% Mupirocin in Managing Staphylococcus aureus and Streptococcus pyogenes Wound Infections.

Cureus.

2025; 17(4):e82366. Published 2025 Apr 16. doi:10.7759/

Enhancing Healing Outcomes in Chronic Non-Healing Leg Ulcers: The Role of Antibiotics, Mupirocin, and Collagen-Based Dressings cureus.82366 11. Alberts A, Bratu AG, Niculescu AG, Grumezescu AM. CollagenBased Wound Dressings: Innovations, Mechanisms, and Clinical Applications. Gels. 2025; 11(4):271. Published 2025 Apr 5. doi:10.3390/gels11040271 12. Kolimi P, Narala S,............

Nyavanandi D, Youssef AAA, Dudhipala N. Innovative Treatment Strategies to Accelerate Wound Healing: Trajectory and Recent Advancements. Cells.

2022;11(15):2439.

Published 2022 Aug 6. doi:10.3390/ cells11152439 13. Farhangniya M,....................

Samadikuchaksaraei A. A Review of Genes Involved in Wound Healing. Med J Islam Repub Iran. 2023; 37:140. Published 2023 Dec 22. doi:10.47176/ mjiri.37.140

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