Burn scars 2X more likely if Vitamin D deficient
Vitamin D Deficiency as a Risk Factor for Hypertrophic Scarring and Reconstructive Surgeries After Burns - April 2026
Aesthetic Surgery Journal Open Forum https://doi.org/10.1093/asjof/ojag074
Philong Nguyen, BS , Joshua Wang, MS , Yousef Tanas, MD , Haidara Bohsas, MD , Alexandra Dunker, BS , Kamryn K Baker, BS , Kevin Vargas, BS , Sudhanvan Iyer, BS , Carolyn Henein, MS , Cameron Bowers, BS
Background Vitamin D plays an important role in immune regulation, collagen remodeling, and wound healing. In the general population, deficiency has been associated with poor wound repair and fibrosis, yet evidence in burn patients remains limited. Burn injuries often result in hypertrophic scarring and significant healthcare utilization for reconstructive and adjunctive procedures.
Objectives: This study examines the impact of preexisting vitamin D deficiency on hypertrophic scarring and scar-related healthcare utilization in a large, multi-institutional cohort of burn patients.
Methods: The TriNetX Research Network was queried for patients ≥18 years old with burn injuries between 2010 and 2023. Patients with vitamin D deficiency, defined as 25-hydroxyvitamin D < 20 ng/mL within one month prior to injury, were matched 1:1 to non-deficient controls using propensity score matching. Matching variables included demographics, body mass index, comorbidities, substance use, vitamin deficiencies (A, C, E, and K), calcidiol levels, and total burn surface area. The primary outcome was hypertrophic scarring. Secondary outcomes included scar-related interventions: Z-plasty and intralesional corticosteroid injections. Cumulative incidence was assessed at 3, 12, and 24 months. Hazard ratios (HRs) with 95% confidence intervals (CIs) were calculated using Cox proportional hazards models.
Results After matching, 6,832 patients were included in each cohort. Vitamin D deficiency was associated with significantly higher rates of hypertrophic scarring at
- 3 months (5.82% vs 2.55%, HR 2.33, 95% CI 1.93–2.81, p < 0.0001),
- 12 months (9.38% vs 4.56%, HR 2.12, 95% CI 1.84–2.46, p < 0.0001), and
- 24 months (10.61% vs 5.26%, HR 2.09, 95% CI 1.83–2.40, p < 0.0001).
Vitamin D deficient patients also demonstrated greater use of reconstructive procedures, including Z-plasty (HR 1.86–2.38) and corticosteroid injection (HR 3.14–3.56).
Conclusions: Vitamin D deficiency is strongly associated with increased hypertrophic scarring and greater reliance on reconstructive and adjunctive procedures following burn injury. These results underscore the potential role of micronutrient status in long-term burn recovery. Prospective studies are needed to determine whether early detection and correction of deficiency can mitigate scarring and reduce healthcare utilization.
Note1: Far more burn scars since 1980s, mainly because people generally survive the burns
Note2: Far more people with dark skins have burn scars ( low vitamin D)
Related in VitaminDWiki
- Less scarring (hypertrophic) if supplementation with Vitamin D got above 25 ng – RCT
- Burns, ulcers, and wounds healed by Vitamin D - many studies
- Topical Vitamin D
- Wounds and pregnancy masks treated by topical Vitamin D
- Psoriasis is treated by topical Vitamin D, etc.
Topical Vitamin D will likely be found to reduce scarring
Claude AI May 2026](https://claude.ai/share/9bae6029-6555-4ddf-a0de-e8cc7ff44822) The mechanistic case is strong, but the direct evidence for topical vitamin D on burn scars specifically is thin. Here's the picture as it stands.
Mechanism is plausible. Keloid fibroblasts express functional VDR, and 1,25(OH)₂D suppresses TGF-β1–induced collagen I, fibronectin, and α-smooth muscle actin, while modulating MMP-9 and PAI-1 and inducing antifibrotic hepatocyte growth factor. The same VDR/Smad antifibrotic axis has been shown in lung, liver, intestine, and skeletal muscle fibroblasts via the TGF-β/Smad signalling cascade. So vitamin D signaling is doing exactly what you'd want during the proliferative/remodeling phase of a burn wound.
Systemic supplementation has reasonable RCT support for burn outcomes. A 2025 Iranian double-blind RCT in hospitalized burn patients found supplementation at 1,000 and 3,000 IU/day improved wound healing and decreased scar thickness, with the 3,000 IU arm showing better Vancouver Scar Scale scores at three months and shorter hospitalization. This builds on the Birmingham observational data showing patients with higher 25(OH)D had better wound healing, fewer complications, and less scarring. Doses used in burn trials are still cautious by your standards, but the signal is consistent.
Intralesional and combination approaches look more promising for established scars. A 2025 trial (Hassan, 30 patients) used intralesional vitamin D₃ injections (with monthly systemic 200,000 IU cholecalciferol in deficient patients) on hypertrophic scars and keloids and reported clinical improvement. Combined topical calcipotriol + nonablative fractional photothermolysis has shown benefit for treating existing keloid/hypertrophic scars where calcipotriol alone did not.
Adjacent topical evidence. A 2021 RCT of low-dose calcipotriol ointment in dystrophic EB wounds showed 88.4% wound area reduction at day 14 vs 65.5% on placebo, plus significant pruritus reduction. And a 2025 preclinical paper on vitamin D2 + colloidal silver nanoparticles in 3D reconstructed human skin showed wound repair and UVB protection. Neither addresses burn scarring directly but both suggest topical D-pathway activation does something useful in injured skin.
Practical read. For an actual burn, the highest-leverage move is making sure 25(OH)D is well-replete before and during healing — burn patients are systematically deficient because injured skin can't make D and ICU dynamics deplete it further. Topical vitamin D as a standalone prevention strategy on a fresh burn does not have RCT support; the one prevention trial was null. For an established hypertrophic scar or keloid post-burn, the combination playbook (intralesional D ± systemic loading ± laser ± silicone) has a more interesting evidence base than topical alone.
The genuine gap: no one has run a topical 1,25D (calcitriol) or high-dose D3 cream RCT specifically on burn wounds during the proliferative phase, with scar outcomes at 6–12 months. That's the trial that would actually answer your question. Given how cheap and safe topical D would be at the burn-care scale, it's a striking omission — likely the same "unpatentable nutrient, no sponsor" dynamic you've written about.
Worth a VitaminDWiki page if you don't already have one — the keloid/hypertrophic angle ties cleanly to your existing fibrosis content, and the burn-specific topical gap is exactly the kind of "obvious untested intervention" framing your audience responds to.