Chronic Wounds
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A regenerative path alongside advanced wound care
Chronic wounds diabetic foot ulcers, pressure injuries, venous or arterial ulcers, post-surgical and radiation wounds stall when inflammation, poor microcirculation, and exhausted local cells overwhelm the body’s repair programs. Dressings, debridement, off‑loading, compression, revascularization where possible, glycemic control, nutrition, and antibiotics remain essential, but they don’t always restart the biology of healing. Our program layers mesenchymal stem/stromal cells (MSCs), especially human umbilical cord–derived MSCs (UC‑MSCs), alongside hyperbaric oxygen therapy (HBOT) and targeted regenerative support to calm inflammatory “noise,” re‑establish microvascular supply, and deliver pro‑repair signals so granulation, epithelialization, and remodelling can proceed.
How UC‑MSCs may help a non‑healing wound
UC‑MSCs act as cellular coordinators rather than replacement tissue. Through paracrine signalling growth factors, cytokines, extracellular vesicles they nudge macrophages toward a pro‑repair state, reduce protease‑heavy inflammation, and encourage fibroblasts and keratinocytes to synthesize healthy extracellular matrix. They also support endothelial cells to rebuild capillary networks and improve oxygen and nutrient delivery at the wound edge.
In select cases, we employ engineered UC‑MSCs designed to enhance expression of two key growth factors: VEGF, which promotes new capillary formation, and PDGF, which drives fibroblast activation and orderly matrix organization. Together, these signals aim to restart the normal cascade—debridement and inflammation resolving into robust granulation, then epithelial closure with better‑quality collagen.
What the research shows
Randomized clinical evidence (local UC‑MSC injection): In patients with long‑standing non‑healing wounds of mixed etiologist, a single peri‑wound injection of UC‑MSCs (after sharp debridement and best practice care) has been associated with faster granulation, improved microcirculatory perfusion and transcutaneous oxygen, reduction in wound area over 2–4 weeks, and good short‑ and 1‑year safety. These signals support the central role of immunomodulation and angiogenesis in moving wounds from “stalled” to “healing.”
Phase I pilot in complex diabetic foot ulcers with PAD (topical + IV UC‑MSCs): In people with diabetic foot ulceration complicated by peripheral arterial disease who were not candidates for further revascularization, adding UC‑MSCs to conservative management was feasible and well‑tolerated. Across the cohort, teams documented rapid wound‑bed improvement, marked granulation within weeks, symptom relief, and favourable limb outcomes at multi‑year follow‑up.
Case experience combining WJ‑MSCs with PRP for pressure injuries: When umbilical‑cord Wharton’s jelly MSCs are combined with autologous platelet‑rich plasma and injected intradermally at ulcer margins (on top of standard prevention and care), clinicians have observed early granulation (days), steady epithelialization, and near‑complete closure by ~6–7 weeks in refractory heel ulcers, with good local tolerability. PRP likely augments MSC potency by supplying a burst of VEGF, PDGF, TGF‑β, EGF, HGF, IGF‑1 and a provisional scaffold that helps MSCs persist where they’re needed.
Mechanistic consensus: Reviews across preclinical and clinical literature highlight MSCs’ multifaceted paracrine activity—VEGF, PDGF, EGF, SDF‑1, IGF, TGF‑β, IL‑6/8 and antimicrobial mediators—driving angiogenesis, matrix deposition, keratinocyte migration, immune quieting, and even indirect antimicrobial effects, with open questions around optimal sourcing, dosing, and delivery that ongoing trials continue to refine.
Bottom line: When layered onto guideline‑concordant wound care, UC‑MSC approaches frequently convert fragile, low‑oxygen wound beds into cleaner, granulating surfaces that are easier to maintain and trend toward closure, with encouraging safety to date. HBOT complements this biology by improving dissolved oxygen, leucocyte function, and collagen cross‑linking; together, oxygenation plus pro‑repair signalling can smooth the glidepath from “stalled” to “healing.”
Where improvements tend to show up
- Early (days to 2 weeks): Cleaner wound bed, healthier granulation tissue, reduced peri wound erythema, pain and malodour down, dressings easier to manage; micro perfusion and TcPO₂ begin to improve.
- Next (2–8 weeks): Sustained reduction in wound area and depth, more robust capillary blush at the margins, thicker epithelial layer with better integrity; fewer setbacks from minor trauma in DFU, longer “quiet” periods in venous ulcers, and a clearer transition from fragile to durable coverage in post‑surgical or radiation wounds.
Why umbilical‑cord sources are a strong fit
UC‑MSCs expand efficiently and maintain a youthful, pro‑repair secretome rich in angiogenic factors, anti‑inflammatory mediators, and extracellular‑vesicle cargo that supports keratinocytes, fibroblasts, and endothelial cells. Compared with many adult‑tissue MSCs, UC‑MSCs show robust paracrine activity at low inflammatory set points—a good match for fragile wound beds that need calm, coordinated signals rather than aggressive stimulation. In engineered applications, enhanced VEGF and PDGF expression aims to amplify capillary sprouting and matrix organization precisely where chronic wounds struggle most.
Other stem‑cell and cell‑free options under study
Beyond UC‑MSCs, wound‑healing research includes bone‑marrow and adipose‑derived MSCs, which share core immunomodulatory and pro‑angiogenic behaviours and appear across a growing clinical literature. Cell‑free approaches—purified secretome or exosomes—deliver many of the same trophic signals without whole‑cell transplantation and can be used topically as adjuncts around the wound edge. Platelet‑rich plasma (PRP) is another supportive tool; while distinct from stem‑cell therapy, it provides a concentrated set of growth factors that can complement MSC‑driven repair. The shared objective across platforms is not merely to “cover” a wound, but to re‑educate the wound micro‑environment so it sustains closure and resists breakdown.
How we integrate this at Vega Stem Cell
The treatment process begins with a careful evaluation of the wound to determine the best therapeutic approach. Stem cell therapy is performed through local injections around the affected area, helping to stimulate tissue repair, reduce inflammation, and relieve pain.
For patients with poor blood circulation such as those with ischemic limbs or vascular insufficiency this approach may be combined with vascular therapy to enhance outcomes. This combination improves oxygen and nutrient delivery, boosts regenerative response, and reduces the risk of complications, supporting faster and more effective healing.
All procedures are carried out under medical supervision in a controlled clinical environment to ensure maximum safety and efficacy throughout the treatment process.
Putting it all together
Chronic wounds persist when hypoxia, inflammation, and stalled cell signalling keep regeneration from taking hold. UC‑MSC therapy especially when combined with HBOT and targeted regenerative support aims to tilt the biology back: calmer cytokine activity, new capillary growth, organized matrix deposition, and sustained epithelial closure. For suitable candidates, this approach can be woven into advanced wound care with success measured in what matters most cleaner beds, shrinking dimensions, less pain and infection risk, and a wound that closes and stays closed.
Link to Articles
https://vegastemcell.com/articles/the-role-of-stem-cells-in-wound-healing-and-scarring/
https://vegastemcell.com/articles/how-to-use-stem-cells-for-chronic-wounds/