Skin and Wound Healing in hEDS

Skin and wound healing issues are common in people with hypermobile Ehlers-Danlos syndrome (hEDS), primarily due to fragile connective tissue. While these problems are typically milder than in classical or vascular forms of EDS, they can still interfere with daily life, delay recovery from injuries or surgery, and lead to visible bruising and scarring. Common symptoms include soft or stretchy skin, easy bruising, slow healing, and thin or wide scars. These complications stem from multiple factors—such as disorganized structural proteins in the skin, overactive repair cells, fragile blood vessels, and minor clotting or immune differences. Management focuses on prevention, gentle care, pain control, and nutritional and emotional support, with some patients benefiting from advanced wound treatments when needed.

Common Skin and Wound‑Related Symptoms in hEDS

• Soft or mildly stretchy skin

  • Soft to the touch with mild hyperextensibility

  • Present in > 50 % of individuals

• Easy bruising

  • Often spontaneous or after minimal trauma

  • Capillary fragility and poor perivascular collagen support

  • Risk of being mistaken for abuse, especially in children

• Slow wound healing

  • Prolonged closure of cuts, surgical sites, or childbirth tears

  • Linked to extracellular matrix (ECM) disarray, myofibroblast over‑activation, and high matrix metalloproteinase (MMP) activity

• Atrophic (“cigarette‑paper”) scars

  • Thin, wide, wrinkled; usually postsurgical or post‑traumatic

• Delayed healing after dental work or childbirth

• Stretch marks (striae) without rapid growth or weight change

Underlying Causes & Mechanisms

• Disorganized skin support structure: The “fabric” inside the skin (collagen, elastin, and other fibers) is loosely or unevenly woven, so cuts close slowly and scars often end up wide and thin.

• Overactive repair cells (myofibroblasts): The cells that pull a wound together stay switched on too long and keep tugging, which can leave weaker, stretched‑out skin.

• High “cleanup” enzymes (MMP‑9 and other MMPs): Enzymes that normally clear away damaged tissue work overtime and chew up new repair tissue faster than the body can replace it.

• Softer, stretchier tissue mechanics: Skin and the thin connective sheets underneath (fascia) are less firm, so stitches have less to grab and new tissue gets less “training” to become strong.

• Fragile tiny blood vessels (capillaries): Small vessels break with even mild bumps, causing easy bruising and bleeding that can slow healing.

• Mild clotting and immune quirks: Platelets and early immune signals can be slightly off‑balance, so clots form more slowly and the first steps of repair don’t run as smoothly.

Prevalence, Severity, and Course

• Most people with hEDS have at least one skin‑related symptom; soft skin and bruising are the most frequent.

• Delayed healing and atrophic scarring occur but are far less common and less severe than in classical or vascular EDS.

• Chronic non‑healing ulcers or spontaneous skin rupture are very rare; their presence should prompt reassessment of the diagnosis or search for comorbid factors.

• Features are usually stable but can worsen with repeated trauma, aging, or nutritional deficits.

Complications by Wound Type

Management and Treatment

Supportive Care

• Injury Prevention – padding bony prominences, supportive clothing, avoiding high‑impact or contact sports

• Skin Protection & Care – gentle cleansers, rich moisturizers, barrier creams, sun protection, minimal use of adhesives/harsh chemicals

• Wound Management – meticulous cleansing, non‑stick dressings, low‑tension or prolonged‑retention sutures, steri‑strips, and close follow‑up

• Bruising Management – compression garments to support capillaries; consider supplements such as ascorbic acid (vitamin C) to bolster collagen cross‑linking

• Scar Management – silicone gels or sheets, pressure therapy, corticosteroid injections, laser or light therapies (data limited)

• Physical Therapy & Exercise – low‑load strengthening, proprioceptive training, core stability, and controlled range‑of‑motion activities

• Pain Management – multimodal approach combining:

  • Heat or cold packs for acute flair control

  • Transcutaneous Electrical Nerve Stimulation (TENS) for neuromodulation of chronic pain

  • Gentle massage or myofascial release when tolerated

  • Over‑the‑counter NSAIDs (e.g., ibuprofen) for inflammatory pain, mindful of GI tolerance

  • Short courses of muscle relaxants for spasm‑related discomfort

  • Referral to pain specialists for refractory pain, considering neuropathic agents or topical anesthetics

• Nutritional Support – adequate protein, vitamin C, zinc, iron, and overall balanced diet; screen and treat GI‑related malabsorption

• Mental‑Health Support – counseling, cognitive‑behavioral therapy, peer groups to address body‑image concerns, anxiety, depression, and medical‑trauma stress

Adjunctive / Specialized Approaches

• Surgical approaches – gentle handling, multilayer closure, non‑absorbable or slow‑absorbable sutures, prophylactic steri‑strips, careful post‑op compression

• Advanced dressings – hydrocolloid, alginate, foam, hydrogel; chosen by exudate level and wound depth

• Negative‑pressure wound therapy (NPWT) for large or slow‑granulating wounds

• Hyperbaric oxygen or electrical stimulation – considered in refractory (resistant to treatment) cases, though hEDS‑specific data are lacking

• Experimental avenues – doxycycline (MMP inhibition), mesenchymal stromal cell infusions, bioengineered skin substitutes; investigational at present

  
  

Prevention

• Gentle handling during medical, dental, and surgical procedures.

• Patient education on minimizing trauma and recognizing skin vulnerability.

• Pre-procedure planning to anticipate complications in dental or obstetric care.

Effectiveness

• Treatments are variably effective; most interventions are supportive (treatments and interventions that aim to manage symptoms, prevent injuries, and enhance the body's natural healing processes without directly addressing the underlying genetic defect).

• There are no disease-modifying therapies, and most individuals continue to experience persistent mild-to-moderate symptoms.

  
  

Other Considerations

• Comorbid bleeding or immune issues – mild platelet defects, mast‑cell activation, or immunoglobulin deficiencies may worsen healing; screen when history suggests.

• Environmental factors – smoking, UV exposure, excessive alcohol, poor sleep, and high psychosocial stress magnify fragility and should be mitigated.

• Multidisciplinary care – coordinated dermatology, surgery, hematology, immunology, physical therapy, nutrition, and psychology maximizes outcomes.

Summary

People with hEDS often experience skin that bruises easily, wounds that heal slowly, and scars that may be thin or wide, though these issues are generally less severe than in other EDS types. These symptoms are caused by a combination of disrupted skin structure, overly active repair processes, and subtle issues with clotting and immune function. While most wounds do eventually heal, they often require extra care and time. Management is supportive and preventive, focusing on injury avoidance, specialized wound care, scar and pain management, nutritional support, and mental health resources. Surgical planning, physical therapy, and multidisciplinary care are also key. Though no treatments can reverse the underlying tissue fragility, good planning and gentle techniques can reduce complications and improve healing outcomes.