Abbreviations
full-thickness skin grafting
INTRODUCTION
Secondary epidermal cysts and milia are benign epithelial lesions that occasionally develop following trauma, burns, or reconstructive surgery. These lesions arise from epidermal cells or adnexal structures implanted within the dermis, leading to the formation of cystic cavities lined with keratinizing squamous epithelium. Although milia are known to occur after dermabrasion and split-thickness skin grafting, their development following full-thickness skin grafting (FTSG) is uncommon. We report a rare case of recurrent secondary milia that developed within the philtral scar after sequential FTSG procedures using retroauricular skin for reconstruction of a philtrum defect caused by a dog-bite injury. To the best of our knowledge, recurrent cystic lesions occurring specifically on the philtrum after FTSG have rarely been described, histologically confirmed, and successfully treated with complete excision.
CASE REPORT
A 29-year-old woman presented with a traumatic defect involving the philtrum and upper lip after being bitten by her pet Jin-do dog. She was evaluated 5 days after the injury. The defect measured 4.5×2.5 cm and exposed the subcutaneous tissue and a portion of the orbicularis oris muscle. The wound margins were irregular and partially epithelialized. During surgery, the irregular wound bed was curetted, and the margins were sharply debrided to expose a uniform wound surface. The philtrum was reconstructed using a full-thickness skin graft harvested from the right retroauricular area and the upper lip defect was repaired using a mucosal V-Y advancement flap. The graft healed well, with full take (
Fig. 1).
Approximately 10 months later, a hypertrophic scar developed on the philtrum, accompanied by mild contracture and pruritus. Scar revision was performed using another full-thickness skin graft harvested from the contralateral retroauricular area (
Fig. 2). Healing remained uneventful. Three months after the revision, the patient noticed the development of white papules associated with tenderness within the grafted area. Intralesional triamcinolone acetonide injections were administered three times at monthly intervals; however, the number of lesions gradually increased. On examination, the grafted skin showed multiple firm, whitish papules measuring 4–6 mm in diameter, with an appearance consistent with milia. The lesions were excised under local anesthesia. The excised specimens consisted of firm keratinous nodules. Histopathological findings showed a keratin-filled dermal cyst lined with stratified squamous epithelium, confirming the diagnosis of secondary milia (
Fig. 3).
Over the following 9 months, the patient experienced two additional recurrences at approximately 3-month intervals. Each recurrence was treated with surgical excision, and histopathological analysis again confirmed milia (
Fig. 4,
Supplementary Fig. 1). After the third excision, the scar remained soft, flat, and stable, with no evidence of recurrence for more than 3 years (
Fig. 5). The patient’s symptoms, including pruritus and pain, resolved completely.
DISCUSSION
Secondary milia are keratin-filled cysts that may arise after trauma, inflammation, or reconstructive surgery [
1,
2]. Although they are well described after dermabrasion and burns, their occurrence after FTSG is uncommon (
Table 1) [
3-
7]. This case illustrates an unusual pattern of recurrent milia developing within grafted skin after sequential FTSG procedures using retroauricular donor skin. Only isolated cases have described similar phenomena. Lee et al. [
8] reported milia formation following facial resurfacing procedures. However, recurrent cystic lesions developing specifically after retroauricular FTSG for philtrum reconstruction have not been previously documented. Accordingly, this case provides insight into potential graft- and recipient-site factors contributing to the development of secondary milia.
Retroauricular skin is preferred in facial reconstruction because of its favorable color and texture match. However, the retroauricular region has been described as an adnexa-rich or se-baceous-associated area in dermatological classification studies [
9-
11]. Because FTSG includes the entire dermis, it inherently transfers sebaceous glands, hair follicles, and eccrine ducts, some of which may survive revascularization. When sebaceousrich graft tissue is transplanted into a recipient site with a different adnexal composition, distortion or obstruction of pilosebaceous ducts may occur, leading to impaired keratin outflow and cyst formation. This process may predispose to keratin accumulation and subsequent secondary milia formation. Although milia are typically sporadic complications of FTSG, donor-site characteristics may have contributed to the development of cystic lesions in this patient.
The patient’s injury resulted from a dog bite, which typically produces irregular wounds with uneven depth. In this case, partial epithelialization was observed in peripheral zones before surgery. Although these areas were curetted, microscopic epidermal remnants may have remained embedded within the wound bed and could have contributed to implantation cyst formation once the graft matured. This mechanism may explain the recurrence despite sequential excisions. These observations highlight the importance of allowing adequate demarcation of traumatic wounds and considering complete excision of epithelialized margins, rather than curettage alone, when preparing the wound bed for grafting.
Following the first FTSG, a hypertrophic scar developed at the grafted philtrum. This condition is characterized by excessive fibroblast activity, increased collagen deposition, and elevated tissue tension. Such structural changes may generate compression or angulation of pilosebaceous ducts, leading to obstruction of glandular outflow. Therefore, the combination of sebaceousrich graft tissue and recipient-site fibrosis may have created a microenvironment favorable for recurrent cyst formation.
Taken together, the recurrent milia observed in this patient likely resulted from multiple interacting mechanisms, including high adnexal density in the donor skin, microscopic epidermal remnants from the initial injury, hypertrophic scarring, and mechanical tension related to dynamic perioral movement. The simultaneous presence of these factors may account for the unusual recurrence of cystic lesions, despite appropriate graft take and otherwise uneventful wound healing. This case underscores several practical considerations for reconstruction of traumatic defects. In irregular bite wounds, complete removal of epithelial remnants through sharp excision may help reduce the risk of milia formation. Donor-site selection may take into account differences in adnexal density, particularly when reconstructing areas with relatively fewer sebaceous glands. Longterm monitoring is recommended, as secondary milia may develop months after grafting, especially in areas prone to scarring or inflammation. Complete surgical excision remains the definitive treatment for established cystic lesions.
Recurrent secondary milia after FTSG are rare but possible complications. In this case, both donor- and recipient-site factors likely contributed to repeated lesion formation. Awareness of these mechanisms may assist surgeons in optimizing woundbed preparation and graft selection to minimize the risk of postoperative cyst formation.