Chung-Woo Lee, Sung-Yun Hwang, Ladan Esmaeili, Dae-Seok Hwang
Maxillary AVN after Le Fort I osteotomy is an exceptionally rare but serious complication. The available evidence supports a multifactorial mechanism in which multiple vascular insults cumulatively impair collateral perfusion rather than a mechanism driven by isolated descending palatine artery injury. Surgical prevention should therefore emphasize preservation of overall maxillary perfusion and collateral soft-tissue attachments.
BACKGROUND: Maxillary avascular necrosis (AVN) after Le Fort I osteotomy is rare but potentially devastating. Although injury to the descending palatine artery has traditionally been regarded as a major cause, the relative contribution of individual vascular and surgical factors remains unclear. This systematic review aimed to synthesize the clinical evidence on maxillary AVN after orthognathic surgery and to evaluate whether postoperative ischemic complications are better explained by isolated arterial injury or cumulative vascular compromise.
MAIN BODY: A systematic literature search of PubMed, Scopus, Web of Science, and Embase was performed from database inception to May 2026 in accordance with PRISMA 2020 guidelines. English-language retrospective cohort studies, prospective cohort studies, and case series reporting maxillary AVN or ischemic complications associated with orthognathic surgery were included. Single-case reports, reviews, conference abstracts, editorials, and studies with insufficient clinical data were excluded. Seven studies were included in the qualitative synthesis. Reported ischemic manifestations ranged from tooth discoloration and pulpal necrosis to gingival necrosis, dentoalveolar sequestration, partial maxillary necrosis, and anterior segment AVN. Among cohort studies, clinically significant ischemic complications were uncommon, with reported rates ranging from 0.2% to 3.3%, whereas tooth discoloration reflecting pulpal ischemia was reported in 3.4% of orthognathic surgery patients. Segmented or multisegment Le Fort I osteotomy, transverse expansion, large maxillary advancement, palatal soft-tissue compromise, cleft-related scarring, and previous palatal surgery were repeatedly described among affected patients. However, no single factor consistently explained all reported cases. The relationship between descending palatine artery injury and ischemic complications was inconsistent, and ligation alone was not uniformly associated with AVN.
CONCLUSION: Maxillary AVN after Le Fort I osteotomy is an exceptionally rare but serious complication. The available evidence supports a multifactorial mechanism in which multiple vascular insults cumulatively impair collateral perfusion rather than a mechanism driven by isolated descending palatine artery injury. Surgical prevention should therefore emphasize preservation of overall maxillary perfusion and collateral soft-tissue attachments.