Sagittal Growth Restriction of the Midface Following Isolated Cleft Lip Repair: A Systematic Review and Meta-Analysis

Author:

Celie Karel-Bart1ORCID,Wlodarczyk Jordan2,Naidu Priyanka3,Tapia Maria Fernanda3,Nagengast Eric1ORCID,Yao Caroline134,Magee William1234

Affiliation:

1. Division of Plastic and Reconstructive Surgery, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA

2. Division of Plastic and Maxillofacial Surgery, Children's Hospital Los Angeles, Los Angeles, CA, USA

3. Operation Smile Incorporated, Virginia Beach, VA, USA

4. Shriners Hospital for Children, Pasadena CA, USA

Abstract

Midface hypoplasia (MFH) is a long-term sequela of cleft lip and palate repair, and is poorly understood. No study has examined the aggregate data on sagittal growth restriction of the midface following repair of the lip, but not palate, in these patients. A systematic review of 3780 articles was performed. Twenty-four studies met inclusion criteria and 11 reported cephalometric measurements amenable to meta-analysis. Patients with Veau class I-III palatal clefts were included so long as they had undergone only lip repair. Groups were compared against both noncleft and unrepaired controls. Cephalometrics were reported for 326 patients (31.3% female). Noncleft controls had an average SNA angle of 81.25° ± 3.12°. The only patients demonstrating hypoplastic SNA angles were those with unilateral CLP with isolated lip repair (77.4° ± 4.22°). Patients with repaired CL had SNA angles similar to noncleft controls (81.4° ± 4.02°). Patients with unrepaired CLP and CL tended toward more protruding maxillae, with SNA angles of 83.3° ± 4.04° and 87.9° ± 3.11°, respectively. Notably, when comparing SNA angles between groups, patients with CLP with isolated lip repair had significantly more hypoplastic angles compared to those with repaired CL ( P < .0001). Patients with CLP with isolated lip repair were also more hypoplastic than noncleft controls ( P < .0001). In contrast, there was no significant difference between the SNA of patients with repaired CL and controls ( P = .648). We found that cleft lip repair only appeared to contribute to MFH in the setting of concurrent cleft palate pathology, suggesting that scarring from lip repair itself is unlikely to be the predominant driver of MFH development. However, studies generally suffered from inadequate reporting of timing, technique, follow-up time, and cleft severity.

Publisher

SAGE Publications

Subject

Otorhinolaryngology,Oral Surgery

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