Since noted by Graber [16], the cause of maxillary growth in CLP patients remains controversial to this day. In our study, we exclusively reviewed ICP patients with Veau types 1 and 2 that underwent surgical repair in our study to determine factors associated with MH. Though the low incidence of MH in our study is similar to that found in the literature [14, 17, 18], our small sample size prevented statistical analysis. However, our results seem to suggest that the age of initial palatal closure and palatoplasty technique are not associated with maxillary growth restriction. Multiple surgeons were involved in our study, and in spite of varied techniques, and differing results in terms of fistula and VPI, the variability did not seem to contribute to maxillary growth in ICP.
Numerous studies have shown the adverse effects of scarring after palatoplasty [5,6,7, 9] and cheiloplasty have on maxillary growth [8, 10, 11]. In our study, we only evaluated ICP patients to isolate the potential effect that palate repair may have on maxillary growth. Only one patient in our cohort developed MH despite a high rate of postoperative complications including VPI and oronasal fistula. This seems to suggest that postoperative complications and the cumulative number of subsequent surgical procedures that address these complications do not contribute to maxillary growth restriction. This may imply that scaring from the initial palatoplasty and subsequent procedures does not affect maxillary growth restriction. Although many authors have focused on the relationship between surgical technique of the initial palatoplasty and maxillary growth [19,20,21,22,23], we believe technical nuances such as raising mucoperiosteal flaps or vomerine flaps may not alter the maxillary growth trajectory. Patient age at the time of repair also did not seem to have an effect either. Our average age at initial palatoplasty exceeded that of the patient requiring MH (19 vs. 14 months). These observations are similar to that of Odom et al. who also noted that timing and techniques for palatal repair do not have a deleterious effect on antero-posterior maxillary growth [14].
The high rate of secondary procedures we observed in our cohort despite a low incidence of MH is also noteworthy. Interestingly, a higher rate of secondary procedures has been reported after cleft palate closure in patients with ICP. As Chorney et al. noted in their case series of 312 patients, patients with Veau type 2 have a statistically higher rate of pharyngeal flap requirement and oronasal fistula repair [21]. Similarly, in their study of 869 non-syndromic cleft palate patients, Jackson et al. found that patients with ICP had the worst speech outcomes and higher rates of secondary surgery for velopharyngeal dysfunction [19]. In our cohort, four patients developed oronasal fistulas and one of these patients required two corrective procedures. This patient as well as others who had multiple corrective surgeries for complications had no evidence of maxillary growth restriction at follow-up. Seventeen patients developed VPI and 4 of these patients required at least 2 revisionary surgeries. Subgroup analysis seemed to suggest that patients whose cleft was repaired prior to 12 months were more likely to develop palatal fistulae, and overall complications where patients whose clefts were repaired between 12 and 18 months had an increased risk to develop VPI. The majority of our patients had their initial corrections performed by non-fellowship trained surgeons prior to 1980. This may explain our high complication rate as evolving surgical techniques significantly improved outcomes after palate repair thereafter. However, in spite of our high reported VPI and fistula rate, we observed a low incidence of MH. Our results seem to suggest that age at palate closure, type of cleft palate (Veau 1 vs. 2) and type of surgical technique may not be associated with MH. Additionally, complications after primary palatoplasty such as VPI and palatal fistula and subsequent procedures may also not restrict maxillary growth.
Due to our low incidence of MH, our ability to deduce statically significant conclusions was limited. Additionally, our study was limited by its retrospective nature and relied on available charting. In our study, MH was defined by clinical judgment to perform LeFort I osteotomy and lacked quantitative lateral cephalograms that may have allowed more objective assessment and comparison to other studies. Larger prospective studies are needed to further evaluate the association of surgical technique and the rate of MH in the ICP patient population.
