Disrupting the intrinsic growth potential of a suture contributes to midfacial hypoplasia.
Children with unoperated cleft palates have nearly normal growth of their faces whereas patients who have had early surgical repair often exhibit midfacial hypoplasia. Surgical repair is responsible for the underlying bone growth arrest but the mechanisms responsible for these surgical sequelae are poorly understood. We simulated the effect of cleft palate repair by raising a mucoperiosteal flap in the murine palate. Three-dimensional micro-CT reconstructions of the palate along with histomorphometric measurements, finite element (FE) modeling, immunohistochemical analyses, and quantitative RT-PCR were employed to follow the skeletal healing process. Inflammatory bone resorption was observed during the first few days after denudation, which destroyed the midpalatal suture complex. FE modeling was used to predict and map the distribution of strains and their associated stresses in the area of denudation and the magnitude and location of hydrostatic and distortional strains corresponded to sites of skeletal tissue destruction. Once re-epithelialization was complete and wound contracture subsided, the midpalatal suture complex reformed. Despite this, growth at the midpalatal suture was reduced, which led to palatal constriction and a narrowing of the dental arch. Thus the simple act of raising a flap, here mimicked by denuding the mucoperiosteum, was sufficient to cause significant destruction to the midpalatal suture complex. Although the bone and cartilage growth plates were re-established, mediolateral skeletal growth was nonetheless compromised and the injured palate never reached its full growth potential. These data strongly suggest that disruption of suture complexes, which have intrinsic growth potential, should be avoided during surgical correction of congenital anomalies.
Department of Oral and Maxillofacial Surgery, West China Stomatology Hospital, Chengdu, China 610041; Division of Plastic and Reconstructive Surgery, Department of Surgery, Stanford School of Medicine, Stanford, CA 94305, USA.
Jingtao
J
Li
College of Medicine, University of Arizona, Tucson, AZ 85721, USA; Division of Plastic and Reconstructive Surgery, Department of Surgery, Stanford School of Medicine, Stanford, CA 94305, USA.
Chelsey A
CA
Johnson
Division of Plastic and Reconstructive Surgery, Department of Surgery, Stanford School of Medicine, Stanford, CA 94305, USA.
Andrew A
AA
Smith
Division of Plastic and Reconstructive Surgery, Department of Surgery, Stanford School of Medicine, Stanford, CA 94305, USA; Dental School, University Paris Descartes PRES Sorbonne Paris Cité, EA 2496, Montrouge, France; AP-HP Odontology Department Bretonneau, Hôpitaux Universitaires Paris Nord Val de Seine, Paris, France.
Benjamin
B
Salmon
Department of Oral and Maxillofacial Surgery, West China Stomatology Hospital, Chengdu, China 610041.
Bing
B
Shi
Division of Plastic and Reconstructive Surgery, Department of Surgery, Stanford School of Medicine, Stanford, CA 94305, USA.
John
J
Brunski
Division of Plastic and Reconstructive Surgery, Department of Surgery, Stanford School of Medicine, Stanford, CA 94305, USA. Electronic address: jhelms@stanford.edu.
Jill A
JA
Helms
D000818:Animals; D000831:Animals, Newborn; D002972:Cleft Palate / Q000473:pathology / Q000601:surgery; D006801:Humans; D007231:Infant, Newborn; D063175:Mandibular Reconstruction / Q000009:adverse effects / Q000379:methods*; D008437:Maxilla / Q000254:growth & development / Q000601:surgery; D051379:Mice; D008810:Mice, Inbred C57BL; D010159:Palate / Q000254:growth & development* / Q000601:surgery*; D013537:Sutures / Q000009:adverse effects; D014945:Wound Healing / Q000502:physiology
Cleft palate; Growth arrest; Midpalatal; Mucoperiosteal denudation; Repair