Velasco MG, Ysunza A, Hernandez X, Marquez C. Diagnosis and treatment of submucous cleft palate: a review of 1008 cases. Cleft Palate J. 1988; 25:171-173
Reiter R, Brosch S, Wefe Hl, Schlomer G, Haase S. The submucous cleft palate: diagnosis and therapy. Int J Pediatr Otorhinol. 2011; 75:85-88
The incidence of submucous cleft palate is between 1:1250–1:6000. It is important for this relatively silent deformity to be identified early and referred appropriately as a delay in diagnosis may affect the patient's quality of speech in the long term. This paper presents a case of submucous cleft palate which was diagnosed late (age 14). Nevertheless, by the appropriate intervention of the multidisciplinary cleft team, the patient was treated successfully.
Clinical Relevance: Dentists and doctors need to be aware of the signs and symptoms associated with submucous cleft palate so that they can refer the patient to an appropriate specialist centre for further investigation and treatment. Moreover, patients with this condition are shown to have a higher incidence of dental abnormalities, such as hypodontia and peg-shaped laterals.
Article
Submucous cleft palate is a subgroup of cleft palates and describes an intact palatal mucosa with a cleft in the musculature of the soft palate. This congenital deformity is a result of incomplete fusion of the muscles of the soft palate during palatogenesis and sometimes the palatine bone is also involved. It occurs at approximately the 6th–7th week of intrauterine life. The incidence of submucous cleft palate is between 1:1250–1:6000.1
The clinical signs associated with this deformity have been described by Calnan in 1954 (also known as the Calnan triad).2 They are:
However, the complete classic triad of signs described by Calnan are only present in 23.9% of cases.4 This may account for the late detection of this condition, particularly when the uvula is intact.
Speech-related abnormalities are generally not fully developed in the early stages of life. They often present themselves late, which can result in delayed detection by the cleft team. The symptoms arise mainly as a result of the abnormal position of levator veli palatine muscle. This muscle is displaced anteriorly which results in increased escape of air from the oropharynx to the nasopharynx, leading to velopharyngeal insufficiency (VPI) and presents as hypernasality. A recent study showed that hypernasal speech was present in 51% of cases of which 22% were severe.4
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