METHOD: A cross sectional study was carried out where caretakers of cleft lip and/or palate were asked to complete the translated Malay language version of Strength Difficulties Questionnaire. The hearing status of the children was analyzed based on recent pure tone audiometric and tympanogram results. The patients' age, gender, type of cleft pathology, age of palatal surgery and behavioural patterns were examined for their potential relationship with hearing status.
RESULTS: A total of 74 children (148 ears) aged between 7 and 17 years with cleft lip and/or palate were recruited. The result showed 37 ears (25.0%) had hearing loss with majority suffered from mild conductive hearing loss. There were 16 ears (10.8%) that had persistent middle ear effusion. Hearing improvement occurred when palatal repair was performed at the age of less than 1 year old. (p = 0.015) There was no significant relationship between patients' gender, age, type of cleft and history of myringotomy with their hearing status. In terms of behavioural patterns, 16.3% were abnormal for total behavioural score, 39.2% for peer problem and 17.6% for conduct problem. For prosocial behaviour, 16.3% were rated low and very low. There was fair correlation between age and hyperactivity problems (r = 0.44). Patients' gender, type of cleft pathology, had been teased apart and hearing status was found not related to behavioural problems.
CONCLUSION: Cleft lip and/or palate patients have a good longterm hearing outcome. Majority had normal hearing and if there is hearing impairment, it is only a mild loss. Early palatal repair surgery before the age of 1 year can significantly reduce the risk of hearing loss. Cleft lip and/or palate patients experienced peer problems. There was no significant correlation between behavioural difficulty and hearing status among school-aged children with cleft lip and palate.
DESIGN: Saliva samples were collected after the morning meal by placing a sterile cotton swab in the vestibule of the oral cavity from cleft lip and palate patients immediately preoperative and 12 weeks postoperative. Normal children were examined as a control group. Samples were cultured; Staphylococcus and Streptococcus isolates were identified and quantified.
PATIENTS: Fifteen cleft lip and palate patients and 22 normal children, aged 3 to 39 months were examined.
RESULTS: Streptococcus mitis biovar 1, Streptococcus salivarius and Streptococcus oralis of the viridans group of streptococci were the most commonly found in normal children, as well as in cleft lip and palate children. In the cleft lip and palate group, mean streptococcal count was 32.41 (29.80) and 46.46 (42.80) in the pre- and postoperative periods, respectively; in the normal group, the count was 20.93 (27.93) and 49.92 (34.72) at 0 week and 12 weeks, respectively. Staphylococcus aureus was the most common Staphylococcus species found in CLP patients, representing 47.4% postoperatively. In the cleft lip and palate children, mean staphylococcal count was 5.34 (8.13) and 0.56 (0.92) in the pre- and postoperative periods, respectively; in normal children, the count was 0.82 (1.98) and 0.60 (2.55) at 0 and 12 weeks, respectively. The differences were statistically significant only for the staphylococcal count between pre- and postoperative periods in children with cleft lip and palate as tested by analysis of variance (p < .05).
CONCLUSIONS: Cleft lip and palate patients had more colonization by S. aureus compared with normal children, and the colony count decreased significantly following surgical repair of the cleft lip and palate.
RESULTS: A significant nonparametric linkage (NPL) score was detected in family 100. Other suggestive NPL and logarithm of the odds (LOD) scores were attained from families 50, 58, 99 and 100 under autosomal recessive mode. Heterogeneity LOD (HLOD) score ≥ 1 was determined for all families, confirming genetic heterogeneity of the population and indicating that a proportion of families might be linked to each other. Several candidate genes in linkage intervals were determined; LPHN2 at 1p31, SATB2 at 2q33.1-q35, PVRL3 at 3q13.3, COL21A1 at 6p12.1, FOXP2 at 7q22.3-q33, FOXG1 and HECTD1 at 14q12 and TOX3 at 16q12.1.
CONCLUSIONS: We have identified several novel and known candidate genes for nonsyndromic cleft lip and/or palate through genome-wide linkage analysis. Further analysis of the involvement of these genes in the condition will shed light on the disease mechanism. Comprehensive genetic testing of the candidate genes is warranted.