The impact of cleft lip and palate repair on maxillofacial growth

Surgical correction is central to current team-approached cleft treatment. Cleft surgeons are always concerned about the impact of their surgical maneuver on the growth of the maxilla. Hypoplastic maxilla, concaved mid-face and deformed dental arch have constantly been reported after cleft treatments. It is very hard to completely circumvent these postoperative complications by current surgical protocols. In this paper, we discussed the factors that inhibit the maxillofacial growth on cleft patients. These factors included pre-surgical intervention, the timing of cleft palate and alveolae repair, surgical design and treatment protocol. Also, we made a review about the influence on the maxillary growth in un-operated cleft patients. On the basis of previous researches, we can conclude that most of scholars express identity of views in these aspects： early palatoplasty lead to maxilla growth inhibition in all dimensions; secondary alveolar bone graft had no influence on maxilla sagittal growth; cleft lip repair inhibited maxilla sagittal length in patients with cleft lip and palate; Veau＇s pushback palatoplasty and Langenbeck＇s palatoplasty with relaxing incisions were most detrimental to growth; Furlow palatoplasty showed little detrimental effect on maxilla growth; timing of hard palate closure, instead of the sequence of hard or soft palate repair, determined the postoperative growth. Stilt, scholars hold controversial viewpoints in some issues, for example, un-operated clefts have normal growth potential or not, pre-surgical intervention and pharyngoplasty inhibited maxillofacial growth or not.

A preliminary study on the teratogenesis of dexamethasone and the preventive effect of vitamin B_(12 )on murine embryonic palatal shelf fusion in vitro

Excessive dexamethasone (Dex) administrated into pregnant mice during critical periods of palatal development can produce a high incidence of cleft palate. Its mechanisms remain unknown. Vitamin B12 has been shown to antagonize the tera- togenic effects of Dex, which, however, remains controversial. In this study, we investigated the effects of Dex and vitamin B12 on murine embryonic palatal shelf fusion using organ culture of murine embryonic shelves. The explanted palatal shelves on em- bryonic day 14 (E14) were cultured for 24, 48, 72 or 96 h in different concentrations of Dex and/or vitamin B12. The palatal shelves were examined histologically for the morphological alterations on the medial edge epithelium (MEE) and fusion rates among different groups. It was found that the palatal shelves were not fused at 72 h or less of culture in Dex group, while they were completely fused in the control and vitamin B12-treated groups at 72 and 96 h, respectively. The MEE still existed and proliferated. In Dex+vitamin B12 group the palatal shelves were fused at each time point in a similar rate to controls. These results may suggest that Dex causes teratogenesis of murine embryonic palatal shelves and vitamin B12 prevents the teratogenic effect of Dex on palatogenesis on murine embryos in vitro.

A preliminary study on the key factors contributing to the attractive lips of Chinese children

Objective:To explore the aesthetic characteristics of the Chinese children lips.Methods: Frontal and profile photographs of 653 healthy children were categorized as the attractive and the unattractive by three laypersons and objectively measured for comparison.Results: The attractive group tended to be smaller in the upper paramedian red lip height,the lower paramedian red lip height,the midline upper red lip height,the central bow angle,and the lip angle,while greater in the Cupid’s bow width.Conclusions:Thinner lips seemed to be more attractive than full ones among Chinese children.

Synergistic injection of the thermosensitive hydrogel and Bi-based alloy bone cement for orthopaedic repair

Low-melting-point alloys have the advantages of good biocompatibility, plasticity, and near-bone mechanical strength, making them suitable as bone defect-filling materials for direct injection into defective bone sites. However, using low-melting-point alloys for orthopedic implants poses the challenge of causing thermal damage to the surrounding bone tissue during injection. In this study, a thermosensitive hydrogel is prepared and synergistically injected into the bone defect site with BiInSn. BiInSn solidifies and releases heat during injection, while the thermosensitive hydrogel absorbs heat and transforms into a gel state,encapsulating BiInSn. Therefore, the surrounding bone tissue is effectively protected from thermal damage. When BiInSn and the thermosensitive hydrogel were injected synergistically, in vitro thermal experiments revealed that the maximum temperature of the surrounding bone tissue reached 42℃. This temperature is below the 47℃ threshold, which causes permanent damage to bone tissues. In vivo experiments demonstrated that rats in the BiInSn-thermosensitive hydrogel group exhibited better recovery at the bone defect sites. These results suggest that the synergistic injection of Bi-based alloy and thermosensitive hydrogel is beneficial in reducing thermal damage to bone tissue, guiding bone tissue growth, and effectively facilitating the repair of bone defects.

Effect of vitamin B12 on cleft palate induced by 2,3.7.8-tetrachlorodibenzo-p-dioxin and dexamethasone in mice

The purpose of this study was to investigate the effect of vitamin B12 on palatal development by co-administration of 2,3,7,8-tetrachlorodibenzo-p-dioxin （TCDD） and dexamethasone （DEX）. We examined the morphological and histological features of the palatal shelf and expression levels of key signaling molecules （trans- forming growth factor-β3 （TGF-β3） and TGF-β3 type I receptor （activin receptor-like kinase 5, ALK5）） during pala- togenesis among a control group （Group A）, TCDD＋DEX exposed group （Group B）, and TCDD＋DEX＋vitamin B12 exposed group （Group C）. While we failed to find that vitamin B12 decreased the incidence of cleft palate induced by TCDD＋DEX treatment, the expression levels of key signaling molecules （TGF-~3 and ALK5） during palatogenesis were significantly modulated. In TCDD＋DEX exposed and TCDD＋DEX＋vitamin B12 exposed groups, palatal shelves could not contact in the midline due to their small sizes. Our results suggest that vitamin B12 may inhibit the expression of some cleft palate inducers such as TGF-β3 and ALK5 in DEX＋TCDD exposed mice, which may be beneficial against palatogenesis to some degree, even though we were unable to observe a protective role of vitamin B12 in morphological and histological alterations of palatal shelves induced by DEX and TCDD.