bromochloroacetic-acid and Cleft-Palate

To evaluate the role of keratinized mucosa around dental implants, correlating with other clinical parameters related to the success of dental implants.. Cross-section.. Institutional tertiary referral hospital.. A total of 202 dental implants fixed in the cleft area of 109 patients with cleft lip and/or palate were evaluated. Interventions: The evaluated clinical parameters were probing depth and gingival and plaque indexes on the buccal surface (three sites).. All clinical parameters were correlated with the width of keratinized mucosa around the implants.. The largest probing depths were detected when the width of keratinized mucosa was 2 mm or more, with a statistically significant difference between the means of the probing depth and keratinized mucosa width.. Even though the present results suggest that peri-implant health can be observed in areas with keratinized mucosa width under 2 mm provided an adequate oral hygiene control is performed, longitudinal randomized studies are necessary to analyze the relationship between the width of keratinized mucosa and the health of peri-implant tissues.

Topics: Adolescent; Adult; Cleft Lip; Cleft Palate; Cross-Sectional Studies; Dental Implants; Female; Homeostasis; Humans; Keratins; Male; Middle Aged; Mouth Mucosa

The margin of a palatal cleft is a unique anatomical site since the palatal mucosa is continuous with the nasal or nasopharyngeal mucosa. The aim of this study was to compare the expression patterns of cytokeratins and basal membrane components of the mucosa in the area of the cleft.. Biopsies from the mucosa of the hard palate and from the cleft margin in the soft palate were obtained from five patients during the primary surgical closure of the cleft. The tissues were processed for haematoxylin-eosin staining and for immunohistochemistry. Antibodies against the cytokeratins (CK) 4, 7, 8, 10, 13, 16 and 18, and the basal membrane components heparan sulphate (HS) and collagen type IV (CIV) were used for immunostaining.. The nasopharyngeal epithelium was thinner than the epithelium of the soft palatal mucosa, and showed less interpapillary ridges. The nasopharyngeal epithelium was stratified but expressed the keratins of a simple epithelium (CK 7, 8 and 18). The expression pattern abruptly changed into that of a typical non-keratinized stratified epithelium (CK 4, 13) at the transition to the soft palatal epithelium. The epithelium of the hard palate was a fully differentiated, keratinized and stratified epithelium (CK 10, 16). The basal membrane was thinner in the nasopharyngeal epithelium, which might be related to the presence of abundant inflammatory cells.. The area around the palatal cleft showed three different types of epithelium. There was an abrupt transition in phenotype of the epithelium from the oral side to the nasopharyngeal side.

Topics: Child, Preschool; Cleft Palate; Epithelium; Humans; Infant; Keratins; Mouth Mucosa; Nasopharynx; Palate, Hard

Oral reconstructions for cleft palate repair are often complicated by a shortage of mucosal tissue. This shortage causes scar tissue formation leading to impaired growth of the dento-maxillary complex. The overall aim of our research is to develop a substitute. which limits the iatrogenic effects of cleft palate surgery. This study describes the culture and characterization of mucosal substitutes containing keratinocytes. Epidermal and oral keratinocytes from a beagle dog were cultured on several skin-derived and collagen-based substrates. Oral keratinocytes cultured on the skin-derived substrates closely resembled normal oral epithelium of the dog. A multi-layered epithelium was formed showing parakeratosis, expression of cytokeratin 16 and the formation of a basement membrane. Epidermal keratinocytes cultured on the skin-derived substrates formed an epithelium which was similar to dog epidermis. In contrast, keratinocytes cultured on the collagen-based substrates invaded the substrate without the formation of a multi-layered epithelium. In conclusion, this study shows that oral canine keratinocytes cultured on skin-derived substrates exhibit a tissue organization that resembles normal oral mucosa. This type of mucosal substitute will therefore be used in further studies for implantation on the palate of beagle dogs. These studies might eventually lead to an improvement of cleft palate surgery in humans.

Topics: Animals; Cell Culture Techniques; Cells, Cultured; Cleft Palate; Collagen; Dogs; Humans; Immunohistochemistry; Keratinocytes; Keratins; Mouth Mucosa; Skin; Tissue Engineering

Hay-Wells syndrome, also known as ankyloblepharon-ectodermal dysplasia-clefting (AEC) syndrome (OMIM 106260), is a rare autosomal dominant disorder characterized by congenital ectodermal dysplasia, including alopecia, scalp infections, dystrophic nails, hypodontia, ankyloblepharon and cleft lip and/or cleft palate. This constellation of clinical signs is unique, but some overlap can be recognized with other ectodermal dysplasia syndromes, for example ectrodactyly--ectodermal dysplasia--cleft lip/palate (EEC; OMIM 604292), limb--mammary syndrome (LMS; OMIM 603543), acro-dermato-ungual-lacrimal-tooth syndrome (ADULT; OMIM 103285) and recessive cleft lip/palate--ectodermal dysplasia (CLPED1; OMIM 225060). We have recently demonstrated that heterozygous mutations in the p63 gene are the major cause of EEC syndrome. Linkage studies suggest that the related LMS and ADULT syndromes are also caused by mutations in the p63 gene. Thus, it appears that p63 gene mutations have highly pleiotropic effects. We have analysed p63 in AEC syndrome patients and identified missense mutations in eight families. All mutations give rise to amino acid substitutions in the sterile alpha motif (SAM) domain, and are predicted to affect protein--protein interactions. In contrast, the vast majority of the mutations found in EEC syndrome are amino acid substitutions in the DNA-binding domain. Thus, a clear genotype--phenotype correlation can be recognized for EEC and AEC syndromes.

Topics: Abnormalities, Multiple; Amino Acid Sequence; Ankylosis; Base Sequence; Binding Sites; Blepharitis; Child; Cleft Lip; Cleft Palate; DNA; DNA Mutational Analysis; DNA-Binding Proteins; Female; Filaggrin Proteins; Genes, Tumor Suppressor; Heterozygote; Humans; Immunohistochemistry; Intermediate Filament Proteins; Keratins; Male; Membrane Proteins; Molecular Sequence Data; Mutation, Missense; Phosphoproteins; Protein Structure, Tertiary; Sequence Alignment; Sequence Homology, Amino Acid; Skin; Syndrome; Trans-Activators; Transcription Factors; Tumor Suppressor Proteins

This study was undertaken to examine the normal and abnormal epithelial alterations of secondary palate in rats. Control and dexamethasone-treated embryos and fetuses of Wistar rats were evaluated by macroscopic and scanning electron microscopic analysis prior to, during, and after fusion of palatal processes. Normal alterations of the surface topography included growth and disorganization of medial edge epithelial cells followed by fusion and posterior migration to both the oral and nasal aspects of the palate. No evidence of epithelial cell death or transformation was observed. Dexamethasone-treated fetuses showed epithelial cells increased in size with a large amount of desquamation, followed by deposition of a disorganized cell layer with keratin-like characteristics. This allowed no fusion of palatal processes.

Topics: Animals; Branchial Region; Cell Movement; Cell Size; Cleft Palate; Dexamethasone; Disease Models, Animal; Embryonic and Fetal Development; Epithelial Cells; Epithelium; Extracellular Matrix; Female; Glucocorticoids; Keratins; Male; Microscopy, Electron, Scanning; Palate, Hard; Rats; Rats, Wistar; Teratogens

Several clinical syndromes are characterized by ectodermal dysplasia (ED) in association with clefting of the lip and/or palate. In these syndromes, alopecia is primarily due to abnormalities of the hair shaft associated with increased hair fragility. Scalp dermatitis is yet another peculiar finding, primarily seen in the ankyloblepharon-ED-clefting (AEC) syndrome. We report on a 16-year-old patient with ectrodactyly-ED-clefting (EEC) syndrome, who exhibited a scarring alopecia due to deep folliculitis. On scanning electron microscopy, irregular torsion and longitudinal grooving of the hair shaft (pili torti et canaliculi) were observed. Quantitative determinations of the elastic and viscous parameters of hair demonstrated a normal viscosity but a significantly reduced hair elasticity, indicating either an abnormal composition or a disordered arrangement of microfibrils within the apparently normal keratin matrix. In contrast to the erosive scalp dermatitis of early onset in the AEC syndrome, alopecia in this case of EEC syndrome demonstrated follicular scarring with onset during puberty. We question a possible role of the anatomical hair abnormality in the pathogenesis of chronic deep folliculitis in this and clinically related syndromes.

Topics: Adolescent; Alopecia; Biophysical Phenomena; Biophysics; Cicatrix; Cleft Lip; Cleft Palate; Dermatomycoses; Ectodermal Dysplasia; Elasticity; Fingers; Folliculitis; Hair; Humans; Keratins; Malassezia; Male; Microscopy, Electron, Scanning; Puberty; Scalp Dermatoses; Staphylococcal Skin Infections; Syndrome; Viscosity

Vital cell labeling techniques were used to trace the fate of the medial edge epithelial (MEE) cells during palatal fusion in vivo. Mouse palatal tissues were labeled in utero with DiI. The fetuses continued to develop in utero and tissues of the secondary palate were examined at several later stages of palatal ontogeny. The presence and distribution of DiI was correlated with the presence of cell phenotype-specific markers. During the initial stages of palatal fusion the DiI-labeled MEE were present in the midline position. These cells were attached to an intact laminin-containing basement membrane and contained keratin intermediate filaments. At later stages of palatogenesis the DiI-labeled MEE were not separated from the mesenchyme by an intact basement membrane and did not contain keratin. In late fetal development, DiI-labeled cells without an epithelial morphology were present in the mesenchyme. The transition of the DiI-labeled cells from an epithelial phenotype to a mesenchymal phenotype is consistent with a fate of epithelial-mesenchymal transformation rather than programmed cell death.

Topics: Animals; Cleft Palate; Ectoderm; Epithelium; Fluorescent Dyes; Immunohistochemistry; Keratins; Laminin; Mesoderm; Mice; Palate