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PubMed1991

Ankyloglossia with deviation of the epiglottis and larynx.

We observed ankyloglossia to be usually accompanied by displacement of the epiglottis and larynx. Infants with this disease developed dyspnea and skin and hair abnormalities. In addition, they had other symptoms, such as a dark forehead, a frowning expression, a dark color around the lips, scanty eyebrows, swelling around the palpebrae, harsh respiratory sounds, hard crying, snoring, and frequent yawning. In spite of these abnormalities, they had been considered to be healthy by their pediatricians. Arterial oxygen percent saturation (SaO2) was measured while the infants were asleep, suckling, and awake. The results revealed that their SaO2 was unstable and slightly low. The symptoms and signs of this disease were very similar to those observed in victims of sudden infant death syndrome before their death. Correction of the ankyloglossia and deviation of the epiglottis and larynx resulted in great improvement of these signs as well as a stabilization and increase of SaO2.

Cyanosis↗
PubMed1985

Assessment of lingual function when ankyloglossia (tongue-tie) is suspected.

Dental specialists are frequently confronted with the task of attempting to determine whether a cause and effect relationship exists between a short or restricting lingual frenum (ankyloglossia or tongue-tie) and a specific oral motor dysfunction. Because there is no standardized definition of what constitutes a condition of tongue-tie, the dental practitioner is often unsure as to the appropriate course of action with a patient with suspected ankyloglossia. This paper describes clinical measures that permit quantifying several anatomic and functional aspects of the tongue. Such baseline analysis provides a more definitive appraisal of lingual function as well as a more objective basis for making pre- and posttreatment comparisons.

Child↗
PubMed1992

Enhanced prevalence of ankyloglossia with maternal cocaine use.

A series of 500 term neonates was examined in a well-baby nursery, 68 of whom tested positive for maternal cocaine use. From logistic multiple regression equations, weight and crown-heel length were significantly smaller in the maternal cocaine-use subset of this case-control study. Partial ankyloglossia, with a prevalence of 4.4 percent in the overall series, was significantly more common in males than in females (6.0% versus 2.3%), while race (black or white) had no influence on trait frequency. Controlling for race and sex, ankyloglossia was 3.5 times more likely to occur in the drug-use series, perhaps as a function of diminished mitotic rates.

Abnormalities, Drug-Induced↗
PubMed1998

Are the features of ankyloglossia limited to the lingual fraenum?

A 16-year-old male patient presented with ankyloglossia accompanied by a complaint of forceful spurting of saliva from the mouth and a unilateral swelling in the submandibular region. Following surgical relief of the ankyloglossia, the spurting of saliva had virtually ceased and the submandibular swelling disappeared without recurrence.

Adolescent↗
PubMed1983

[Superior ankyloglossia].

Three cases of congenital superior ankyloglossia, two central and one lateral, are presented. All children had also other malformations. The embryology, etiology and syndromes including ankyloglossia are analysed and the authors review the world literature during de five last years founding only a few similar cases.

Female↗
PubMed1994

The transverse-vertical frenuloplasty for ankyloglossia.

Ankyloglossia is a congenital anomaly in which the frenulum is attached to the tip of the tongue to varying degrees. Children affected by this condition may be unhindered or they may have a variety of problems to include dysfunctional breast-feeding and speech mechanics. This article describes the indications for and surgical technique of the transverse-vertical frenuloplasty for the treatment of ankyloglossia.

Child, Preschool↗
PubMed2005

[Use of Z plasty for ankyloglossia: report of 38 cases].

Z plasty was used in 38 children (male 22, female 16) aged from 0.5 to 6 years with ankyloglossia. There were no infection, dehiscence and tongue adhesion. The wound healed more quickly, and tongue protrusion improved from 13.5 mm preoperatively to 24.6 mm postoperatively. Similarly, tongue elevation improved from 4.8 to 20.6 mm.

Ankyloglossia↗
PubMed1993

The localization of a gene causing X-linked cleft palate and ankyloglossia (CPX) in an Icelandic kindred is between DXS326 and DXYS1X.

The locus responsible for X-linked, nonsyndromic cleft palate and/or ankyloglossia (CPX) has previously been mapped to the proximal long arm of the human X chromosome between Xq21.31 and q21.33 in an Icelandic kindred. We have extended these studies by analyzing an additional 14 informative markers in the family as well as including several newly investigated family members. Recombination analysis indicates that the CPX locus is more proximal than previously thought, within the interval Xq21.1-q21.31. Two recombinants place DXYS1X as the distal flanking marker, while one recombinant defines DXS326 as the proximal flanking marker, an interval of less than 5 cM. Each of the flanking markers recombines with the CPX locus, giving 2-point lod scores of Zmax = 4.16 at theta = 0.08 (DXS326) and Zmax = 5.80 at theta = 0.06 (DXYS1X).

Abnormalities, Multiple↗
PubMed1995

Refinement of the X-linked cleft palate and ankyloglossia (CPX) localisation by genetic mapping in an Icelandic kindred.

The gene responsible for X-linked cleft palate and ankyloglossia (CPX) has previously been localized to the proximal region of the q arm of the X chromosome in both Icelandic and North American Indian kindreds. In this study, further linkage analysis has been performed on the Icelandic family and has resulted in a significant reduction in the size of the interval containing the mutated gene. A new polymorphism at DXS95, together with DXS1002 and DXS349, defines the proximal boundary of the CPX interval, whereas DXYS1X defines the distal boundary. Multipoint analysis supports this localisation with a peak lod score of 12.7, more than 2 lod score units higher than the next most likely position. In order to assess the physical size of the CPX interval prior to initiating yeast artificial chromosome cloning, metaphase fluorescence in situ hybridisation analysis was performed with the closest flanking markers. The size of the interval between DXS95 and DXYS1X was estimated to be approximately 2-3 Mb.

Chromosome Mapping↗
PubMed1988

Macroglossia and ankyloglossia in Beckwith-Wiedemann syndrome.

Since the recognition of the Beckwith-Wiedemann syndrome was first noted in 1963, the number of associated anomalies has vastly increased. The rate of appearance of this abnormality is 1 in 13,5000 births. This article presents a case that includes macroglossia and ankyloglossia along with a bifid uvula and a submucous cleft of the palate. A discussion of treatment follows.

Ankylosis↗
PubMed2002

Cloning and expression analysis of the chick ortholog of TBX22, the gene mutated in X-linked cleft palate and ankyloglossia.

T-box genes constitute a conserved gene family with important roles in many developmental processes. Several family members have been implicated in human congenital diseases. Recently, mutations in TBX22 were found to cause X-linked cleft palate (CPX and ankyloglossia), a semidominant X-linked disorder affecting formation of the secondary palate. Here, we have cloned the chick ortholog of human TBX22 and have analyzed its expression during embryogenesis. Expression is very prominent in the somites and in the myotome, and in the mandible and maxilla of the developing jaw. Other sites of expression include the limbs, the cranial mesenchyme and the eye. Hence, Tbx22 expression domains encompass the regions important for the development of the disease phenotype.

Amino Acid Sequence↗
PubMed2001

The T-box transcription factor gene TBX22 is mutated in X-linked cleft palate and ankyloglossia.

Formation of the secondary palate is a complex step during craniofacial development. Disturbance of the events affecting palatogenesis results in a failure of the palate to close. As a consequence of deformity, an affected child will have problems with feeding, speech, hearing, dentition and psychological development. Cleft palate occurs frequently, affecting approximately 1 in 1,500 births; it is usually considered a sporadic occurrence resulting from an interaction between genetic and environmental factors. Although several susceptibility loci have been implicated, attempts to link genetic variation to functional effects have met with little success. Cleft palate with ankyloglossia (CPX; MIM 303400) is inherited as a semidominant X-linked disorder previously described in several large families of different ethnic origins and has been the subject of several studies that localized the causative gene to Xq21 (refs. 10-13). Here we show that CPX is caused by mutations in the gene encoding the recently described T-box transcription factor TBX22 (ref. 14). Members of the T-box gene family are known to play essential roles in early vertebrate development, especially in mesoderm specification. We demonstrate that TBX22 is a major gene determinant crucial to human palatogenesis. The spectrum of nonsense, splice-site, frameshift and missense mutations we have identified in this study indicates that the cleft phenotype results from a complete loss of TBX22 function.

Amino Acid Sequence↗
PubMed2004

Neonatal lethality of LGR5 null mice is associated with ankyloglossia and gastrointestinal distension.

The physiological role of an orphan G protein-coupled receptor, LGR5, was investigated by targeted deletion of this seven-transmembrane protein containing a large N-terminal extracellular domain with leucine-rich repeats. LGR5 null mice exhibited 100% neonatal lethality characterized by gastrointestinal tract dilation with air and an absence of milk in the stomach. Gross and histological examination revealed fusion of the tongue to the floor of oral cavity in the mutant newborns and immunostaining of LGR5 expression in the epithelium of the tongue and in the mandible of the wild-type embryos. The observed ankyloglossia phenotype provides a model for understanding the genetic basis of this craniofacial defect in humans and an opportunity to elucidate the physiological role of the LGR5 signaling system during embryonic development.

Animals↗
PubMed1993

Congenital ankyloglossia with deviation of the epiglottis and larynx: symptoms and respiratory function in adults.

We operated on 38 adult patients with congenital ankyloglossia with deviation of the epiglottis and larynx. The results were as follows. 1) Most patients had Angle's class III malocclusion, irregular alignment of the upper teeth, and high hard palate. 2) Fifty percent of the patients in our study population had obstructive respiratory failure. Their vital capacity increased significantly after the operation, but changes of forced expiratory volume in 1 second were not prominent. 3) Subjective symptoms of this disease were stiffness of the shoulders, a cold feeling in the extremities, an obstructed feeling in the throat, insomnia, fatigue, dry skin, irritability and/or anxiety, and nervousness. These improved postoperatively. 4) Objective symptoms included snoring, muscle cramps, difficulty in playing wind instruments, hoarseness, and incorrect articulation. The objective symptoms, except for incorrect articulation, improved postoperatively.

Adult↗
PubMed2003

Complete ventral ankyloglossia in three related dogs.

Two 8-month-old and one 7.5-month-old Anatolian Shepherd dogs were examined because of excessive drooling and poor weight gain. The 2 older dogs were full brothers, and the younger dog was their half sister; all 3 had the same sire. Physical examination revealed that the dogs were unable to protrude their tongues properly. In all 3, the tip of the tongue was notched and deviated ventrally when the dog attempted to protrude the tongue. In addition, a thin tissue band between the sublingual surface of the tongue and the floor of the oral cavity was seen; this tissue band extended from the lingual frenulum to the gingiva of the mandibular incisors. Frenuloplasty was performed to correct the complete ventral ankyloglossia. Immediately after surgery, the tongue was more mobile, and during recheck examinations, the dogs appeared to be able to use their tongues normally and could protrude their tongues when panting. They had gained weight and weighed almost as much as their healthy siblings. In all 3 dogs, the tip of the tongue retained a "W" shape.

Animals↗
PubMedDate not supplied

Ankyloglossia and its influence on maxillary and mandibular development. (A seven year follow-up case report).

The consequences of not treating improper tongue function may be very important as this organ can influence face development and dental therapy. The role of the tongue in the development of the skeletal structures of the face has been considered in different perspectives over the years. For some, the tongue adapts to the "tongue box," for others the "tongue box" has been created and stabilized by the morphogenetic action of the tongue during development and growth. A case of ankyloglossia treated with lingual frenectomy and followed clinically and radiologically for seven years is reported. Spontaneous upper arch expansion occurred and therefore orthodontic treatment following surgical intervention was unnecessary.

Child↗