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It is not a pooled estimate for the umbrella condition."}],"comparison":{"collapseColumnsLabel":"Show initial comparisons","defaultColumnKeys":["MONDO:0011234/OMIM:602483","MONDO:0013013/OMIM:612798","MONDO:0013845/OMIM:614669","MONDO:0014312/OMIM:615706"],"expandColumnsLabel":"Compare all source entries","intro":"Compare the original source entries. Different entries may describe different patient groups.","primaryFeatureIds":[],"scopeNoteHtml":"

Each column keeps its native condition scope. Initial features are displayed alphabetically, not ranked by clinical importance. Counts remain separate, and an empty cell does not mean a feature cannot occur.

"},"coverage":{"countRecords":63,"emptyColumnKeys":[],"hpoRelease":"2026-06-23","narrativeSourceChanges":[],"records":136,"sourceGroups":{"omim":32,"orphanet":33,"published":71}},"features":[{"hpoId":"HP:0000377","label":"Abnormal pinna morphology","primary":false},{"hpoId":"HP:0003319","label":"Abnormality of the cervical spine","primary":false},{"hpoId":"HP:0009895","label":"Abnormality of the crus of the helix","primary":false},{"hpoId":"HP:0010754","label":"Abnormality of the temporomandibular joint","primary":false},{"hpoId":"HP:0031013","label":"Ankylosis","primary":false},{"hpoId":"HP:0009102","label":"Anterior open-bite malocclusion","primary":false},{"hpoId":"HP:0008772","label":"Aplasia/Hypoplasia of the external ear","primary":false},{"hpoId":"HP:0002104","label":"Apnea","primary":false},{"hpoId":"HP:0000729","label":"Autistic behavior","primary":false},{"hpoId":"HP:0000193","label":"Bifid uvula","primary":false},{"hpoId":"HP:0008513","label":"Bilateral conductive hearing 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cheeks","primary":false},{"hpoId":"HP:0001290","label":"Generalized hypotonia","primary":false},{"hpoId":"HP:0001263","label":"Global developmental delay","primary":false},{"hpoId":"HP:0000162","label":"Glossoptosis","primary":false},{"hpoId":"HP:0011802","label":"Hamartoma of tongue","primary":false},{"hpoId":"HP:0000364","label":"Hearing abnormality","primary":false},{"hpoId":"HP:0000365","label":"Hearing loss","primary":false},{"hpoId":"HP:0002079","label":"Hypoplasia of the corpus callosum","primary":false},{"hpoId":"HP:0008559","label":"Hypoplastic superior helix","primary":false},{"hpoId":"HP:0001252","label":"Hypotonia","primary":false},{"hpoId":"HP:0005216","label":"Impaired mastication","primary":false},{"hpoId":"HP:0008751","label":"Laryngeal cleft","primary":false},{"hpoId":"HP:0001140","label":"Limbal dermoid","primary":false},{"hpoId":"HP:0000040","label":"Long penis","primary":false},{"hpoId":"HP:0000369","label":"Low-set 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Ancestor membership does not transfer phenotype values between groups.","importantHtml":""},"sections":[{"bodyHtml":"

Variants (also called mutations) in several genes, including the GNAI3, EDN1, and PLCB4 genes, can cause auriculocondylar syndrome. These genes provide instructions for making proteins that are involved in chemical signaling. These proteins help transmit information from the outside of the cell to the inside of the cell. This information helps the cell to grow, divide, or take on specialized functions.

Studies suggest that the proteins produced from the GNAI3, EDN1, and PLCB4 genes are involved in a signaling pathway that regulates the movement (migration) and maturation (differentiation) of cells called neural crest cells. During early development, the neural crest cells that are regulated by this signaling pathway form the first and second pharyngeal arches, which ultimately become the jawbones, the muscles that create facial expressions, the inner and outer ears, and other bones and tissues of the head and face.

The GNAI3, EDN1, and PLCB4 gene variants that cause auriculocondylar syndrome cause cells to produce proteins that do not function properly. These altered proteins impair the migration and differentiation of neural crest cells, leading to abnormalities of the structures that are formed from the first and second pharyngeal arches.

Variants have not been found in everyone who has the characteristic features of auriculocondylar syndrome. In these cases, the cause of the condition is unknown.

MedlinePlus Genetics: Causes

","key":"forms","title":"What causes Auriculocondylar syndrome?"},{"bodyHtml":"

A hallmark of this condition is an ear abnormality called a question mark ear, in which the ears have a distinctive question mark shape that is caused by a split that separates the upper part of the ear from the earlobe. Other ear abnormalities that can occur in people with auriculocondylar syndrome include cupped ears, ears with fewer folds and grooves than usual, narrow ear canals, small skin tags in front of or behind the ears, and ears that are rotated backward. Some affected individuals also have hearing loss.

Affected individuals often have a small lower jaw (micrognathia), which is caused by the underdevelopment of the upper portion of the mandible (condyle). These abnormalities can impair the function of the temporomandibular joint (TMJ), which connects the lower jaw to the skull. Problems with the TMJ affect how the upper and lower jaws fit together and can make it difficult to open and close the mouth. Because micrognathia often causes problems with breathing, many infants with auriculocondylar syndrome will need a breathing tube.

Other features of auriculocondylar syndrome can include prominent cheeks, an unusually small mouth (microstomia), a tongue that is placed further back in the mouth than normal (glossoptosis), differences in the size and shape of facial features between the right and left sides of the face (facial asymmetry), and an opening in the roof of the mouth (cleft palate). In rare cases, people with auriculocondylar syndrome have developmental delays and intellectual disabilities.

Source: MedlinePlus Genetics

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