Primary condylar hyperplasia

Summary

Primary condylar hyperplasia (MONDO:0018793) is a disease. A subtype of temporomandibular joint disorder — broader associated-gene and molecular evidence is on the parent page (see Disease family below).

At a glance

• Prevalence: Unknown (Worldwide) [Orphanet-validated]
• Phenotypes (HPO): 6

Clinical features

Signs & symptoms

Clinical features (HPO)

6 HPO clinical features (Orphanet curated; top 6 by frequency):

HPO ID	Term	Frequency
HP:3000077	Abnormal mandible condylar process morphology	Very frequent (80-99%)
HP:0000306	Abnormality of the chin	Frequent (30-79%)
HP:0000324	Facial asymmetry	Frequent (30-79%)
HP:0009102	Anterior open-bite malocclusion	Frequent (30-79%)
HP:0010754	Abnormality of the temporomandibular joint	Frequent (30-79%)
HP:0001572	Macrodontia	Occasional (5-29%)

Identifiers

Disease identifiers

Field	Value
Canonical name	primary condylar hyperplasia
Mondo ID	MONDO:0018793
Orphanet	477781
UMLS	C5568570
MedGen	1799993
GARD	0021966
Is cancer (heuristic)	no

Also known as: type 1 condylar hyperplasia

Disease family

This is a subtype of temporomandibular joint disorder. Genetic, therapeutic, and trial evidence is largely curated at the broader-term level — see the parent page for the associated-gene cohort and molecular evidence.

Classification path: disease › human disease › disease by body system or component › musculoskeletal system disorder › skeletal system disorder › arthropathy › temporomandibular joint disorder › primary condylar hyperplasia

Related subtypes (2): congenital temporomandibular joint ankylosis, temporomandibular joint dysfunction syndrome

Genetics & variants

GWAS landscape

No GWAS associations recorded — common-variant (GWAS) studies don’t cover this disease (typical for Mendelian / rare diseases). See the curated gene cohort and Mendelian overlap below.

Variant details and genetic-evidence tiers

No tiered GWAS variants or ClinVar records for this disease.

Genes & proteins

No associated-gene cohort resolved for this disease. Atlas builds the molecular and therapeutic sections — associated genes, protein families, druggability, pathways, interactions, and drug associations — by aggregating over a disease’s associated genes (resolved via GWAS / GenCC / ClinVar / CIViC), and none resolved here. This is expected for antibody-mediated, autoimmune, or otherwise non-gene-defined conditions; the curated evidence for this disease is its clinical features, GWAS susceptibility, and clinical trials (above).

Function

No pathway enrichment — requires an associated-gene cohort.

Therapeutics

No druggable-target or therapeutic data for this disease’s cohort.

Clinical trials & evidence

Clinical trials

Clinical trials: 0.