Secondary avascular necrosis

Summary

Secondary avascular necrosis (MONDO:0018374) is a disease (an umbrella term covering 6 Mondo subtypes). A subtype of avascular necrosis — broader associated-gene and molecular evidence is on the parent page (see Disease family below).

At a glance

• Umbrella term: 6 Mondo subtypes

Clinical features

No curated clinical features (Orphanet) for this disease.

Identifiers

Disease identifiers

Field	Value
Canonical name	secondary avascular necrosis
Mondo ID	MONDO:0018374
Orphanet	399169
UMLS	C5680036
MedGen	1842971
GARD	0021659
Is cancer (heuristic)	no

Also known as: secondary AVN

Disease family

This is a subtype of avascular necrosis. 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 › bone disorder › osteonecrosis › avascular necrosis › secondary avascular necrosis

Related subtypes (2): dysbaric osteonecrosis, primary avascular necrosis

Subtypes (6): Gaucher disease type I, hereditary thrombophilia due to congenital histidine-rich (poly-L) glycoprotein deficiency, hereditary antithrombin deficiency, traumatic avascular necrosis, secondary non-traumatic avascular necrosis, osteonecrosis of the jaw

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.