Test Directory

Test Code
1589
Test Name
Metaphyseal Dysplasia With With Maxillary Hypoplasia Or Without Brachydactyly
CPT Codes
81479
Expected Turnaround Time
Typically 2 to 4 weeks from receipt of a sample in the laboratory. All cases involving ongoing pregnancies will be expedited.
Clinical Utility
Genetic analysis to provide a molecular diagnosis of this disorder. Recommended for individuals with a personal and/or family history of this disorder to ensure appropriate treatment and establish recurrence risk for family members.
Specimen and Container Info

Non-Prenatal Specimens

Preferred/Alternate

Specimen Type

Containers

Volume

Preferred Specimen Type

Whole Blood

Lavender Top (EDTA)

3 mL

Alternate Specimen Type

Genomic DNA

1.5 mL Tube

3 µg (at a concentration of at least 30 ng/µl), preferably in TE solution.

Alternate Specimen Type

Fibroblasts

T-25 Flasks

2 confluent T-25 flasks, filled to capacity

Alternate Specimen Type

Saliva (Whole blood is recommended for CNV)

DNA Self-Collection Kit or Oragene Saliva Collection Kit for Young Children

Follow kit instructions (www.dnagenotek.com)

Prenatal Specimens

Either specimen type below is acceptable.

Specimen Type

Containers

Volume

Cultured cells

T-25 Flasks

2 confluent T-25 flasks derived from amnio or CVS samples.

Genomic DNA

1.5 mL Tube

3 µg (at a concentration of at least 30 ng/µl), preferably in TE solution.

NOTE: For specimens from outside of North America, the preferred specimen type is Genomic DNA. HNL Genomics does not recommend shipping whole blood or cultured cells from any location other than the United States, Canada, or Mexico.

Transport Instructions
  • Transport at room temperature within 24 hours.
  • If the specimen cannot be transported to the lab within 24 hours, refrigerate for up to 72 hours.
  • Do not freeze or expose to extreme temperatures, refrigerate for up to 72 hours if cannot be transported to lab within 24 hours. 
Stability Requirements

Room Temperature

24 hours

Refrigerated

72 hours

Causes for Rejection
  • Improperly labeled specimen (minimum of two patient identifiers)
  • Inappropriate specimen type
  • Incomplete or incorrect test request form
  • Insufficient volume
  • Specimen has leaked in transit
  • Specimen without a test order
Methodology
Next Generation Sequencing and Copy Number Variation Analysis
Performing Location
Genomics - Snowdrift
Description

RUNX2 related disorders - Cleidocranial dysplasia (CCD; MIM 119600) is an autosomal dominant disorder caused by mutations in the runt-related transcription factor 2 gene (RUNX2, CBFA1). The RUNX2 product is involved in the differentiation of mesenchymal precursor cells towards osteoblasts. The phenotypic affects of mutations in RUNX2 are potentially protean in consequence. Findings may include moderate short stature, delayed fontanelle closure, parietal, frontal and occipital bossing, open fontanelle in adults, hypertelorism, a low nasal bridge, cleft palate and or a narrow high arched palate with midface hypoplasia or micrognathia. Deafness and various dental abnormalities may also occur. Skeletal findings may include osteosclerosis, increased bone fragility, calvarial thickening, small, hypoplastic or absent clavicles, short ribs, spondylolysis, spondylolisthesis, scoliosis, kyphosis, wide pubic symphysis with delayed mineralization, hypoplastic iliac wing, a broad femoral head with a short neck and coxa vara. The hands may display brachydactyly, a long second metacarpal, short middle phalanges of the second and fifth fingers and abnormal cone shaped phalangeal epiphyses. Syringomyelia has also been observed. Missense, nonsense, splice site, deletion and insertion mutations are the most common mutation types described in RUNX2. Chromosomal translocations and large deletions have been rarely reported.

Metaphyseal dysplasia with maxillary hypoplasia with or without brachydactyly (MDMHB; MIM 156510) is an autosomal dominant disorder caused by an intragenic duplication of exons 3 to 5 of RUNX2.  While cleidocranial dysplasia results from loss of function mutations in RUNX2, MBMHB appears to be due to a gain of function of RUNX2.  MDMHB is characterized by metaphyseal flaring and thin diaphyseal cortices of the long bones, enlargement of the medial halves of the clavicles, maxillary hypoplasia, and dystrophic teeth. The hands may display brachydactyly with short fifth metacarpals and short middle phalanges of the second and fifth fingers.  Other features include mild short stature, wide ischial and pubic bones, mild thickening of frontal and parietal skull bones, platyspondyly, multiple small vertebral fractures, and osteoporosis.

Testing Schedule
Monday-Friday
Genes
RUNX2
MIM
156510
Disease Group
Skeletal Disorders