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Resolving BMP-dependent mechanisms of mandibular outgrowth

Award Number: R03DE035131
ORGANIZATION: NATIONAL INSTITUTE OF DENTAL AND CRANIOFACIAL RESEARCH
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 07/01/2026
PERIOD OF PERFORMANCE END DATE: 06/30/2028

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Resolving BMP-dependent mechanisms of mandibular outgrowth - PROJECT SUMMARY The mandible (lower jaw) is critical for speech and mastication. In patients with micrognathia, a common congenital anomaly occurring about 1 in every 1500 births, the mandible fails to properly grow, demanding invasive and extensive surgical interventions like distraction osteogenesis to repair mandible length. Despite the prevalence of the anomaly, the precise cellular and molecular mechanisms that sustain mandible growth remain unclear. This gap in knowledge hinders treatment options. Bmp signaling is a critical regulator of skeletal shape and size throughout the vertebrate skeleton. However, given the complex redundancy within the pathway and sensitivity of progenitors to altered levels and/or duration of Bmp signaling across development, understanding how Bmp regulators collaborate to ensure proper skeletal formation is critical. In particular, several studies have demonstrated a vital role for the Bmp antagonist Noggin (Nog) in the suppression of chondrocyte proliferation across facial cartilages. In contrast to Nog, other Bmp antagonists like Gremlin 1 appear to be dispensable for early mandible patterning and growth. In zebrafish, we demonstrate a conserved role for nog2 and nog3 in modulating chondrocyte number. However, strikingly, we identify a range of craniofacial defects in grem1a-/-; nog2-/-; nog3+/- zebrafish, including a truncated lower jaw. Unlike many models for micrognathia where disruption of the initial cartilaginous skeleton precedes micrognathia, we find that grem1a-/-; nog2-/-; nog3+/- zebrafish display normal patterning of the early cartilaginous skeleton, but later mandible growth is disrupted. This model enables us to explore previously unknown but fundamental mechanisms of mandible outgrowth. In the proposal, we seek to understand the mechanisms of mandible growth and the spatiotemporal requirements for Bmp antagonists during this process. The proposal aligns with NIDCR’s mission to understand biological processes relevant to craniofacial health, as the outlined project seeks to understand the mechanisms that support mandible growth. Results from this study will initiate a research program that interrogates the mechanisms of sustained growth throughout the craniofacial skeleton, including the mandible and how disrupting the regulatory networks that control these processes lead to micrognathia and other craniofacial defects.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2026 ( Subtotal = $315,000 )
2026	2026	UNIVERSITY OF CALIFORNIA, LOS ANGELES	10889 WILSHIRE BLVD STE 700	LOS ANGELES	CA	90024	LOS ANGELES	USA	Oral Diseases and Disorders Research	000	1	7/1/2026	NEW	$315,000
														Subtotal = $315,000

Grand Total All Awards = $315,000

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Resolving BMP-dependent mechanisms of mandibular outgrowth

Award Number: R03DE035131

ORGANIZATION: NATIONAL INSTITUTE OF DENTAL AND CRANIOFACIAL RESEARCH

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)

PERIOD OF PERFORMANCE START DATE: 07/01/2026

PERIOD OF PERFORMANCE END DATE: 06/30/2028

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