Official websites use .gov

A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS

A lock ( 🔒 ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

Need Help

The role of taste receptor cells in periodontal homeostasis

Award Number: R01DE035102
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: 05/01/2026
PERIOD OF PERFORMANCE END DATE: 04/30/2031

Group Awards By:

View Award Description

The role of taste receptor cells in periodontal homeostasis - Project Summary Periodontal disease, caused by bacterial infection and inflammation of the gums and supporting bone, affects nearly 50% of U.S. adults over the age of 30, with approximately 9% suffering from severe periodontitis. The hallmark of this disease is the progressive destruction of alveolar bone, ultimately leading to tooth loss and significant oral disability. Periodontitis is particularly prevalent among older adults and is associated with increased risk for systemic conditions such as atherosclerosis, rheumatoid arthritis, and diabetes mellitus. The disease arises from polymicrobial dysbiosis that disrupts the balanced oral microbiota, alongside impaired host innate immune responses that contribute to tissue destruction. While the roles of microbial communities and immune dysfunction in periodontitis are well established, the specific gingival cell types involved in protective responses remain poorly understood. Recent studies have identified taste-like chemosensory cells—solitary chemosensory cells (SCCs) and tuft cells—in various mucosal tissues as key sentinels that detect microbial signals and initiate innate immune responses. Building on this, our preliminary work has identified SCCs and macrophages (MΦ) in the mouse gingiva as components of the epithelial barrier that protect against bacterial invasion. Both cell types express bitter taste receptors and associated signaling components, respond to bitter and bacterial stimuli, and activate innate immune pathways that mitigate periodontal inflammation and bone loss. This proposal aims to expand upon these findings by: • Aim 1: Investigating how taste signaling in gingival macrophages contributes to both the pathogenesis and protection mechanisms in periodontal disease. • Aim 2: Identifying the protective mechanisms by which gingival SCCs and MΦ reduce periodontal bone loss in response to bitter compound stimulation. Overall, this study represents a significant advancement in our understanding of periodontal disease pathophysiology. Activating SCCs and MΦ through bitter compounds offers a novel, non-invasive therapeutic strategy. Furthermore, this approach holds promise for clinical translation through advanced delivery systems such as nanoparticles and hydrogels.


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 = $522,405 )
2026	2026	TRUSTEES OF THE UNIVERSITY OF PENNSYLVANIA, THE	3451 WALNUT ST	PHILADELPHIA	PA	19104	PHILADELPHIA	USA	Oral Diseases and Disorders Research	000	1	4/27/2026	NEW	$522,405
														Subtotal = $522,405

Grand Total All Awards = $522,405

Top

All Categories

About

Search

Reports

Data Submission

Award Information

The role of taste receptor cells in periodontal homeostasis

Award Number: R01DE035102

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: 05/01/2026

PERIOD OF PERFORMANCE END DATE: 04/30/2031

Federal Websites

Department of Health & Human Services

HHS Operating Divisions

HHS Staff Divisions

Download A Document Viewer