Help for Dental Inflammation and Bone Loss May Soon Be at Hand

Researchers at Brazil’s University of Sao Paulo have discovered mechanisms involved in dental pulp inflammation and root apex damage. Such findings may be key in developing therapeutic approaches to mitigate damage such as bone loss resulting from endodontic infection.1

In conducting two studies on mice, the researchers focused on a key mechanism element, a tumor necrosis factor-a receptor (TNFR1), which becomes pro-inflammatory when binding to the cytokine TNF-a. They found that in one instance, the TNF-a-TNFR1 signaling pathway protected teeth and allowed repair. In another case, this pathway led to an inflammatory process and bone loss. The difference depended on whether or not certain microorganisms were present.1


TNF-a is a pro-inflammatory cytokine that promotes biomineralization in dental pulp. TNFR1 is a receptor. It should be remembered that inflammation can be beneficial — a sign that the immune system is working. The TNF cytokines regulate this process as well as signal immune cells to kill tumor cells.1,2

Some cells release cytokines while other cells house cytokine receptors. Once the cytokine TNF-a binds to the receptor, it tells the receptor what to do. Subsequently, the cell may then launch an attack on an invasive virus and increase defenses to prevent future invasions.2


To better understand the role of the TNF-a-TNFR1 signaling pathway, the researchers conducted two studies. In one, the researchers sought to establish the role of the TNF-a-TNFR1 axis in dental pulp repair following pulp capping in vivo. They found that when dental pulp capping, in which bioactive material is placed over exposed pulp, was performed, TNFR1 played a role in forming reparative dentin and healing.

On the other hand, when TNFR1 was genetically removed or deactivated (ablated), key mineralization protein expression was inhibited, which, in turn, led to the development of dental pulp necrosis and apical periodontitis. Such findings demonstrate the importance of this pro-inflammatory signaling pathway in cell differentiation and protein synthesis that control dental biomineralization, an important process in dental healing.1,3


The other study investigated the role of the TNF-a-TNFR1 inflammatory axis in experimentally induced periapical inflammation and bone resorption in vivo. An author in both study articles, Francisco Wanderley Garcia de Paula-Silva, a professor at the University of Sao Paulo’s Ribeirao Preto Dental School, explained that they were studying periapical lesions, “… a very specific type of lesion involving the penetration of bacteria into the dental root canal and resulting in contamination of the canal.”1

The research showed that the TNF-a-TNFR1pathway figures significantly into inflammation and bone loss in the event of root canal contamination by microorganisms. Blocking the pathway in this instance, reduced adverse effects.1,4


The researchers are now turning their attention to therapeutic approaches based on the results of these two studies. Said de Paula-Silva, “We realized from these research findings that a treatment protocol could be developed if this inflammatory response is blocked by inhibiting the receptor. We’re still in the initial stages, based on an animal model, but it’s a very interesting target.”1


  1. EurekAlert. Discovery of mechanism involved in dental inflammation paves way to therapies against bone loss.
  2. Cleveland Clinic. Cytokines.
  3. de Almeida-Junior A, Curcino Araujo LD, Chaves Lamarque GC, et al. Reparative dentin formation following dental pulp capping is mediated by TNFR1 in vivo. J Endod. 2023;49:1329-1336.
  4. Almeida-Junior LA, de Carvalho MS, Almeida LKY, et al. TNF-a-TNFR1 signaling mediates inflammation and bone resorption in apical periodontitis. J Endod. 2023;49:1319-1328.
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