The findings of the study, published in the journal Scientific Reports, show that anti-inflammatory drugs commonly taken by children may be associated with dental enamel defects, found in about 20% of children globally.
Researchers from Brazil’s Ribeirão Preto Dental School (FORP-USP) and School of Pharmaceutical Sciences (FCFRP-USP), investigated the effects of celecoxib and indomethacin, classified by the World Health Organisation as the first line of painkillers along with paracetamol.
The researchers said in recent years, they have been encountering increasing cases of hypominerlisation among the children reporting to healthcare institutions with symptoms of white or yellow tooth spots and dental sensitivity and fragility.
Researchers said that animal studies indicate that there may be a direct correlation between dental enamel diseases (DED) and sickness in the early years of life, including high fever, requiring treatment with NSAIDs.
“These diseases are typically treated with NSAIDs, which inhibit the activity of cyclooxygenase (COX, a key inflammatory enzyme) and reduce the production of prostaglandin (which also promotes inflammation),” Professor Francisco de Paula-Silva, of FORP-USP’s Paediatric Department and last author of the article said.
“However, COX and prostaglandins are known to be physiological for dental enamel, and we, therefore, wondered whether these drugs interfered in the normal formation of this structure,” he added.
Using rats to study the problem, the researchers found that after treating the animals with celecoxib and indomethacin for 28 days, the teeth fractured more easily during extraction despite no visible differences between the teeth of control and treated rats.
Imaging and the chemical composition analysis further revealed that the dental mineralisation of the treated rats affected and teeth contained lower than usual levels of calcium and phosphates, two minerals crucial for forming dental enamel.
“Right now, the study at least offers us a clue to the identity of a new player that may be involved in the development of DEDs. Hitherto we have been totally in the dark,” said Paula-Silva.
“We only achieved these important findings thanks to the efforts of FORP-USP’s Dental Enamel Clinic and collaboration with Lúcia Helena Faccioli, a professor at FCFRP-USP. She made a crucial contribution to our understanding of the role played by lipidic mediators related to inflammatory diseases that affect teeth.”
The researchers now plan to conduct a clinical study to confirm the research findings in the animal model.
“We are going to analyse the medical history of the children with DEDs and their use of these drugs, and we will set up a clinical study that will correlate the two datasets to see if the same thing happens to humans. If so, we can make recommendations on which drugs should not be used for which patients. We can also help work out an appropriate treatment protocol in future,” said Paula-Silva.