Research from the Faculty of Dentistry, Universitas Gadjah Mada, has demonstrated something intriguing. Eugenol, an active compound long known in dental practice, can significantly reduce the number of inflammatory cells in inflamed dental pulp. The study was conducted by drg. Raras Ajeng Enggardipta, MDSc., Sp.KG, together with researchers from the Department of Conservative Dentistry and Department of Oral Biology at the Faculty of Dentistry, Universitas Gadjah Mada, and was published in the August 2016 issue of Indonesian Dentistry Magazine. Using 30 Sprague-Dawley rats as experimental animals, the study sought to answer a question that has long concerned clinicians: How effective is eugenol at reducing pulp inflammation?
Eugenol is certainly not an unfamiliar name in dentistry. Its full chemical name is 4-allyl-2-methoxyphenol, and it is a major component of clove oil, which has been used for centuries to relieve toothache. In modern clinical practice, eugenol is used as a temporary treatment for patients with irreversible pulpitis, a condition in which the dental pulp or nerve has become severely inflamed and cannot recover on its own, typically causing intense spontaneous pain that is difficult to control with ordinary painkillers.
Before patients receive root canal treatment from a dental specialist, eugenol may be applied to cotton and placed inside the tooth cavity to provide temporary symptom relief. The Indonesian Ministry of Health has even included this procedure in basic treatment guidelines for community health centers (Puskesmas). However, scientific evidence explaining how eugenol works at the cellular level remains limited, and this was the gap the study sought to address.
The researchers divided the 30 rats into two groups: a treatment group that received eugenol and a control group that received only distilled water. The maxillary first molar of each rat was drilled until the pulp chamber was reached, deliberately creating a condition of pulpitis. After treatment, the pulp tissue was examined on days 1, 3, 5, 7, and 14. Histological specimens were stained with hematoxylin and eosin, and the numbers of three major types of inflammatory cells—neutrophils, macrophages, and lymphocytes—were counted.
The results were surprising in a positive sense. In the eugenol-treated group, inflammatory cell infiltration was consistently lower than in the control group at every observation point. The difference was statistically significant (p<0.05), indicating that it was unlikely to have occurred by chance.
“Administration of eugenol can reduce the number of inflammatory cells, namely neutrophils, macrophages, and lymphocytes, in the dental pulp of inflamed Sprague-Dawley rats.” — drg. Raras Ajeng Enggardipta, MDSc., Sp.KG, et al., Indonesian Dentistry Magazine, 2016
Neutrophils, the first responders to an injury, were most abundant on the first day and gradually declined thereafter. Macrophages peaked on day 5 before decreasing as the inflammatory phase subsided. Lymphocytes followed a similar pattern. Throughout all phases, the eugenol group consistently showed lower cell counts.
The mechanism behind eugenol’s anti-inflammatory effect is related to its ability to inhibit several key chemical signals involved in inflammation. Eugenol is known to suppress the production of pro-inflammatory cytokines such as IL-1 and TNF-α, two molecules that play important roles in dilating blood vessels and recruiting inflammatory cells to injured tissue. Without these signals, fewer inflammatory cells migrate to the damaged pulp tissue.
In addition, eugenol inhibits IFN-γ, a cytokine involved in transforming monocytes into macrophages at sites of inflammation. By inhibiting this pathway, the number of macrophages formed around the injury is also reduced. This multilayered effect explains why eugenol can suppress all three types of inflammatory cells rather than affecting only one.
Interestingly, by days 7 and 14, the differences in neutrophil and lymphocyte counts between the two groups were no longer statistically significant. This may be because the inflammatory phase had naturally subsided and the body had begun entering the proliferative or healing phase in both the eugenol and control groups. For macrophages, however, the difference remained significant through day 14, suggesting a longer-lasting effect of eugenol on this cell type.
These findings are more than laboratory data. In the context of primary healthcare, eugenol is readily accessible, relatively inexpensive, and already available at basic healthcare facilities such as Puskesmas. This study provides a stronger scientific basis for using eugenol as a temporary treatment for pulpitis before patients are referred to dental specialists.
For comparison, arsenic trioxide was an older alternative once used to devitalize painful dental pulp. However, it is toxic to surrounding tissues and can cause gingival necrosis, bone damage, and even osteomyelitis of the jaw. With growing evidence of eugenol’s anti-inflammatory effectiveness, this safer option is gaining stronger scientific justification.
The researchers also emphasized that further studies are needed to directly measure IL-1 and TNF-α levels and determine the optimal anti-inflammatory dose of eugenol for human dental pulp. In other words, the story of eugenol is far from over, and these findings have merely opened the next chapter.
Author: drg. Achmad Zam Zam Aghasy, M.Kes., Annisa Dwi Noviyanti
Photo: FreePik
Source DOI: http://dx.doi.org/10.22146/majkedgiind.8730