The paper published in the Journal of Dentistry, uncovered a link between PI and activated fibroblasts. Activated fibroblasts are cells in the connective tissue that have started to proliferate abnormally. The study also identified three specific marker genes that were overexpressed in PI but not in periodontitis.
The number of people receiving dental implants continues to increase annually, as more individuals become aware of the advantages of replacing missing teeth. However, this rise has also been accompanied by a growing prevalence of PI. While treatment protocols for PI often mirror those designed for managing periodontitis, they have proven to be less effective. Peri-implantitis also has a higher chance of recurrence than periodontitis, posing greater challenges for management.
Researchers said that understanding the key differences in the pathophysiology of PI and periodontitis is essential for developing more specialised and effective treatments for PI.
Yun Hak Kim, a lead researcher on the study at Pusan National University, said, “This study provides essential insights into the role of activated fibroblasts as a distinctive factor in the pathogenesis of PI versus periodontitis. Although PI and periodontitis share clinical similarities, they exhibit distinct biological pathways.
“This research identifies three key biomarkers—ACTA2, FAP, and PDGFRβ—that are markedly overexpressed in PI. These biomarkers have the potential to facilitate differential diagnosis and contribute to the development of PI-specific therapeutic approaches.”
The study
To understand the genetic, immunological and other physiological factors underlying PI and periodontitis, researchers collected gingival tissue from patients with both conditions. The samples were then processed and analysed for RNA obtained from the gingival tissue. The study identified the three genes that could serve as disease-specific biomarkers for PI, which could help clinicians diagnose the condition and make more informed decisions regarding treatment.
Biomarker-based diagnostics could minimise misdiagnoses between PI and periodontitis and enhance patient prognoses. By providing targeted treatment strategies for high-risk patients, particularly in PI, this approach may contribute to reducing recurrence rates and improving overall therapeutic effectiveness.
While the treatment approaches for periodontitis and PI follow a similar protocol, controlling PI with this approach can be challenging. The differentially expressed genes identified in the study could be pivotal in developing new treatment approaches for PI that target its unique pathophysiology.
Yun Hak said, “Over the next five to 10 years, this study’s findings could serve as a fundamental basis for the development of highly specialised, targeted therapies addressing PI, specifically focusing on its unique biological and immunological characteristics compared to periodontitis.
“This targeted approach could significantly contribute to extending the durability and success rates of dental implants, especially for patients at elevated risk of peri-implantitis due to underlying inflammatory conditions. Additionally, by elucidating the role of activated fibroblasts in PI, this research offers valuable insights that could advance our understanding and treatment of other chronic inflammatory diseases with similar cellular mechanisms.”