FKG UNAIR Lecturer Finds LPS of Bacteria Causing Local Isolate Periodontal Tissue Damage

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Illustration by Feri Fenoria

UNAIR NEWS – Dental disease cases in the community are dominated by caries and periodontal diseases. Periondontal disease is one of the diseases caused by gram-negative bacteria. The Actinobacillus actinomycetemcomitans bacteria produce a poison called Lipopolysaccharide (LPS).

Lipopolysaccharide (LPS) is a component or A. actinomycetemcomitans which is part of the cell wall with virulence factor. LPS interacts with serum proteins through receptors on the surface of epithelial cells. High LPS concentrations increase interleukin (IL) – 1β and IL-6 which results in periodontal tissue damage due to the response of epithelial cytokines, neutrophils, fibroblasts, and monocytes.

A lecturer in Oral Biology, Faculty of Dental Medicine (FKG) Universitas Airlangga (UNAIR), Dr. Rini Devijanti Ridwan, drg., M. Kes conducted a research related to the effect of LPS on dental health. In conducting the research, she was assisted by three oral biology lecturers, Prof. Dr. Tuti Kusumaningsih, drg., M. Kes., Sidarningsih, drg., M. Kes., and Dr. Sherman Salim, drg., MS., Sp. Pros (K).

Rini had isolated LPS and tested it on Wistar mice. LPS from these local isolate bacteria caused some damage to the periodontal tissue and alveolar bone. Isolation was carried out relying on the measurement of osteoblasts, osteoclasts, IL-6, Matrix Metallopeptidase 1 (MMP-1) and RANKL expression.

The results of his research proved that LPS from Actinobacillus actinomycetemcomitans induces expression of IL-6, osteoclastogenesis, and bone resorption. LPS induction in Wistar mice will stimulate an increase in IL-6, causing greater alveolar bone damage. LPS interferes with homeostasis or collective metabolism of genes through phagocytic collagen through fibroblasts.

It implies that IL-6 contributes to the progression of alveolar bone damage from indicators on RANKL that regulate the pathological and physical state of biological conditions or bone resorption. During the pathological inflammation phase of the periodontitis state, RANKL expression was obtained on B cells, T cells, and monocytes.

T-cell and B-cell activation are cellular sources or RANKL in alveolar bone resorption during inflammation. These results support the conclusion that LPS from local isolate A. actinomycetemcomitans over a period of 7 days and 14 days caused periodontal tissue damage and alveolar bone damage in Wistar mice.

It can be concluded that A. actinomycetemcomitans is the major cause of aggressive periodontitis. Aggressive periodontitis attacks many people in a fairly young age.

“Aggressive periodontitis attacks humans at the age of 30-35 years,” she said.

She also revealed that aggressive periodontitis damage is very fast and progressive. The damage seen in this case is shaky teeth even though the condition of the oral cavity is good. Geographical conditions also affect the type of A. actinomycetemcomitans bacteria.

Author: Aditya Novrian

Editor: Khefti Almawalia

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