It's not just the gums that are affected by periodontitis
Last reviewed: 07.06.2024
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Tokyo scientists have studied the processes of bone mass loss against the background of periodontitis - a common gum disease. It turned out that double-stranded RNA molecules are capable of triggering a specific immune response that provokes deterioration of the bone system.
Infectious and inflammatory gum diseases affect not only the soft tissues but also the underlying alveolar bones that hold the tooth row. Periodontal bone erosion occurs, which, if not treated appropriately, leads to tooth loss.
Massive microbial plaque in the region of the neck of the teeth is often the cause of periodontal pathologies. The main substances present in the external bacterial membranes are lipopolysaccharides. They provide support for the microbial cell and its defense against immunocyte attack, but at the same time, are capable of inducing an inflammatory response by activating TLR4 receptors on immune cells, which subsequently identify pathogenic bacteria.
In healthy bone tissue, new bone building material is deposited by stromal osteoblasts. At the same time, osteoclasts contribute to the destruction of old bone tissue to remove its mineral content. There is a strict balance between these processes, which makes it possible to maintain the constancy of bone mass. The protein agent RANKL takes an active part in this support. The hormone-like component E2-prostaglandin is produced by osteoblasts and stimulates the activity of RANKL in periodontitis. E2-prostaglandin production is altered and bone mass equilibrium is disturbed.
In their work, the researchers used bone marrow structures and rodent osteoblasts, as well as a synthetic analog of dsRNA. It was observed that dsRNAinduced the differentiation of most osteoclasts - structures that destroy bone tissue. As a result, more E2-prostaglandin was produced, RANKL was activated, and osteoclast differentiation was stimulated. At the same time, mature osteoclasts became "long-lived", bone tissue was subjected to increased adsorption when the inflammatory process caused by microbial infection was activated.
Understanding the mechanism by which the inflammatory response that causes bone damage in periodontitis may be triggered by the entry of dsRNAvia bacteria or by the accumulation of immunocytes in tissues is a major breakthrough in the knowledge of the complications of gingival pathologies.
To date, Tokyo scientists plan to investigate other mechanisms of periodontitis progression. This is necessary to create new drugs and treatment methods to prevent bone destruction in infectious-inflammatory processes.
The research article was published in the pages of the Journal of BiochemistryJournal of Biochemistry.