How mechanical stress can accelerate bone destruction in periodontitis?

Excessive bite force does not cause alveolar bone loss but significantly worsens it when combined with periodontitis, report researchers in a new study. While traumatic occlusion has long been suspected to exacerbate periodontitis, the molecular mechanisms behind this link were poorly understood. Now, using mouse models of both conditions separately and combined, the researchers conducted comprehensive gene expression analysis across multiple periodontal tissues, identifying key inflammatory pathways upregulated in bone when both conditions were present.

Periodontitis, or inflammation of the tooth-supporting tissues, is one of the most common chronic diseases worldwide and a leading cause of tooth loss in adults. It develops when bacterial buildup around the teeth triggers persistent inflammation, gradually destroying their supporting bone and tissue structures. While bacterial infection is the primary driver of periodontitis, other factors also influence how severely and quickly the condition progresses. These include lifestyle habits such as alcohol consumption and smoking, autoimmune disorders, and-as researchers have long suspected—the way teeth come together when biting or grinding.

When teeth are repeatedly subjected to abnormal or excessive bite forces, known as ‘traumatic occlusion,’ supporting structures come under intense mechanical stress. For decades, dentists and scientists have hypothesized that this overload can worsen periodontitis excessively, so that occlusal adjustment (reshaping of the biting surfaces) is already used in clinical practice as a part of gum disease treatment. However, the evidence supporting this link is somewhat limited, and the molecular mechanisms behind it remain poorly understood.

To address this knowledge gap, a research team led by Assistant Professor Yosuke Tsuchiya from the Department of Periodontology, Graduate School of Medical and Dental Sciences, Institute of Science Tokyo (Science Tokyo), Japan, investigated how traumatic occlusion affects gene expression in periodontal tissues, both with and without periodontitis. Their paper, published online in the Journal of Clinical Periodontology on March 26, 2026, presents the first comprehensive analysis of this kind.

The researchers employed mouse models of periodontitis and traumatic occlusion. To recreate periodontitis, they placed a small silk thread around a molar tooth to trigger bacterial-driven inflammation. To induce traumatic occlusion, they slightly increased the height of the biting surface of the molar tooth using composite resin, thus generating excessive force on it when biting. Mice were divided into four groups: control, periodontitis only, traumatic occlusion only, and a group with both conditions combined.

Using advanced imaging techniques, including micro-computed tomography, the team measured bone loss around the teeth. They also performed transcriptome analysis to examine the activity of thousands of genes in gum tissue, bone, and the periodontal ligament shortly after disease induction. This enabled them to capture early changes in gene expression associated with each condition. Additionally, they investigated the effects of long-term traumatic occlusion alone over a period of 8 weeks.

Interestingly, mice exposed only to traumatic occlusion did not show significant bone loss, even after prolonged exposure. However, when traumatic occlusion was combined with periodontitis, bone loss became significantly more severe. The team’s gene level analysis revealed crucial details, as Tsuchiya explains, “Multiple signaling pathways associated with inflammation and bone metabolism were upregulated in the bone tissue of mice from the combined group.” This confirms that excessive bite force does not directly cause damage but instead amplifies the destructive effects of existing dysregulation caused by periodontitis.

These findings carry meaningful implications for how gum disease is treated. “This study is the first to demonstrate the molecular basis by which traumatic occlusion exacerbates periodontitis, and may provide scientific evidence supporting the clinical application of occlusal adjustment in periodontal therapy,” concludes Tsuchiya. By revealing the biological mechanisms at play, their research may also point toward the future basis of occlusal treatment in periodontal therapy.

Reference:

Tsuchiya, Y., Y.Ohsugi, T.Hirota, et al. 2026. “Traumatic Occlusion Exacerbates Bone Resorption by Modifying Gene Expression in the Bone Tissue of Ligature-Induced Periodontitis in Mice.” Journal of Clinical Periodontology53, no. 6: 838–848. https://doi.org/10.1111/jcpe.70112.