Research Corner - Innate immune training of osteoclastogenesis promotes inflammatory bone loss in mice
Mr Alex Pollard, our Honorary Editor, has written a precis of an article that was recently published.
Innate immune training of osteoclastogenesis promotes inflammatory bone loss in mice
This interesting study published in Developmental Cell explores a concept that challenges long-held assumptions about our immune system. In particular, the idea that the innate immune system lacks memory. Innate immunity has traditionally been considered the more primitive arm of the immune system and was thought to respond the same way each time it encountered an antigen (potential threat). However, this study shows that under certain conditions the innate immune cells can be “trained” to respond more aggressively when re-exposed, a phenomenon termed trained immunity. This raises interesting questions about the role of 'trained' innate cells in chronic inflammatory diseases like periodontitis.
The researchers set out to investigate whether immune training could impact on bone loss using a mouse model. The immune system was primed with β-glucan—a component of fungal cell walls known to induce this phenomena. The “trained” mice were later challenged with models of periodontitis and arthritis and experienced more osteoclast activity and significantly more inflammatory bone loss than untrained controls.
For those of us interested in periodontology, the results of the study are compelling. If this type of immune memory exists in humans, it could help explain why some patients are more susceptible to periodontitis and more prone to bone loss. Several systemic factors such as diet and infections are thought to influence immune training and could tip the balance toward bone loss in susceptible individuals. These results and this line of research raise the question as to whether we might one day modulate these responses as part of our therapeutic approach.
It is important to recognise the limits of this study. The findings come from animal models and while mice are a valuable tool for understanding basic mechanisms, we can’t yet assume these processes take place the same way in humans. However, it does offer interesting avenues for future studies.
Overall, I felt that this study reminds us (if we needed it) how deeply interconnected systemic and oral health are. It also adds another layer of complexity to our understanding of the host response in periodontitis. As always, individualised care with a keen eye on a patients' individual risk factor profile remain at the heart of what we do.