Periodontal disease includes infectious diseases such as gingivitis, periodontal disease. gingivitis and periodontitis, ch. periodontosis. Aggressive bacteria affect the supporting tissues of the teeth. In recent decades, there is increasing evidence that periodontal disease is not limited to the mouth, but can have far-reaching effects on the entire body. The connection between periodontal disease and systemic diseases such as cardiovascular diseases, diabetes, respiratory diseases, rheumatoid arthritis and osteoporosis has become the subject of many studies. Key to understanding these connections is a relatively new branch of science – osteoimmunology.
Relationship of periodontal disease with other systemic diseases
Periodontal disease is a chronic inflammation caused by bacteria present in dental plaque. These bacteria activate an immune response that leads to the breakdown of periodontal tissues. This inflammatory process does not end only in the mouth, but has a systemic effect on the body. The chronic inflammation that characterizes periodontal disease triggers a cascade of immune responses that affect various organ systems.
Cardiovascular diseases:
Epidemiological studies have shown that individuals with periodontal disease are more susceptible to developing atherosclerosis, coronary heart disease, and stroke. It is assumed that bacteria from the oral cavity can enter the bloodstream and contribute to the formation of atherosclerotic plaques. In addition, systemic inflammation resulting from periodontal disease increases inflammatory markers such as C-reactive protein (CRP), further contributing to the development of cardiovascular disease.
Diabetes:
There is a bidirectional relationship between periodontal disease and diabetes. People with poorly controlled diabetes are more prone to developing periodontal disease due to a reduced ability of the immune system to fight infection. At the same time, chronic inflammation and periodontal disease can impair control of blood glucose levels, leading to more difficult-to-control diabetes.
Osteoporosis:
There is evidence that postmenopausal women who have osteoporosis are at increased risk of alveolar bone loss, which may contribute to periodontal disease. Osteoporosis affects bone density throughout the body, including the dental ridge, leading to increased susceptibility to periodontal destruction.
Oncological diseases:
In recent years, research has shown that periodontal disease is associated with an increased risk of various types of cancer, including cancer of the mouth, esophagus, pancreas, and bowel (colorectal cancer). The chronic inflammation that characterizes periodontal disease can create an environment that encourages the development of cancer cells. Studies have shown that people with advanced periodontal disease are more likely to develop these types of cancer. Also, some bacteria associated with periodontal disease, such as Fusobacterium nucleatum, are also associated with bowel cancer. A 2022 review study focuses on the link between the oral microbiome, periodontal disease and the development of colorectal cancer. Research has shown that bacteria associated with periodontal disease can contribute to inflammation and changes in the gut microbiota, increasing the risk of developing colorectal cancer.
Neurological diseases:
Research in recent years has also shown a link between periodontal disease and an increased risk of developing neurological diseases, including Alzheimer’s disease. One of the key bacteria associated with periodontal disease, Porphyromonas gingivalis, produces proteolytic enzymes called gingipains. Gingipains can pass into brain tissue, where they cause inflammation and contribute to the formation of the amyloid plaques that characterize Alzheimer’s disease. In addition, gingipains promote neurodegenerative processes, which may increase the risk of developing other neurological diseases. A 2019 study investigates the presence of Porphyromonas gingivalis and its secretions (gingipains) in the brains of Alzheimer’s patients. The results showed that the presence of these bacteria and their enzymes is associated with the development of neurodegenerative changes, which indicates a possible causal influence of periodontal disease on the development of Alzheimer’s disease. The study also opens up the possibility of developing new therapies that could prevent or slow the progression of neurological diseases by inhibiting the activity of gingipains.
Osteoimmunology and periodontal disease
Osteoimmunology is an interdisciplinary field that studies the interactions between the immune system and bone metabolism. This science is becoming crucial in understanding the pathophysiology of periodontal disease and its systemic consequences.
In periodontal disease, there is an interaction between immune cells and osteoclasts – the cells responsible for breaking down bone. Chronic inflammation leads to the activation of osteoclasts and consequent bone breakdown, which is characteristic of advanced periodontal disease. Osteoimmunological mechanisms thus explain why periodontal disease not only affects soft tissue, but also leads to bone loss, which has both oral and systemic consequences.
Cytokines such as interleukin-1 (IL-1), interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) play a key role in osteoimmunological processes, as they stimulate inflammation and simultaneously activate osteoclasts. This not only leads to the destruction of dental bone, but can also affect the development of osteoporosis and other bone diseases. In addition, research suggests that inflammation resulting from periodontal disease can cause systemic activation of these cytokines, affecting bone metabolism throughout the body.
CONCLUDING REMARKS
Understanding the connection between periodontal disease and other systemic diseases, by incorporating the concepts of osteoimmunology, enables us to have a comprehensive approach to the diagnosis and treatment of these conditions. Comprehensive management of periodontal disease is not only important for maintaining the health of the oral cavity, but also for the prevention and management of various systemic diseases. In the future, further research in the field of osteoimmunology could contribute to the development of new therapeutic approaches that would simultaneously target inflammation and bone metabolism, thus improving treatment outcomes in both periodontal disease and other related diseases.
SOURCES
- Tonetti, M. S., & Van Dyke, T. E. (2013). Periodontitis and atherosclerotic cardiovascular disease: consensus report of the Joint EFP/AAP Workshop on Periodontitis and Systemic Diseases. Journal of Clinical Periodontology, 40(s14), S24-S29.
- Preshaw, P. M., Alba, A. L., Herrera, D., Jepsen, S., Konstantinidis, A., Makrilakis, K., & Taylor, R. (2012). Periodontitis and diabetes: a two-way relationship. Diabetologia, 55(1), 21-31.
- Takayanagi, H. (2009). Osteoimmunology and the effects of the immune system on bone. Nature Reviews Rheumatology, 5(12), 667-676.
- Khosla, S., & Monroe, D. G. (2020). Regulation of bone metabolism by sex steroids. Cold Spring Harbor perspectives in medicine, 10(1), a031211.
- Graves, D. T., & Corrêa, J. D. (2020). Osteoimmunology in the context of periodontal disease. Immunological Reviews, 294(1), 177-191.
- Cao, Y., & Wu, K. (2022). Oral microbiome, periodontal disease, and their role in the development of colorectal cancer. Periodontology 2000, 89(1), 127-138.
- Dominy, S. S., Lynch, C., Ermini, F., Benedyk, M., Marczyk, A., Konradi, A., … & Potempa, J. (2019). Porphyromonas gingivalis in Alzheimer’s disease brains: Evidence for disease causation and treatment with small-molecule inhibitors. Science Advances, 5(1), eaau3333.
-
Alghamdi B, Jeon HH, Ni J, Qiu D, Liu A, Hong JJ, Ali M, Wang A, Troka M, Graves DT. Osteoimmunology in Periodontitis and Orthodontic Tooth Movement. Curr Osteoporos Rep. 2023 Apr;21(2):128-146. doi: 10.1007/s11914-023-00774-x. Epub 2023 Mar 2. PMID: 36862360; PMCID: PMC10696608.
-
Zhang M, Liu Y, Afzali H, Graves DT. An update on periodontal inflammation and bone loss. Front Immunol. 2024 Jun 11;15:1385436. doi: 10.3389/fimmu.2024.1385436. PMID: 38919613; PMCID: PMC11196616.
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