Comprehensive research conducted over the past decades has shown that there is a definite connection between periodontal and systemic conditions, leading to the development and consolidation of the “periodontal medicine” concept. The 2018 classification of periodontal conditions uses this concept as a key element of the precise diagnosis of and individualized therapeutical protocols for periodontitis patients. The topic of this review is the pathogenic connections that exist between periodontal disease and metabolic/digestive tract conditions. It is important to remember that the oral cavity is a key element of the digestive tract and that any conditions affecting its integrity and function (such as periodontitis or oral cancer) can have a significant impact on the metabolic and gastrointestinal status of a patient. Thus, significant diseases with links to metabolic or digestive disruptions were chosen for inclusion in the review, such as diabetes mellitus, hepatic conditions and gastric cancers. Periodontal pathogenic mechanisms share several significant elements with these conditions, including mutual pro-inflammatory mediators, bacterial elements and genetic predisposition. Consequently, periodontal screening should be recommended for affected patients, and conversely, periodontitis patients should be considered for careful monitoring of their metabolic and digestive status.
Non-surgical periodontal therapy (NSPT) is the first essential step for the management of any periodontitis patient. This study aims to evaluate the impact of NSPT on pro-inflammatory mediators’ regulation and on clinical parameters in periodontitis patients who suffer from chronic hepatitis C. At baseline, selected patients were clinically evaluated for their periodontal status. A subsequent quantitative assessment of C-reactive protein and pentraxin-3 in samples of gingival fluid was performed by Enzyme-Linked Immunosorbent Assay (ELISA). Afterwards, NSPT was performed. Three months after NSPT, the clinical and ELISA assessments were repeated. The results show an improvement of the clinical parameters in periodontitis patients at the three-month recall. In chronic hepatitis C patients with periodontitis, the gingival fluid levels of pro-inflammatory markers reduced significantly. The targeted markers also expressed significant correlations with the clinical parameters used for the assessment of periodontitis’ severity. The results suggest that, while chronic hepatitis C patients exhibited a more negative periodontal status at baseline as compared to non-hepatitis ones, NSPT is effective in decreasing the local periodontal inflammatory reaction and in proving the periodontal status of this type of patients. Given the limitation of the study, periodontal screening and NSPT should be included in the integrated therapeutical approach of chronic hepatitis C patients, for its impact on the local inflammatory response.
Osteopenic bone disease occurs frequently in patients with chronic liver cirrhosis, which most frequently presents with hepatic osteodystrophy. Thus, the relationship between nutritional status and bone mineral density has been poorly measured in liver cirrhosis. This single-center study consisted of a group of 70 patients diagnosed with liver cirrhosis. The nutritional status was evaluated with the Controlling Nutritional Status index, and volumetric vertebral bone mineral density was measured with quantitative computed tomography. Among the 70 patients included, osteopenia and osteoporosis were found in 71% and 24.3%, respectively. Malnutrition assessed with the Controlling Nutritional Status index was observed in 56 (80%) patients and was more frequent in alcoholic cirrhosis patients than viral cirrhosis patients (87.24% vs. 65.22%). Significant positive correlation with Controlling Nutritional Status score was found with Model for End-Stage Liver Disease (rho = 0.576, p-value < 0.0001), Child–Pugh score (rho = 0.670, p-value < 0.0001), International Normalized Ratio (rho = 0.517, p-value = 0.001), aspartate aminotransferase (rho = 0.293, p-value = 0.045), and bilirubin (rho =0.395, p-value = 0.02). Among the liver cirrhosis patients, 15 had osteoporosis and 49 had osteopenia at the lumbar spine (L1-L4 vertebrae), as determined by bone mass density via quantitative computed tomography. A non-significant relationship between Controlling Nutritional Status index-assessed nutritional status and bone mass density was documented. Regarding osteoporosis, no differences were found between the viral and alcohol types of liver cirrhosis patients (p-value = 0.870). Age, obesity, grade of varices, Child–Pugh score, and Model for End-Stage Liver Disease score were associated with osteoporosis in patients with liver cirrhosis.
Data about the association between primary sclerosing cholangitis (PSC) and metabolic bone disease are still unclear. PSC is a chronic cholestatic liver disease (CCLD) which affects the biliary tract, and it has a highly variable natural history. We systematically searched until 28 February 2022 MEDLINE, Cochrane Central Register of Controlled Trials, the ISI Web of Science, and SCOPUS, for studies in patients with PSC. We identified 343 references to potential studies. After screening them, we included eight studies (893 PSC patients, 398 primary biliary cirrhosis (PBC) patients, and 673 healthy controls) for the present meta-analysis. Pooled analyses found no difference in BMD-LS (Z = 0.02, p-value = 0.98) between PSC patients and healthy controls. BMD-LS was statistically lower in PBC patients than in PSC patients (Mean Difference, MD, 0.06, 95% CI 0.03 to 0.09, p-value = 0.0007). The lumbar spine T-score was higher in the PSC patients compared with PBC patients (MD 0.23, 95% CI 0.04 to 0.42, p-value = 0.02). Given the limited literature available, better designed, and larger scale primary studies will be required to confirm our conclusion.
Periodontitis is characterized by low-grade inflammation of the periodontal tissues, the structures that support and connect the teeth to the maxilla and mandible. This inflammation is caused by the accumulation of subgingival bacterial biofilm and gradually leads to the extensive damage of these tissues and the consequent loss of teeth. Hepatitis B is a major global health concern; infection with the hepatitis B virus causes significant inflammation of the liver and the possibility of its gradual evolution to cirrhosis. Hepatitis D, caused by infection with the delta hepatitis virus, is manifest only in patients already infected with the type B virus in a simultaneous (co-infected) or superimposed (superinfected) manner. The dental and periodontal status of patients with hepatitis B/D could exhibit significant changes, increasing the risk of periodontitis onset. Moreover, the progression of liver changes in these patients could be linked to periodontitis; therefore, motivating good oral and periodontal health could result in the prevention and limitation of pathological effects. Given that both types of diseases have a significant inflammatory component, common pro-inflammatory mediators could drive and augment the local inflammation at both a periodontal and hepatic level. This suggests that integrated management of these patients should be proposed, as therapeutical means could deliver an improvement to both periodontal and hepatic statuses. The aim of this review is to gather existing information on the proposed subject and to organize significant data in order to improve scientific accuracy and comprehension on this topic while generating future perspectives for research.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.