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Mitochondrial Function and Root-Filled Teeth – Detrimental and Unknown Interfaces in Systemic Immune Diseases

BACKGROUND: Mitochondriopathy has recently been linked to several immune system diseases. Historically, there have been many conversations regarding the possible toxic effects of root-filled teeth (RFT), although discussions about the possible decreases in adenosine triphosphate (ATP) activity on th...

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Detalles Bibliográficos
Autores principales: Lechner, Johann, Mayer, Wolfgang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7360410/
https://www.ncbi.nlm.nih.gov/pubmed/32765044
http://dx.doi.org/10.2147/IJGM.S258170
Descripción
Sumario:BACKGROUND: Mitochondriopathy has recently been linked to several immune system diseases. Historically, there have been many conversations regarding the possible toxic effects of root-filled teeth (RFT), although discussions about the possible decreases in adenosine triphosphate (ATP) activity on the mitochondrial membrane, as caused by dental toxins, are rare. In fact, only a few methods currently exist to assess toxin release in teeth. OBJECTIVE: An experimental clinical study design is used to investigate the extent to which RFT release toxins in a solution created specifically following extraction (Tox-sol). Our laboratory is investigating the extent to which these Tox-sols reduce ATP activity in patients. PATIENTS AND METHODS: RFTs were identified and extracted to assess their local toxin release using a semi-quantitative volatile sulfur compound indicator (VSCI). These RFTs are placed in an aqueous solution at room temperature for 24 hours and subsequently removed. The resulting solution (Tox-sol) is diluted to 1:100; peripheral blood mononuclear cells (PBMCs) obtained from patients were added to the solution in the laboratory. The remaining ATP activity was measured on the mitochondrial membrane and was compared with the baseline ATP activity of each patient. RESULTS: The total population (n=30) showed a ~10% reduction in ATP activity following 24 hours of exposure to the Tox-sol. Three groups emerged with greatly reduced (n=16), neutral (n=10), and increased (n=4) ATP activity. In four different disease groups (rheumatism, neurological disorders, allergies, and tumors), a non-disease specific inhibition of ATP activity was observed. DISCUSSION: The study design was limited, as patients were exposed to the Tox-sol and PBMC fraction for only 24 hours. The actual exposure time in a patient’s mouth can continue for years and the actual levels can increase over time. Disease-specific effects of Tox-sol were not found. CONCLUSION: Within the short exposure time of 24 hours, and at a dilution of 1:100, the Tox-sol caused a median decrease in ATP activity of ~15% in 50% of test subjects. A practical VSCI reliably showed the effects of toxic sulfur compounds on the RFT. The toxic degradation products of biogenic amines from RFT can thus serve as possible contributing factors in the development of mitochondriopathies.