Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0031099 (periodontitis)
 12,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The specific activities of the succinate dehydrogenase-coenzyme Q10 reductase in mitochondria were determined for patients from a normal periodontal practice. The criteria for selection were patients having a bone score of 1.0-4.0 and a pocket depth of 2.5-5.2 mm. All 29 patients showed a deficiency of 20-63% of CoQ10-enzyme activity in gingival biopsies. The mean value was elevated (P less than 0.001) over that of controls. For corresponding blood samples, 24/28 (86%) showed deficiencies of 20-66% and a higher (P less than 0.001) mean value than that of controls. Periodontal patients frequently have significant gingival and leucocytic deficiencies of CoQ10. The leucocytic deficiency indicates a systemic nutritional imbalance and is not likely caused by neglected oral hygiene. A gingival deficiency could predispose this tissue to periodontitis and this disease could even augment the deficiency. These results support previously suggested adjunctive use of CoQ10 with oral hygiene for improved treatment presumably through bioenergetics.
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PMID:Bioenergetics in clinical medicine. IX. Gingival and leucocytic deficiencies of coenzyme Q10 in patients with periodontal disease. 95 67

Eight patients under routine care for periodontitis received oral treatment with a form of coenzyme Q (7 / CoQ10 and 1 / hexahydrocoenzyme Q4). An unchanged plaque score showed the patients cooperated and were under plaque control. The periodontal score decreased (p less than 0.01) on CoQ treatment. Unexpectedly, the periodontal pocket depth decreased (P less than 0.05) on CoQ treatment since all patients were considered candidates for surgical intervention. Healing was so excellent 5-7 days post-biopsy that the biopsy sites were difficult to locate. The healing was viewed as extraordinarily effective. The mean value of the specific activities of the succinate dehydrogenase-coenzyme Q10 reductase of gingival biopsies increased (P less than 0.05) during treatment which could correlate with the extraordinarily healing. Treatment of periodontitis with coenzyme Q should be considered as adjunctive treatment with current dental practice.
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PMID:Bioenergetics in clinical medicine. II. Adjunctive treatment with coenzyme Q in periodontal therapy. 110 47

Topical application of Coenzyme Q10 (CoQ10) to the periodontal pocket was evaluated with and without subgingival mechanical debridement. Ten male patients with adult periodontitis participated and 30 periodontal pockets were selected. During the first 3 weeks, the patients did not receive any periodontal therapy except the topical application of CoQ10. After the first 3-week period, root planning and subgingival scaling were performed in all sites. CoQ10 was applied in 20 of the pockets once a week for a period of 6 weeks. Soybean oil was applied to the remaining 10 sites as a control. In the first 3-week period, significant reductions in gingival crevicular fluid flow, probing depth and attachment loss were found only at experimental sites. After mechanical subgingival debridement, significant decreases in the plaque index, gingival crevicular fluid flow, probing depth and attachment loss were found both at experimental and control sites. However, significant improvements in the modified gingival index, bleeding on probing and peptidase activity derived from periodontopathic bacteria were observed only at experimental sites. These results suggest that topical application of CoQ10 improves adult periodontitis not only as a sole treatment but also in combination with traditional nonsurgical periodontal therapy.
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PMID:Effect of topical application of coenzyme Q10 on adult periodontitis. 775 36

Oxidative stress is one of the factors that could explain the pathophysiological mechanism of inflammatory conditions that occur in cardiovascular disease (CVD) and periodontitis. Such inflammatory response is often evoked by specific bacteria, as the lipopolysaccharide (LPS) of Porphyromonas gingivalis is a key factor in this process. The aim of this research was to study the role of mitochondrial dysfunction in peripheral blood mononuclear cells (PBMCs) from periodontitis patients and to evaluate the influence of LPS on fibroblasts to better understand the pathophysiology of periodontitis and its relationship with CVD. PBMCs from patients showed lower CoQ10 levels and citrate synthase activity, together with high levels of ROS production. LPS-treated fibroblasts provoked increased oxidative stress and mitochondrial dysfunction by a decrease in mitochondrial protein expression, mitochondrial mass, and mitochondrial membrane potential. Our study supports the hypothesis that LPS-mediated mitochondrial dysfunction could be at the origin of oxidative stress in periodontal patients. Abnormal PBMC performance may promote oxidative stress and alter cytokine homeostasis. In conclusion, mitochondrial dysfunction could represent a possible link to understanding the interrelationships between two prominent inflammatory diseases: periodontitis and CVD.
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PMID:Mitochondrial dysfunction promoted by Porphyromonas gingivalis lipopolysaccharide as a possible link between cardiovascular disease and periodontitis. 2135 1