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Query: UMLS:C0031099 (periodontitis)
 12,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report two cases of septic pulmonary embolism associated with periodontitis. Chest CT revealed multiple nodular shadows with features characteristic of septic pulmonary embolism in both patients. Both patients had toothache, fever, and chest pain, and showed findings of periodontitis at initial presentation. Antimicrobial agents combined with dental surgery were successful in treatment. While septic pulmonary embolism from the lesions of periodontitis appears to be rare, periodontitis remains important in the differential diagnosis of septic pulmonary embolism.
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PMID:Septic pulmonary embolism associated with periodontal disease: reports of two cases and review of the literature. 1183 86

Dental infection can be an important source for septic pulmonary embolism (SPE), but only a few cases of SPE accompanying dental infection have been reported. The aim of this study was to characterize the clinical features of SPE induced by dental infection. Patients who fulfilled the diagnostic criteria described in the text were recruited in a retrospective fashion. All 9 patients were men, with a median age of 59 years (range:47 to 74 years). Eight patients had chest pain (88.9%), 5 had a preceding toothache (55.6%) and 3 had preceding gingival swelling (33.3%). Blood cultures obtained from 7 patients were negative. Periodontitis was found in all of the cases, periapical periodontitis in 5 cases, and gingival abscess in 3 cases. The median duration of hospitalization was 15 days, and symptoms were mild in some cases. In addition to antimicrobial therapy, tooth extraction was performed in 3 cases, tooth scaling in 6. SPE induced by dental infection has prominent clinical characteristics such as male preponderance, chest pain, preceding toothache, and mild clinical course.
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PMID:Septic pulmonary embolism induced by dental infection. 2397 Mar 24

Obesity is a risk factor for a plethora of severe morbidities and premature death. Most supporting evidence comes from observational studies that are prone to chance, bias and confounding. Even data on the protective effects of weight loss from randomized controlled trials will be susceptible to confounding and bias if treatment assignment cannot be masked, which is usually the case with lifestyle and surgical interventions. Thus, whilst obesity is widely considered the major modifiable risk factor for many chronic diseases, its causes and consequences are often difficult to determine. Addressing this is important, as the prevention and treatment of any disease requires that interventions focus on causal risk factors. Disease prediction, although not dependent on knowing the causes, is nevertheless enhanced by such knowledge. Here, we provide an overview of some of the barriers to causal inference in obesity research and discuss analytical approaches, such as Mendelian randomization, that can help to overcome these obstacles. In a systematic review of the literature in this field, we found: (i) probable causal relationships between adiposity and bone health/disease, cancers (colorectal, lung and kidney cancers), cardiometabolic traits (blood pressure, fasting insulin, inflammatory markers and lipids), uric acid concentrations, coronary heart disease and venous thrombosis (in the presence of pulmonary embolism), (ii) possible causal relationships between adiposity and gray matter volume, depression and common mental disorders, oesophageal cancer, macroalbuminuria, end-stage renal disease, diabetic kidney disease, nuclear cataract and gall stone disease, and (iii) no evidence for causal relationships between adiposity and Alzheimer's disease, pancreatic cancer, venous thrombosis (in the absence of pulmonary embolism), liver function and periodontitis.
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PMID:Causal inference in obesity research. 2793 71

Both periodontitis and chronic obstructive pulmonary disease (COPD) are among the most common diseases associated with smoking. These conditions frequently present alongside comorbidities including diabetes, coronary heart disease, duodenal ulcer, deep vein thrombosis, pulmonary embolism, osteoporosis and muscle atrophy. Chronic inflammation contributes to the pathology of both periodontitis and COPD, and in patients suffering from both conditions treatment of periodontitis may lead to relief from COPD symptoms as well. Smoking contributes to the underlying pathophysiology by causing local inflammation, increasing the production of proinflammatory cytokines and most importantly, by locally increasing the activity of proteolytic enzymes which degrade the extracellular matrix in both periodontal and lung interstitial tissue. The increase in protease activity and extracellular matrix degradation may explain why periodontitis and COPD comorbidity is so common, a finding which also indicates that therapeutic interventions targeting protease activity and the inflammatory response may be beneficial for both conditions.
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PMID:Review of the association between periodontitis and chronic obstructive pulmonary disease in smokers. 3096 66