Does periodontal disease cause cardiovascular disease? Analysis of epidemiological evidences

This article reports a critical analysis of epidemiologic studies that evaluated periodontal disease as a cause of cardiovascular disease. Thirty-five studies were identified through a manual search of the special abstracts volumes of the Journal of Dental Research, as well as an electronic search on MEDLINE, LILACS, and ISI and inspection of the articles' bibliographies. Inclusion criteria were: articles in any language published between 1989 and 2000 reporting the presence or absence of an association between periodontal and cardiovascular diseases. Available studies are scarce, and interpretations are limited by potential bias and confounding. The studies analyzed (whether separately or jointly) fail to provide convincing epidemiologic evidence for a causal association between periodontal and cardiovascular diseases. Although the possibility that oral diseases can cause cardiovascular diseases cannot be discarded, until better data are available, periodontal disease should not be incriminated as a cause of cardiovascular disease.     

Menière's disease

Menière's disease is an idiopathic condition classically described as a triad of vertigo, deafness and tinnitus. A wide differential diagnosis exists, but acoustic neuroma must be actively excluded. Various medical and surgical treatment options are available, although two-thirds of patients spontaneously resolve with time.     

Menière and his disease

Prosper Menière (1799-1862) was born in Angers, where his father was a merchant. He finished his medical studies in Paris and subsequently became an assistant at the H?tel Dieu, first to the surgeon Dupuytren and later to the internist Chomel. Meanwhile he helped to combat an epidemic of cholera in the south of France, and he was personal physician to the imprisoned Duchess de Berry, who had returned from exile to reclaim the throne for the Bourbon dynasty. In 1838 he specialised in otology after he had been made head of the Institute for Deaf Mutes in Paris. In 1861 he described a group of patients who suffered recurrent attacks of vertigo as well as abnormal sounds and whose hearing deteriorated over the years. He attributed this condition to a disorder of the inner ear; this went against the prevailing opinion, which attributed most vertiginous attacks to cerebral congestion.     

Quo vadis motor neuron disease?

Motor neuron disease (MND), also known as amyotrophic lateral sclerosis, is a relentlessly progressive neurodegenerative condition that is invariably fatal, usually within 3 to 5 years of diagnosis. The aetio-pathogenesis of MND remains unresolved and no effective treatments exist. The only Food and Drug Administration approved disease modifying therapy is riluzole, a glutamate antagonist, which prolongs survival by up to 3 mo. Current management is largely symptomatic/supportive. There is therefore a desperate and unmet clinical need for discovery of disease mechanisms to guide novel therapeutic strategy. In this review, we start by introducing the organizational anatomy of the motor system, before providing a clinical overview of its dysfunction specifically in MND. We then summarize insights gained from pathological, genetic and animal models and conclude by speculating on optimal strategies to drive the step change in discovery, which is so desperately needed in this arena.     

More illness and less disease? A 20-year perspective on chronic disease and medication

BACKGROUND: The implication of medication is that a drug is given against an illness. Over the last few decades an expanding number of drugs have appeared that focus on reducing risk factors and lifestyle conditions. Aims: To investigate the apprehension in respect of chronic disease among the working population in a Swedish community in 2000 compared with 1980. METHODS: In 1980 and 2000 an analogous questionnaire assessing chronic diseases and medication was mailed to 250 randomly selected persons from a local population between 25 and 70 years of age. RESULTS: Some 80% of the persons (n = 201) replied in 1980 and 78% (n = 195) in 2000. Individuals declaring a chronic disease increased from 23% (46/201) in 1980 to 39.5% in 2000 (p = 0.0005). Corresponding figures for men were 20.6% (20/97) in 1980 and 40.8% (40/98) in 2000 (p = 0,004) and for women 25.0% (26/104) in 1980 and 38.1% (37/97) in 2000 (p = 0.064). Persons who regularly see a doctor increased from 13% to 26% (p = 0.002) and the use of drugs for chronic diseases increased from 19% to 33% (p = 0.002). In 2000 an average of 2.3 drugs per person were used among those with a chronic disease, an increase of 53% since 1980. CONCLUSION: Stated chronic diseases and use of drugs for such diseases increased greatly between1980 and 2000. Prescribing drugs for a "risk" with no apparent illness may be confused with the remedy for an illness.     

Atherosclerosis: an infectious disease?

Traditional risk factors do not fully account for atherogenesis. There is increasing evidence that infectious pathogens, such as Helicobacter pylori, cytomegalovirus, and Chlamydia pneumoniae, may promote the atherosclerotic cascade. Proposed mechanisms include macrophage transformation, endothelial injury, chronic inflammation, and thrombosis. Specific antibiotic therapy may affect outcome.     

Cerebrovascular disease and gait and balance impairment in mild to moderate Alzheimer’s disease

Objectives

Gait and movement abnormalities are traditionally considered infrequent in patients with mild/moderate Alzheimer’s disease (AD). However, an increased risk of falls and gait abnormalities has been detected, even in early stages of the disease. Whether these abnormalities are associated with cerebrovascular disease, which has a high prevalence in AD, remains unclear.

Design

Cross-sectional study.

Setting

Dementia outpatient clinics.

Participants

24 mild/moderate AD patients with (AD+CVD) and 20 without (AD-CVD) cerebrovascular disease without a history of stroke and antipsychotic medications.

Measurements

Physical performance, measured with the Short Physical Performance Battery [SPPB], a summary measure combining 4-meter gait speed, balance and muscle strength, and with 8-meter gait speed with a turn was compared between the two groups.

Results

AD+CVD patients showed a significant higher prevalence of 4-meter gait speed slower than 0,8 m/s (37.5% Vs 5%, p-value=0.01) and balance impairment (37.5% Vs 10%, p-value=0.038), as well as a slower 8-meter gait speed with a turn (mean+SD=0.6±0.2 Vs 0.8±0.2, p-value=0.024). These associations were confirmed in multivariable models. No differences were observed for muscle strength.

Conclusion

In our sample, AD with cerebrovascular disease had worse gait and balance than AD without cerebrovascular disease. If confirmed, these results may have clinical implications, since cerebrovascular disease can be potentially prevented.     

Vaginal cancer: an iatrogenic disease?

Presently we are witnessing two unique occurrences in the field of public health: the first demonstration of transplacental carcinogenesis in humans and the first drug-induced cancer epidemic in women under age 30. This article examines the current status of the vaginal cancer epidemic and possible reasons for the failure of governmental health agencies to recall and test the generation of females who were exposed to diethylstilbestrol (DES) in utero. Epidemiologic evidence indicates that the large majority of "DES daughters" may develop adenosis. The carcinogenicity of other estrogens in wide use is examined. It is pointed out that, although vaginal cancer in daughters exposed to DES in utero provided the clinical evidence to secure a Food and Drug Administration ban on DES as an additive to cattle feed, the FDA approved a new use of DES as a "morning-after pill" contraceptive even though the contraceptive contains 833,000 times the amount of DES banned for human consumption in beef. The lack of standards of informed consent in the testing of the morning-after pill on university women and the additional risk this presents to DES daughters are discussed. The sociopolitical and economic contributing factors to the vaginal cancer epidemic and the extent to which the scientific direction of medical care is influenced by economic factors are examined. Public health measures which might prevent the occurrence of such man-made epidemics in the future are recommended.     

Niacin metabolism and Parkinson’s disease

Epidemiological surveys suggest an important role for niacin in the causes of Parkinson’s disease, in that niacin deficiency, the nutritional condition that causes pellagra, appears to protect against Parkinson’s disease. Absorbed niacin is used in the synthesis of nicotinamide adenine dinucleotide (NAD) in the body, and in the metabolic process NAD releases nicotinamide by poly(ADP-ribosyl)ation, the activation of which has been reported to mediate 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced Parkinson’s disease. Recently nicotinamide N-methyltransferase (EC2.1.1.1) activity has been discovered in the human brain, and the released nicotinamide may be methylated to 1-methylnicotinamide (MNA), via this enzyme, in the brain. A deficiency in mitochondrial NADH: ubiquinone oxidoreductase (complex 1) activity is believed to be a critical factor in the development of Parkinson’s disease. MNA has been found to destroy several subunits of cerebral complex 1, leading to the suggestion that MNA is concerned in the pathogenesis of Parkinson’s disease. Based on these findings, it is hypothesized that niacin is a causal substance in the development of Parkinson’s disease through the following processes: NAD produced from niacin releases nicotinamide via poly(ADP-ribosyl)ation, activated by the hydroxyl radical. Released excess nicotinamide is methylated to MNA in the cytoplasm, and superoxides formed by MNA via complex I destroy complex 1 subunits directly, or indirectly via mitochondrial DNA damage. Hereditary or environmental factors may cause acceleration of this cycle, resulting in neuronal death.     

Does ambient temperature affect foodborne disease?

BACKGROUND: Foodborne illness is a significant public health issue in most countries, including Australia. We examined the association between temperature and salmonellosis notifications, and compared these associations for 5 Australian cities. METHODS: Log-linear models describing monthly salmonellosis notifications in terms of calendar time and monthly average temperatures were fitted over the period 1991 to 2001 for each city. We used a negative binomial chance model to accommodate overdispersion in the counts. RESULTS: The long-term trend showed an increase in salmonellosis notifications in each of the 5 cities. There was a positive association between monthly salmonellosis notifications and mean monthly temperature of the previous month in every city. Seasonal patterns in salmonellosis notifications were fully explained by changes in temperature. DISCUSSION: The strength of the association, the consistency across 5 cities, and a plausible biologic pathway suggest that higher ambient temperatures are a cause of higher salmonellosis notifications. The lag of 1 month suggests that temperature might be more influential earlier in the production process rather than at the food preparation stage. This knowledge can help to guide policy on food preparation and distribution. It also suggests a basis for an early warning system for increased risk from salmonellosis, and raises yet another possible health problem with global warming.     

Liver disease and ��natural�� hepatotoxins

The author discusses the role of “natural” hepatotoxic substances, derived from plants and fungi, in the etiology of liver disease, especially in tropical and subtropical countries. The hazards involved in even the occasional use of natural hepatotoxins and the difficulty in tracing the causative factors of chronic diseases are illustrated by the example of the pyrrolizidine (Senecio) alkaloids. The ingestion by rats of a single dose of these alkaloids can induce chronic liver lesions and even hepatoma which, however, may not become apparent for 1½-2½ years.