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Recent epidemiologic surveys and studies have provided important information on the prevalence, extent, and severity of periodontal diseases in the United States. Over 50% of adults had gingivitis on an average of 3 to 4 teeth. Subgingival calculus was present in 67% of the population. Adult periodontitis, measured by the presence of periodontal pockets > or = 4 mm, was found in about 30% of the population on an average of 3 to 4 teeth. Severe pockets > or = 6 mm were found in less than 5% of the population. Attachment loss > or = 3 mm was found in 40% of the population. Gingival recession accounted for a significant amount of attachment loss. The prevalence of early-onset periodontitis ranged from less than 1% in 14- to 17-year-olds to 3.6% in young adults aged 18 to 34. Extensive and severe periodontitis was much more prevalent in minorities, people with less than a high school education, and those who had seen a dentist infrequently and had subgingival calculus. Smoking and diabetes have been identified as risk factors, especially diabetics with poor metabolic control, a long duration of the disease, and extensive subgingival calculus. Under managed care, there has been an expansion of soft tissue management programs in the offices of general dentists and referral guidelines which limit referral of patients with moderate periodontitis. Quality-assurance mechanisms will be essential for the diagnosis and treatment of persons with periodontitis.
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PMID:Periodontal diseases in the United States population. 952 27

As interest in women's health issues grows, there is increasing concern that today's practice of medicine may not meet the health needs of women. A primary reason is the gender bias that has been inherent in medical education, research and clinical practice. The prevailing medical viewpoint has often been that the male body is considered to be the norm and that the female body exactly the same except for the reproductive function. This attitude has led to a lack of interest in researching gender differences and a consequent lack of knowledge of women's health issues. Fortunately, there is a movement for change. The Women's Health Interschool Curriculum Committee was formed in January 1992 to develop curricula concerning women's health and examine bias that may exist in existing curricula. The Canadian Women's Health Network has been growing across the country and there have been calls to create a new specialty in women's health. According to Angell, this proposal for a new specialty was provocatively debated in the Journal of Women's Health, which started publication in 1992. There is also a growing concern on how to conduct better research to address women's health needs. As more attention is paid to women's health issues, what will happen in the area of oral health? In health care, it would seem that the mouth has become completely separated from the rest of the body. Health conferences rarely have any oral health content at all. To correct this problem, there must be an increase in general awareness of the importance of oral health as it relates to the overall health of both women and men. Good oral health is more than just decay-free teeth. Oral health encompasses the teeth, the supporting periodontal structures, soft tissues of the mouth and oral pharynx area, temporomandibular joints and muscles of mastication. The mouth is a gateway to the body and will also reflect many systemic health problems, such as diabetes, leukemia and lupus. The second step would be the recognition that women may have different oral health needs and issues than men. The common view may be that teeth are gender free, but how can this be when teeth exist in a body, and that body is male or female? For many years, the primary acknowledged difference between men and women's oral health was pregnancy gingivitis. Like medicine, dentistry must re-examine the viewpoint that women's oral health differs from men's only as it is influenced by reproductive processes. There are many areas where women's oral health may differ from that of men. This paper will explore the literature for potential women's oral health issues in the areas of oral hygiene behaviours, esthetics, eating disorders, temporomandibular disorders, and hormonal influences on periodontal health.
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PMID:Women's oral health issues: an exploration of the literature. 961 Mar 37

Diabetes mellitus is a systemic disease that affects more than 12 million people in the United States and represents a risk factor for periodontitis with odds ratios of 2.1 to 3.0. New data support the concept that in diabetes-associated periodontitis, the altered host inflammatory response plays a critical role. We have recently examined the gingival crevicular fluid (GCF) mediator level, monocytic secretion, and clinical presentation of 39 insulin-dependent diabetes mellitus (IDDM) patients and 64 non-diabetic patients with various degrees of periodontal health and disease. First, we found that there was an unexpected high level of GCF mediators among the IDDM subjects, even in the gingivitis and mild periodontitis patients. Furthermore, the GCF and monocytic mediator responses were obviously bimodal in distribution with respect to periodontal status. Gingivitis patients and mild periodontitis patients represented one low response group, and the moderate and severe periodontitis subjects the high response group. Accordingly, these 4 periodontal subgroups were pooled to form 2 main groups for analyses--group A (AAP Types I-II) and group B (AAP Types III-IV). Diabetics had significantly higher GCF levels of both PGE2 and IL-1 beta when compared to non-diabetic controls with similar periodontal status. Within the diabetic group, the GCF levels of these inflammatory mediators were almost 2-fold higher in group B subjects when compared to diabetics from group A. Among diabetics, GCF TNF-alpha levels were only marginally detectable and no significant difference was found between group A and group B patients. Insulin-dependent diabetic patients with gingivitis or mild periodontitis (group A) and moderate to severe periodontitis (group B) have abnormal monocytic inflammatory secretion in response to LPS challenge from Porphyromonas gingivalis (P. gingivalis) as compared to non-diabetic periodontal patients. Data suggest that the diabetic state results in a significantly upregulated monocytic secretion of PGE2 (4.2-fold), IL-1 beta (4.4-fold), and TNF-alpha (4.6-fold) when compared to non-diabetic controls. Within diabetics, LPS dose-response curves demonstrated that monocytes from group B patients secreted approximately 3 times more PGE2 and 6.2 times more TNF-alpha than those from group A; however, there was no significant difference in monocytic IL-1 beta secretion between the 2 diabetic groups. This upregulated monocytic trait is thought to exist independently of the presence of severe periodontal disease since, in non-diabetic patients with adult periodontitis, Gram-negative bacterial infections alone are not sufficient to elicit a systemic hyperresponsive monocytic trait. Between group A and group B diabetics, there was no significant difference in metabolic control as expressed by mean level of glycosylated hemoglobin (HbA1c). In conclusion, our data suggest that diabetic patients have exaggerated inflammatory responses when compared to non-diabetic controls. Furthermore, within diabetics, individuals with moderate to severe periodontitis (group B) have significantly elevated monocytic secretion of PGE2 and TNF-alpha upon LPS challenge and significantly higher GCF levels of PGE2 and IL-1 beta when compared to patients with gingivitis or mild periodontal disease (group A). Thus, we suggest that insulin-dependent diabetes mellitus is a significant risk factor for more severe periodontal disease because, as compared to non-diabetics, diabetic subjects react with an abnormally high degree of inflammation to an equivalent bacterial burden.
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PMID:PGE2, IL-1 beta, and TNF-alpha responses in diabetics as modifiers of periodontal disease expression. 972 89

Periodontitis is now seen as resulting from a complex interplay of bacterial infection and host response, often modified by behavioral factors. There has been a fundamental change in the prevailing periodontal disease model of the 1960s, which suggested that the susceptibility to periodontitis increases with age, and that all individuals are susceptible to severe periodontal disease. More recent research has changed the belief in universal susceptibility to the current view that only some 5-20% of any population suffer from severe generalized periodontitis, and that only moderate disease affects a majority of adults. One major risk factor is smoking, as there is now a clear association between smoking and periodontal disease independent of oral hygiene, age, or any other risk factor. In human periodontitis, there is no simple, direct pathogen-disease link. There are three pathogens that have a strong association with progressive periodontal disease: Actinobacillus actinomycetemcomitans, spirochetes of acute necrotizing gingivitis, and Porphyromonas gingivalis. These pathogens may be the cause of continued loss of periodontal attachment in all periodontal disease classifications despite diligent periodontal therapy. This loss of attachment, or destruction of the periodontal ligament and loss of adjacent supporting bone, is seen in adult periodontitis, as well as in early-onset periodontitis, which affects young persons who otherwise appear healthy. The three forms of early-onset periodontitis are prepubertal periodontitis, localized and generalized juvenile periodontitis, and rapidly progressive periodontitis. They are distinguished from adult periodontitis by the age of onset of the disease, the rapid rate of disease progression, manifestations of defects in host response, and the composition of the subgingival microflora. Prepubertal periodontitis is associated with attachment loss around teeth of the deciduous and/or permanent dentition, and is often associated with severe congenital defects of hematological origin, and alterations in neutrophil chemotaxis function. Periodontitis may also be associated with systemic conditions such as metabolic disorders (diabetes mellitus, female hormonal alterations), drug-induced disorders, hematologic disorders/leukemia, and immune system disorders. These systemic disorders have been documented as capable of affecting the periodontium and/or treatment of periodontal disease. In order to rationally treat and prevent periodontal disease, we need to know the etiologic agents for specific patients, and the mechanism of bacterial pathogenesis in periodontitis. In systemic diseases in which the periodontal tissues are affected as well, early detection and carefully managed therapeutics with the physician and periodontist working together may prove beneficial to the patient's general health and quality of life.
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PMID:Periodontal disease: an overview for physicians. 984 64

One hundred and two dentate patients with type II diabetes mellitus and 98 non-diabetic subjects were examined for oral conditions and metabolic state. Self-reported health behaviour was analysed. From factor analysis four factors emerged: general health behaviour (GHB), perceived fatigue (PF), diet control (DC) and regular diet (RD). In diabetics PF, DC and RD were significantly higher than that in non-diabetics. Patients with diabetes were more likely to control their disease through a programme of decreased kilojoule intake leading to weight management. However, they tended to tire. The mean gingivitis index was significantly higher (p < 0.01) among diabetics (2.39) than among non-diabetics (1.99). The number of missing teeth was significantly higher (p < 0.01) for diabetics (6.7) when compared with non-diabetics (4.3). On the other hand, aetiological factors (plaque, calculus) and the level of dental health behaviour as expressed in the HU-DBI scores were similar. Probing pocket depth did not differ statistically between groups. The increasing number of missing teeth in diabetics may primarily result from severe periodontitis with tooth mobility or deep pockets. Findings in this study suggest that the difference in the severity of periodontitis between diabetics and non-diabetics was significant although aetiological factors and the level of dental health behaviour were similar.
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PMID:Comparison of health behaviour and oral/medical conditions in non-insulin-dependent (type II) diabetics and non-diabetics. 984 81

Although diabetes mellitus is known to aggravate periodontal disease, the precise relationship between these two entities is far from being completely understood. Further study of this relationship was therefore undertaken in the form of observation of both naturally occurring gingivitis in rats (ODUS/Odu) and effects produced by induction of experimental diabetes mellitus by injection of streptozotocin (STZ: 65 mg/kg, i.v.). At one and 3 mon after STZ injection, liquid paraffin was injected intraperitoneally. Four days thereafter, pocket probing depths of rats were measured and blood samples as well as peritoneal macrophages were collected from both experimental animals and non diabetic controls. Both chemotaxis and phagocytosis of macrophages were studied. At one and 3 mon after STZ injection, pocket probing depths of diabetic animals were significantly deeper than those of controls (p < 0.001). Pocket probing depths were deeper at 3 mon after STZ injection than after 1 mon in diabetic animals. At three months after STZ injection, there was a high degree of positive correlation between pocket probing depths, blood glucose levels, triglyceride, and hemoglobin A1c levels (p < 0.01). Also, macrophage chemotaxis was more suppressed in diabetic rats than it was in controls. Additionally, both phagocytosis ratios and phagocytosis indices of macrophages in the diabetes group were significantly more suppressed than those in controls in both experimental periods (p < 0.001). Findings suggest that both chemotaxis and phagocytosis are compromised in macrophages from rats rendered diabetic by STZ injection. Thus as host defense mechanisms become weakened, there is a corresponding progression of periodontal disease.
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PMID:The effect of leukocyte function of streptozotocin-induced diabetes in naturally occurring gingivitis rat. 987 87

Bad breath, or halitosis, affects between 50 and 65% of the population. Despite its frequency, this problem is often unaccepted and declared taboo. In about 8% of the cases, bad breath is related to an ENT pathology (sinusitis, tonsillitis, ...). More rarely it is caused by a metabolic (diabetes, trimethylaminuremia, ...) or gastric dysfunction. Ninety percent of the cases however, are associated to an oral disease: either gingivitis due to an inadequate removal of dental plaque, especially from interdental spaces, or periodontitis (alveolar bone destruction), or bacterial accumulation on the dorsum of the tongue. In most cases, an intensive disinfection of the mouth by scaling and root planing and/or instruction of a perfect oral hygiene will be sufficient to solve the problem. Perfumed mouthwashes or toothpastes will only give a short-term masking effect. An effective collaboration between a dentist or a periodontist and an ENT specialist is of great importance to dealt with bad breath.
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PMID:[Halitosis: a multidisciplinary problem]. 1008 8

Children with insulin-dependent diabetes mellitus have a lower salivary flow rate, pH and buffer capacity, but a higher glucose content and peroxidase, IgA, magnesium and calcium concentration, in comparison with healthy children. Nevertheless the incidence of caries is lower than normal in diabetic children with good metabolic control. Periodontal disease usually starts at puberty as mild gingivitis with bleeding and gingival recession, and it may develop into severe periodontitis, especially in children with poor control of diabetes. Microangiopathy, impaired immune response, different bacterial microflora and collagen metabolism are involved in the pathogenesis of diabetic periodontal disease. The gingival flora is mostly composed of Gram-negative, anaerobic bacteria, while collagen has a lower solubility and is atrophic and inadequate to support the occlusion forces. For these reasons, prevention of periodontitis is important in diabetic children; they should receive oral hygiene instruction and visit a dentist at least twice a year.
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PMID:Oral health in children and adolescents with IDDM--a review. 1070 31

Previous studies have proposed common psychological factors between oral health behavior and diabetes self-care. The aim here was to describe and analyse more comprehensively the relationships between dental and diabetes health behavior on the basis of attribution theory. The likeness between subjects' own assessments, similarities of the causes given to success and failure, and the predictive power of own dental assessments concerning the metabolic balance of diabetes were studied. The research population was composed of 149 IDDM patients. Data were collected by means of a quantitative questionnaire, a clinical oral examination and from patient records. It was found that from the patients reporting success with avoiding gingivitis 82% also reported success with metabolic status and they also had lower mean HbA1c levels than patients assessing failure with gingivitis. There were some correlations between causes of failure: not bothering to clean approximal surfaces correlated with non-adherence to diabetes treatment instructions, and laziness as the cause of caries correlated with non-adherence to diabetes treatment instructions and with poor motivation for diabetes care. It can be concluded that there are some common determinants for both dental health behavior and diabetes self-care. This connection should be taken into account in health education by health care professionals.
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PMID:Attributions to dental and diabetes health outcomes. 1074 68

Children with insulin-dependent diabetes mellitus have a lower salivary flow rate, pH and buffer capacity, but a higher glucose content and peroxidase, IgA, magnesium and calcium concentration, in comparison with healthy children. Nevertheless the incidence of caries is lower than normal in diabetic children with good metabolic control. Periodontal disease usually starts at puberty as mild gingivitis with bleeding and gingival recession, and it may develop into severe periodontitis, especially in children with poor control of diabetes. Microangiopathy, impaired immune response, different bacterial microflora and collagen metabolism are involved in the pathogenesis of diabetic periodontal disease. The gingival flora is mostly composed of Gram-negative, anaerobic bacteria, while collagen has a lower solubility and is atrophic and inadequate to support the occlusion forces. For these reasons, prevention of periodontitis is important in diabetic children; they should receive oral hygiene instruction and visit a dentist at least twice a year.
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PMID:Oral health in children and adolescents with IDDM--a review. 1085 89


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