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PubMed2004

Relationship of periodontal disease and tooth loss to prevalence of coronary heart disease.

BACKGROUND: Studies relating periodontal disease to coronary heart disease (CHD) have provided equivocal results using tooth loss and/or clinical signs of periodontal disease as measures of periodontal exposure. METHODS: The purpose of this cross-sectional study was to evaluate the relationship of tooth loss and periodontitis to prevalent CHD at the Atherosclerosis Risk in Communities (ARIC) visit 4 using both tooth loss and clinical signs of disease in a population-based sample of 8,363 men and women aged 52 to 75 years from four U.S. communities. Each subject participated in a complete periodontal examination, assessment of missing teeth, assessment of prevalent CHD, and a number of laboratory tests and questionnaires. High attachment loss was defined as > or = 10% of sites with attachment loss > 3 mm and high tooth loss was defined as fewer than 17 remaining teeth. RESULTS: Individuals with both high attachment loss and high tooth loss (odds ratio [OR] 1.5, 95% confidence interval [CI] 1.1 to 2.0) and edentulous individuals (OR 1.8, CI 1.4 to 2.4) had elevated odds of prevalent CHD compared to individuals with low attachment loss and low tooth loss, while controlling for a number of traditional risk factors for CHD. CONCLUSIONS: These results suggest that tooth loss and periodontal disease are associated with prevalent CHD, but only when both are present. The weaker relationships between periodontal disease and CHD that have been found among older adults may be due to older adults having fewer teeth. Future longitudinal studies should be designed to ascertain the cause of tooth loss during follow-up.

Black or African American↗
PubMed1989

Trends in tooth loss due to caries and periodontal disease by tooth type.

Although the patterns of dental disease is gradually changing, caries and periodontal disease still account for the most important reason for extractions in most countries. However their relative contributions towards overall tooth mortality figures varies. The aim of this study is to investigate the types of teeth usually associated with extractions due to caries or periodontal disease and its relation to the age at which the tooth was lost. The highest proportion of extractions due to caries occurred between 21 to 30 years of age while that for periodontal disease occurred between 41 to 50 years. For caries, the greatest proportion of extractions involved the posterior teeth. The most frequently extracted teeth due to caries are the molars, in particular the first permanent molar. However, for periodontal disease a slightly greater proportion of anterior teeth were lost than the posteriors. This trend is more marked in the lower jaw than the upper. Overall, extractions related to caries tend to increase posteriorly, while that for periodontal disease tend to increase anteriorly.

Adolescent↗
PubMed1981

Charcot-Marie-Tooth's disease with severe trophic and sensory disorders. Study of a case following along a half a century with anatomical studies.

Plantar ulcers of neurological origin are known to be associated with several disorders, some of which may be familial. We present the case report together with the clinical and post-mortem data of a patient with peroneal muscular atrophy of the Charcot-Marie-Tooth type and plantar ulcers as a prominent feature. At least three other members of her family had Charcot-Marie-Tooth disease. The family pedigree is included. The discussion stresses the difference between patients with Charcot-Marie-Tooth disease with associated manifestations, bony destruction of the feet and plantar ulcers and patients with hereditary motor and hereditary sensory radicular neuropathies.

Charcot-Marie-Tooth Disease↗
PubMed1993

Molecular analyses of unrelated Charcot-Marie-Tooth (CMT) disease patients suggest a high frequency of the CMTIA duplication.

Charcot-Marie-Tooth disease (CMT) is the most common inherited peripheral neuropathy. One form of CMT, CMT type 1A, is characterized by uniformly decreased nerve conduction velocities, usually shows autosomal dominant inheritance, and is associated with a large submicroscopic duplication of the p11.2-p12 region of chromosome 17. A cohort of 75 unrelated patients diagnosed clinically with CMT and evaluated by electrophysiological methods were analyzed molecularly for the presence of the CMT1A DNA duplication. Three methodologies were used to assess the duplication: measurement of dosage differences between RFLP alleles, analysis of polymorphic (GT)n repeats, and detection of a junction fragment by pulsed-field gel electrophoresis. The CMT1A duplication was found in 68% of the 63 unrelated CMT patients with electrophysiological studies consistent with CMT type 1 (CMT1). The CMT1A duplication was detected as a de novo event in two CMT1 families. Twelve CMT patients who did not have decreased nerve conduction velocities consistent with a diagnosis of CMT type 2 (CMT2) were found not to have the CMT1A duplication. The most informative molecular method was the detection of the CMT1A duplication-specific junction fragment. Given the high frequency of the CMT1A duplication in CMT patients and the high frequency of new mutations, we conclude that a molecular test for the CMT1A DNA duplication is very useful in the differential diagnosis of patients with peripheral neuropathies.

Charcot-Marie-Tooth Disease↗
PubMed1996

Molecular diagnosis of Charcot-Marie-Tooth 1A disease and hereditary neuropathy with liability to pressure palsies by quantifying CMT1A-REP sequences: consequences of recombinations at variant sites on chromosomes 17p11.2-12.

The most frequent form of Charcot-Marie-Tooth disease (CMT1A; OMIM118.220) is the result of a duplication on chromosome 17 in pll.2-p12. This region contains PMP22, a gene expressed in peripheral myelin. The mutation results from an unequal crossing-over involving repeated sequences, CMT1A-REP, located on both sides of the duplicated region. The reciprocal product of this recombination is a deletion of the same region, which is associated with hereditary neuropathy with liability to pressure palsies (HNPP; OMIM162.500). Proximal and distal CMT1A-REP sequences can be distinguished by the presence of a variant EcoRI site. We quantified the number of these repeat sequences in 36 CMT1A and 40 HNPP patients. CMT1A-REP sequences are involved in almost all of the mutations. The majority of recombination breakpoints occur distally from the variant EcoRI site. However, a few have a breakpoint proximal to this site, which creates the risk of misinterpretation with respect to a duplicated/deleted status.

Charcot-Marie-Tooth Disease↗
PubMed1981

Unusual presentation of Charcot Marie-Tooth disease-incoordination with absent of minimal wasting-Report of 2 cases.

Two patients are reported presenting with incoordination mimicking cerebellar disease in the upper and lower limbs, ataxia of gait, absent tendon reflexes and little or no clinically detectable wasting. Motor conduction velocity in the upper limbs was substantially reduced in one patient whereas it was normal and slightly reduced in the other. It is concluded that in Charcot-Marie Tooth disease incoordination may mimic cerebellar disease and when this is so it is due to the association of varying degrees of proprioceptive deafferentation and a dyskinesia similar to that produced by familial (essential) tremor.

Adolescent↗
PubMed2004

[Prevalence of dental anxiety in 144 patients with cardiovascular diseases before tooth extraction].

OBJECTIVE: To determine the prevalence of dental anxiety (DA) in patients with cardiovascular diseases before tooth extraction so as to provide psychotherapy. METHODS: 144 patients with cardiovascular diseases were asked to complete a questionnaire modified from Corah Dental Anxiety Scale (DAS) while awaiting for tooth extraction. RESULTS: The incidence rate of DA in these patients was 7.6%. Anxiety level on anesthesia procedure was the highest. DAS score was higher among patients with the following factors: inactive perception, female, below 60 years old, experiences of painful tooth extraction, a documented history of single cardiovascular disease, under ECG monitoring for the first time and complicated tooth extraction. CONCLUSION: DA existed in patients with cardiovascular diseases before tooth extraction and was related to many factors. Medical staff should take necessary measures to provide them with psychotherapy and nursing guidance before tooth extraction.

Adult↗
PubMed1996

Correlation between the histopathologic, genotypic, and phenotypic features of hereditary peripheral neuropathies in childhood.

In recent years, there have been remarkable advances in the understanding of the molecular genetic basis of the hereditary polyneuropathies. Linkage of the genes for Charcot-Marie-Tooth disease to chromosomes 1 and then 17 was followed by the discovery that the commonest form of Charcot-Marie-Tooth disease (CMT1A) was due to a duplication of DNA at 17p11.2-12. This duplication was shown to contain the gene for peripheral myelin protein PMP22. The finding that mutations of the myelin protein PMP22 gene were present in some Charcot-Marie-Tooth disease cases lacking the duplication confirmed the myelin protein PMP22 gene as the site of the defect in Charcot-Marie-Tooth disease. Similarly, defects of the myelin protein P0 gene on chromosome 1 have been demonstrated in a rarer form of Charcot-Marie-Tooth disease (CMT1B). A deletion of DNA at 17p11.2-12 results in the disorder hereditary neuropathy with liability to pressure palsies. Other mutations of the myelin protein PMP22 and myelin protein P0 genes have been associated with the clinical syndrome known as Dejerine-Sottas disease. An X-linked form of Charcot-Marie-Tooth disease (CMTX) has been characterized and shown to be due to mutations of the gap junction protein, connexin 32. Transgenic murine models with inactivated myelin protein PMP22 and myelin protein P0 genes have shown pathologic changes strinkingly similar to those seen in human patients with disturbances of those genes. In this paper, the clinical and histopathologic characteristics of these conditions are discussed in relation to the genotypic basis. It will be argued that there is still an important place for the clinician and nerve pathologist in a medical world immersed in the wonders of molecular genetics.

Adolescent↗
PubMed2006

Effects of smoking and drinking habits on the incidence of periodontal disease and tooth loss among Japanese males: a 4-yr longitudinal study.

OBJECTIVE: We investigated the risk of periodontal disease and tooth loss, associated with habits of smoking and alcohol consumption, in a longitudinal study. SUBJECTS AND METHODS: The subjects were 1332 Japanese males, 30-59 yr of age, who were free from periodontal disease at the baseline check-up, and who underwent a second check-up 4 yr later. Periodontal disease was diagnosed using the community periodontal index score, based on the clinical probing of pocket depth (> or = 4 mm). Smoking and alcohol consumption patterns were evaluated using a self-administered questionnaire. RESULTS: A dose-response relationship was observed between the amount of smoking and the incidence of periodontal disease in each age group. The overall odds ratios (95% confidence intervals), adjusted for age and alcohol, were 1.51 (0.95-2.22), 1.58 (1.13-2.22) and 2.81 (1.96-4.03), among smokers consuming 1-19, 20 or 21 or more cigarettes per day, respectively, with a significant linear trend (p < 0.0001). A similar association was found between smoking and tooth loss, except for the 50-59-yr-old age group. The adjusted odds ratios were 1.26 (0.60-2.64), 2.01 (1.21-2.32) and 2.06 (1.23-3.48), respectively. A significant linear trend between smoking and tooth loss was also observed (p = 0.01). Ex-smokers showed no significant difference compared with nonsmokers. We also found a significant linear trend between alcohol consumption and tooth loss among 30-39-yr-old subjects, while no relationship was observed between alcohol consumption and periodontal disease. CONCLUSION: Cigarette smoking was found to be an independent risk factor for periodontal disease and tooth loss. Alcohol consumption was a limited risk factor for tooth loss in the younger age group, but was unrelated to periodontal disease. To prevent periodontal disease and tooth loss, health practitioners need to encourage people to stop smoking or not to start.

Adult↗
PubMed1998

Periodontal disease and tooth loss.

Numerous epidemiological studies have shown that caries is the main reason for tooth loss. More recent epidemiological data seem to show an increasing trend of tooth loss due to periodontal reasons rather than caries. In considering the issue of periodontal disease and tooth loss the following observations were made. The presence of initial attachment loss, bone height and the habit of smoking significantly increase the risk of tooth mortality. There is a strong correlation between smoking, the severity of periodontal disease and tooth mortality. Cross-sectional population surveys of tooth loss reported lower anterior teeth to be the most frequently extracted due to periodontal reasons, followed by upper anteriors and upper second molars. However, in long term maintenance studies, molars were lost most frequently. Periodontal reasons for tooth loss were mainly mobility followed by furcation involvement. Periodontal surgery did not significantly enhance tooth retention in high risk groups. Ethnic differences observed were not significant and would need further investigations to address variables such as cultural differences, health habits, diet and socio-economic status. In conclusion, periodontal tooth mortality was found to be associated with the loss of periodontal attachment and risk groups with advanced periodontitis contributing to major tooth loss in a minority of the population.

Alveolar Bone Loss↗
PubMed2000

Treatment of the cavus foot. Deformity in the pediatric patient with Charcot-Marie-Tooth.

The orthopedic management of foot and ankle problems associated with Charcot-Marie-Tooth disease is becoming better understood but is still evolving. It is now known that Charcot-Marie-Tooth disease should be considered a spectrum of neurologic disorders with variable inheritance patterns, clinical course, and severity of deformities. Over half of the patients with Charcot-Marie-Tooth disease develop foot and ankle problems of which the cavovarus deformity is by far the commonest. Other clinical problems include weakness, parathesias, pain, and an unsteady gait. The cavovarus deformity seems to develop from a relative imbalance between the peroneus longus and tibialis anterior muscles and from an imbalance between the tibialis posterior and peroneus brevis muscles. Treatment of the cavovarus foot deformities should be individualized for each patient after careful preoperative evaluation. Surgery using a variety of soft tissue procedures and osteotomies seems to be the treatment of choice for the progressive cavovarus deformity in younger patients. For a patient who has severely rigid deformities a triple arthrodesis may be the only option but is considered by most to be a salvage procedure. It always should be kept in mind that Charcot-Marie-Tooth disease is a progressive neurologic disorder and the deformities can progress despite surgical intervention. Even though the results of treatment in this disease are difficult to evaluate because of the wide [figure: see text] spectrum of disease, it seems reasonable to believe that early surgical intervention in the flexible cavus foot can restore normal foot posture and help prevent or delay the need for more extensive bony procedures.

Adolescent↗
PubMed1989

Health maintenance issues of the elderly. Oral health.

The risk for the most serious oral disease, oral cancer, increases with age as does the prevalence of other oral soft tissue diseases. Tooth loss is not part of normal aging. As more elderly retain their natural dentition, they are at continued risk for tooth-related diseases such as caries and periodontal disease. Preventive dental programs, including an oral exam as part of the physical examination, will be indicated for adults.

Aged↗
PubMed2003

Hereditary neuropathies.

PURPOSE OF REVIEW: This review will update recent advances in the genetics, clinico-electrophysiological, pathological data and pathophysiology of Charcot-Marie-Tooth disease and related disorders. RECENT FINDINGS: Hereditary neuropathies continue to be in a state of constant flux, reflecting the rapid advances in the description of causative genes, three additional Charcot-Marie-Tooth genes having been identified in recent months. Such an ever-increasing body of genetic data provides valuable clues to the pathogenetic mechanisms of both nerve demyelination and nerve axonal degeneration. The classification of Charcot-Marie-Tooth disease is increasingly more complex as there are approximately 26 loci; for clinicians to reach a simplified classification is a pressing need. Genotypic-phenotypic correlations are still incomplete and will require further research, starting from both refined molecular investigations and detailed clinical, electrophysiological, and pathological studies. Recent epidemiological surveys have corroborated the fact that Charcot-Marie-Tooth disease is the most common type of hereditary neuropathy. SUMMARY: Advances in molecular genetics in hereditary neuropathies, and mainly in Charcot-Marie-Tooth disease, have enriched our knowledge of this heterogeneous group of disorders. In spite of this there remain important and basic issues, such as an updated and revised classification of Charcot-Marie-Tooth disorders, the better delineation of phenotypic-genotypic correlations, and further research to map as yet non-localized loci or to identify unknown gene mutations.

Animals↗
PubMed2000

Neurophysiology and molecular genetics of Charcot-Marie-Tooth type 1 neuropathy in Croatian children: follow-up study.

AIM: Longitudinal assessment of clinical and neurophysiological abnormalities in childhood and adolescence and incidence analysis of tandem Charcot-Marie-Tooth disease type 1A gene duplication in Croatian children with Charcot-Marie-Tooth type 1 neuropathy. METHODS: Eight Croatian children with Charcot-Marie-Tooth type 1 neuropathy, aged 4-19 years, were studied clinically, neurophysiologically, and neuropathologically during 1-11 years of follow-up. All children were examined at least once, and in 4 children the measurements were repeated. Molecular genetic analysis was performed in all patients and their family members in order to determine the presence of the Charcot-Marie-Tooth disease type 1A duplication on chromosome 17p11.2-p12, using restriction fragment length polymorphic and short tandem repeat markers. RESULTS: Clubfoot was the most frequently observed clinical feature in children under 10 years of age, whereas muscle hypotrophy, scoliosis, and contractures developed in the second decade of life. All patients showed decreased motor nerve conduction velocity (7-30 m/s) and prolonged distal motor latencies on the first and follow-up examinations. Compound muscle action potential amplitude reduction (0.1-1.25 mV) was recorded in the first and second decade of life. In 6 out of 8 children, molecular genetic studies demonstrated the presence of the 1.5 megabase tandem Charcot-Marie-Tooth disease type 1A duplication in 17p11.2-p12, mostly of paternal origin. CONCLUSION: Pronounced neurographic abnormalities and mild clinical features characterize Charcot-Marie-Tooth type 1 neuropathy in the first decade. There were no significant differences in neurographic abnormalities in the first or second decade of life between Croatian children with and without Charcot-Marie-Tooth type 1A duplication.

Adolescent↗
PubMed2004

Hereditary sensory neuropathies.

PURPOSE OF REVIEW: The hereditary sensory neuropathies, also known as the hereditary sensory and autonomic neuropathies, are a clinically and genetically heterogeneous group of disorders. As they are not as common as Charcot-Marie-Tooth disease, they do not receive the same level of attention, but there have been major advances in the identification of the causative genes in the past decade. Certain forms of hereditary sensory and autonomic neuropathy, especially hereditary sensory and autonomic neuropathy type I, which has minimal autonomic involvement and is more accurately termed hereditary sensory neuropathy type I, can present in a very similar fashion to certain forms of Charcot-Marie-Tooth disease (Charcot-Marie-Tooth type 2B, see below), and therefore it is important that clinicians who regularly manage patients with neuropathy are familiar with the latest developments in the hereditary sensory and autonomic neuropathies. This review will concentrate on the recent genetic advances in hereditary sensory and autonomic neuropathy, and especially on those forms that overlap clinically with Charcot-Marie-Tooth disease, hence the title of the review 'Hereditary sensory neuropathies' rather than hereditary sensory and autonomic neuropathies.

Acyltransferases↗
PubMed1994

Genetic basis of inherited peripheral neuropathies.

Progress in the elucidation of the genetic basis for inherited peripheral neuropathies has been remarkable over the last years. In particular, the molecular mechanisms underlying the autosomal dominantly inherited disorders Charcot-Marie-Tooth disease type 1A (CMT1A), Charcot-Marie-Tooth disease type 1B (CMT1B), and hereditary neuropathy with liability to pressure palsies (HNPP) have been determined. While mutation in the gene encoding the major myelin protein, P0 has been associated with CMT1B, CMT1A and HNPP have been shown to be associated with reciprocal recombination events leading either to a large submicroscopic duplication in CMT1A, or the corresponding DNA deletion in HNPP. Available evidence is consistent with the hypothesis that one or more genes within the relevant rearranged segment of 1.5 Mb on chromosome 17 is sensitive to gene dosage providing a novel mechanism for inherited human disorders. It is likely that the gene encoding the peripheral myelin protein PMP22 is at least one of the genes involved since the PMP22 gene maps within the CMT1A duplication (or HNPP deletion), and point mutations within it have been shown to cause a CMT phenotype in humans and comparable neuropathies in rodents (trembler and tremblerJ). The mechanism(s) by which gene dosage and point mutations affecting the same gene might lead to a similar phenotype are currently unknown but recent transgenic mouse experiments suggest that similar mechanisms may also underlie other genetic diseases.

Animals↗
PubMed1992

[A case of intrathoracic chest wall type lipoma].

Intrathoracic lipoma is a comparatively rare disease. We have recently experienced a case of intrathoracic chest wall type lipoma associated with Charcot-Marie-Tooth disease. The case was a 16-year-old man, in whom preoperative examination of his foot-drop due to Charcot-Marie-Tooth disease pointed out an abnormal chest shadow. Image diagnosis led to intrathoracic chest wall type lipoma. The tumor was easily resectable and was lipoma pathohistologically as well. The literature presented us with 22 cases of such lipoma, which appeared to be predominant for age not more than 10 and age 41-60 and to occur favorably in postero-superior chest wall. Preoperative diagnosis of the present disease became possible to a certain extent by means of CT, MRI. However, in view of imperfect differentiation between lipoma and liposarcoma, surgical resection should be considered, if possibly. No case of intrathoracic lipoma associated with Charcot-Marie-Tooth disease had been reported in the literature, and the causal relationship there between also remains unknown, but to be further examined.

Adolescent↗