| 1. |
- Bryndahl, Fredrik, et al.
(författare)
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Bilateral TMJ Disk Displacement Induces Mandibular Retrognathia
- 2006
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Ingår i: Journal of Dental Research. - : SAGE Publications. - 0022-0345 .- 1544-0591. ; 85:12, s. 1118-1123
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Tidskriftsartikel (refereegranskat)abstract
- Unilateral non-reducing TMJ disk displacement has been shown to retard mandibular growth on the ipsilateral side, with facial asymmetry a sequela. We hypothesized that bilateral affliction would impair mandibular growth bilaterally, generating mandibular retrognathia. Non-reducing TMJ disk displacement was surgically created in 10 growing New Zealand White rabbits. Ten additional rabbits served as a sham-operated control group. Facial growth was followed in serial cephalograms, with tantalum implants, during a period corresponding to childhood and adolescence in man. The results verified that bilateral non-reducing TMJ disk displacement retarded mandibular growth bilaterally, the extent corresponding to mandibular retrognathia in man. Maxillary growth was also retarded, but to a lesser degree. Growth impairment fluctuated over time, the most striking retardation occurring during periods of general growth acceleration. This should be taken into consideration when orthodontic treatment, aimed at stimulating mandibular growth, is initiated in adolescent individuals with non-reducing TMJ disk displacement.
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| 2. |
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| 3. |
- Fritschi, B Zinsli, et al.
(författare)
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Staphylococcus aureus and other bacteria in untreated periodontitis.
- 2008
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Ingår i: Journal of Dental Research. - 0022-0345 .- 1544-0591. ; 87:6, s. 589-593
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Tidskriftsartikel (refereegranskat)abstract
- Whether the subgingival microbiota differ between individuals with chronic and those with aggressive periodontitis, and whether smoking influences bacterial composition, is controversial. We hypothesized that the subgingival microbiota do not differ between sites in individuals with chronic or aggressive periodontitis, or by smoking status. Bacterial counts and proportional distributions were assessed in 84 individuals with chronic periodontitis and 22 with aggressive periodontitis. No differences in probing pocket depth by periodontal status were found (mean, 0.11 mm; 95% CI, 0.6 to 0.8, p = 0.74). Including Staphylococcus aureus, Parvimonas micra, and Prevotella intermedia, 7/40 species were found at higher levels in those with aggressive periodontitis (p < 0.001). Smokers had higher counts of Tannerella forsythia (p < 0.01). The prevalence of S. aureus in non-smokers with aggressive periodontitis was 60.5%. The null hypothesis was rejected, in that P. intermedia, S. aureus, and S. mutans were robust in diagnosing sites in individuals with aggressive periodontitis. S. aureus, S. sanguinis, and T. forsythia differentiated smoking status.
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| 4. |
- Häggman-Henrikson, Birgitta, et al.
(författare)
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Head Immobilization can Impair Jaw Function
- 2006
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Ingår i: Journal of Dental Research. - : SAGE Publications. - 0022-0345 .- 1544-0591. ; 85:11, s. 1001-1005
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Tidskriftsartikel (refereegranskat)abstract
- Findings that jaw-opening/-closing relies on both mandibular and head movements suggest that jaw and neck muscles are jointly activated in jaw function. This study tested the hypothesis that rhythmic jaw activities involve an active repositioning of the head, and that head fixation can impair jaw function. Concomitant mandiular and head-neck movements were recorded during rhythmic jaw activities in 12 healthy adults, with and without fixation of the head. In four participants, the movement recording was combined with simultaneous registration of myoelectric activity in jaw and neck muscles. The results showed neck muscle activity during jaw opening with and without head fixation. Notably, head fixation led to reduced mandibular movements and shorter duration of jaw-opening/-closing cycles. The findings suggest recruitment of neck muscles in jaw activities, and that head fixation can impair jaw function. The results underline the jaw and neck neuromuscular relationship in jaw function.
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| 5. |
- Iwasaki, K, et al.
(författare)
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Amelotin--a Novel Secreted, Ameloblast-specific Protein
- 2005
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Ingår i: Journal of dental research. - : SAGE Publications. - 0022-0345 .- 1544-0591. ; 84:12, s. 1127-1132
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Tidskriftsartikel (refereegranskat)abstract
- We aimed to analyze the differential gene expression in various murine dental tissues, expecting to find novel factors that are involved in tooth formation. We here describe the identification of a novel ameloblast-specific gene, amelotin (AMTN), by differential display polymerase chain-reaction (DD-PCR) analysis of microdissected ameloblasts, odontoblasts, dental pulp, and alveolar bone cells of 10-day-old mouse incisors. The conceptually translated protein sequence was unique and showed significant homology only with its human orthologue. The amelotin genes from mouse and human displayed a similar exon-intron structure and were expressed from loci on chromosomes 5 and 4, respectively, which have been associated with various forms of amelogenesis imperfecta. Expression of amelotin mRNA was restricted to maturation-stage ameloblasts in developing murine molars and incisors. Amelotin protein was efficiently secreted from transfected cells in culture. Taken together, our findings suggest that amelotin is a novel factor produced by ameloblasts that plays a critical role in the formation of dental enamel.
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| 6. |
- Lerner, Ulf H
(författare)
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Bone remodeling in post-menopausal osteoporosis.
- 2006
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Ingår i: Journal of dental research. - : SAGE Publications. - 0022-0345 .- 1544-0591. ; 85:7, s. 584-95
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Tidskriftsartikel (refereegranskat)abstract
- Bone mass in the skeleton is dependent on the coordinated activities of bone-forming osteoblasts and bone-resorbing osteoclasts in discrete bone multi-cellular units. Remodeling of bone in these units is important not only for maintaining bone mass, but also to repair microdamage, to prevent accumulation of too much old bone, and for mineral homeostasis. The activities of osteoblasts and osteoclasts are controlled by a variety of hormones and cytokines, as well as by mechanical loading. Most importantly, sex hormones are very crucial for keeping bone mass in balance, and the lack of either estrogen or testosterone leads to decreased bone mass and increased risk for osteoporosis. The prevalence of osteoporotic fractures is increasing dramatically in the Western part of the world and is a major health problem in many countries. In the present review, the cellular and molecular mechanisms controlling bone remodeling and the influence of sex hormones on these processes are summarized. In a separate paper in this issue, the pathogenesis of post-menopausal osteoporosis will be compared with that of inflammation-induced bone remodeling, including the evidence for and against the hypothesis that concomitant post-menopausal osteoporotic disease influences the progression of periodontal disease.
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| 7. |
- Lerner, Ulf H
(författare)
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Inflammation-induced bone remodeling in periodontal disease and the influence of post-menopausal osteoporosis.
- 2006
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Ingår i: Journal of dental research. - : SAGE Publications. - 0022-0345 .- 1544-0591. ; 85:7, s. 596-607
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Tidskriftsartikel (refereegranskat)abstract
- During physiological conditions, the skeleton is remodeled in so-called bone multi-cellular units. Such units have been estimated to exist at 1-2 x 10(6) sites in the adult skeleton. The number and activities of these units are regulated by a variety of hormones and cytokines. In post-menopausal osteoporosis, lack of estrogen leads to increased numbers of bone multi-cellular units and to uncoupling of bone formation and bone resorption, resulting in too little bone laid down by osteoblasts compared with the amount of bone resorbed by osteoclasts. Inflammatory processes in the vicinity of the skeleton, e.g., marginal and apical periodontitis, will affect the remodeling of the nearby bone tissue in such a way that, in most patients, the amount of bone resorbed exceeds that being formed, resulting in net bone loss (inflammation-induced osteolysis). In some patients, however, inflammation-induced bone formation exceeds resorption, and a sclerotic lesion will develop. The cellular and molecular pathogenetic mechanisms in inflammation-induced osteolysis and sclerosis are discussed in the present review. The cytokines believed to be involved in inflammation-induced remodeling are very similar to those suggested to play crucial roles in post-menopausal osteoporosis. In patients with periodontal disease and concomitant post-menopausal osteoporosis, the possibility exists that the lack of estrogen influences the activities of bone cells and immune cells in such a way that the progression of alveolar bone loss will be enhanced. In the present paper, the evidence for and against this hypothesis is presented.
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| 8. |
- Lundgren, T, et al.
(författare)
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Impaired cytotoxicity in Papillon-Lefèvre syndrome
- 2005
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Ingår i: Journal of Dental Research. - 0022-0345 .- 1544-0591. ; 84:5, s. 414-417
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Tidskriftsartikel (refereegranskat)abstract
- Papillon-Lefèvre syndrome (PLS), palmoplantar hyperkeratosis with periodontitis, has been genetically characterized. However, suspected associated immune dysfunctions remain elusive. The purpose of this study was to evaluate peripheral blood lymphocyte levels and natural killer (NK) cell cytotoxicity in PLS. Twenty patients and 20 healthy controls were examined. Peripheral blood lymphocytes were analyzed by flow cytometry for surface markers. NK cell cytotoxicity against K562 cells was determined by means of a 51Cr release assay. White blood cell differential and proportions of B-, T-, T-helper, T-suppressor, and NK cells revealed only sporadic borderline variations from control values. In contrast, NK cell cytotoxicity was consistently and severely depressed (32-53% of control values) in all patients. To the best of our knowledge, this newly described impairment of NK cell cytotoxic function is the first consistent immune dysfunction reported in PLS. This suggests that the impaired NK cell cytotoxicity might contribute to the pathogenesis of PLS-associated periodontitis.
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| 9. |
- Lundgren, T, et al.
(författare)
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Impaired cytotoxicity in Papillon-Lefèvre syndrome.
- 2005
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Ingår i: Journal of Dental Research. - : SAGE Publications. - 0022-0345 .- 1544-0591. ; 84:5, s. 414-417
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Tidskriftsartikel (refereegranskat)abstract
- Papillon-Lefèvre syndrome (PLS), palmoplantar hyperkeratosis with periodontitis, has been genetically characterized. However, suspected associated immune dysfunctions remain elusive. The purpose of this study was to evaluate peripheral blood lymphocyte levels and natural killer (NK) cell cytotoxicity in PLS. Twenty patients and 20 healthy controls were examined. Peripheral blood lymphocytes were analyzed by flow cytometry for surface markers. NK cell cytotoxicity against K562 cells was determined by means of a 51Cr release assay. White blood cell differential and proportions of B-, T-, T-helper, T-suppressor, and NK cells revealed only sporadic borderline variations from control values. In contrast, NK cell cytotoxicity was consistently and severely depressed (32-53% of control values) in all patients. To the best of our knowledge, this newly described impairment of NK cell cytotoxic function is the first consistent immune dysfunction reported in PLS. This suggests that the impaired NK cell cytotoxicity might contribute to the pathogenesis of PLS-associated periodontitis.
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| 10. |
- Mucci, LA, et al.
(författare)
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Environmental and heritable factors in the etiology of oral diseases--a population-based study of Swedish twins
- 2005
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Ingår i: Journal of dental research. - : SAGE Publications. - 0022-0345 .- 1544-0591. ; 84:9, s. 800-805
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Tidskriftsartikel (refereegranskat)abstract
- A population-based twin study is a useful design for quantification of the effects of genes and environmental factors in disease etiology. We used data from 10,000 Swedish twin pairs to quantify genetic and environmental contributions to tooth loss and periodontal health. Oral health information was obtained from telephone interviews. Structural equation models measured the relative importance of genetic and environmental factors. Genetic factors contributed to 14% of variation in tooth loss among women, and 39% among men. Non-shared environmental factors accounted for one-quarter of risk; environmental factors shared by twins comprised the remainder. Heritability estimates of periodontal disease were 39% and 33% for women and men, respectively, while non-shared environmental factors accounted for the remaining variation. Heritability for both conditions varied as a function of age and smoking status. Analysis of data from this large, population-based study demonstrates a moderate role of genetic factors in oral diseases, and suggests potential gene-environment interactions.
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