
Editorial
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This article reviews the life story and contributions of Sumter Smith Arnim (1904-1990), a noted author, lecturer, teacher, and researcher in preventive dentistry. Following in the footsteps of Levi Spear Parmly, MD, DDS (1790-1859), and Charles C. Bass, MD (1875-1975), Arnim developed and popularized a wide range of preventive concepts and practices, especially dental plaque control
Previous studies have shown that growth hormone can influence the expression of N-acetylgalactosamine-containing molecules in the extracellular matrix of developing rat incisors. N-acetylgalactosamine is a principal component of proteoglycans containing chondroitin sulfate and dermatan sulfate, as well as of some glycoproteins. Since chondroitin sulfate proteoglycans are identifiable components in enamel, dentin, and cementum, we have tested the hypothesis that growth hormone modulates their expression in developing rat incisors. The distribution of the chondroitin-sulfate-rich proteoglycans, decorin and biglycan, was investigated. We used the Lewis dwarf rat as a model because their circulating growth hormone levels are markedly reduced. Polyclonal antibodies against decorin and biglycan were used to localize these two proteoglycans. Semi-quantitative assessments of the staining patterns and intensities were made for each proteoglycan within compartments of the developing teeth. In normal Lewis rats, decorin and biglycan differentially expressed throughout the enamel organ, dental papilla, and dental follicle. Decorin displayed a wide distribution throughout all three regions and was closely associated with different cellular components. In contrast, biglycan showed little association with cells and was identified in the predentin and osteoid matrices. The expression of both proteoglycans was dramatically decreased in the growth-hormone-deficient animals. Administration of growth hormone to the dwarf rats markedly elevated the expression of both proteoglycans, approximating the distribution and intensity of staining seen in normal animals. These findings confirm that growth hormone status can modulate the expression of decorin and biglycan, and hence matrix deposition, in the rat tooth.
The kinematic center of the temporomandibular condyle is that condylar point which follows as much as possible the same movement path during different types of mandibular movements. In this study, the location of the kinematic center with respect to the palpated lateral pole of the condyle was investigated. Also, the lengths of the condylar movement path reconstructed by means of the kinematic center and the palpated condyle were compared. Mandibular movements were recorded with 6 degrees of freedom in 20 healthy subjects. A software procedure calculated the location of the kinematic center as that mandibular point for which the protrusive and opening movement path showed a minimal difference. For each subject, its average location was calculated on the basis of 16 pairs of protrusive and opening movements. The kinematic center was located posteriorly and superiorly with respect to the palpated condylar point (p < 0.0001). The standard deviation in the anterior-posterior coordinate of the average kinematic center was smaller than that in the superior-inferior coordinate (p < 0.0001). During opening, the path length of the kinematic center is longer than that of the palpated lateral pole of the condyle (p < 0.0001). In contrast to left-right differences found in the path lengths of the lateral pole of the condyle, no left-right differences were found for the kinematic center.
Rabbit masseter motor units (22) were studied by stimulation of trigeminal motoneurons. We tested the hypotheses that masseter motor units facilitate fine motor control by concentrating fibers in small areas and that the distribution of motor unit fibers depends on the fiber type. The twitch contraction time and the isometric tetanic force were registered. The motor unit fibers were depleted of their glycogen by prolonged stimulation. Serial sections of the entire muscle were stained with the periodic acid Schiff (PAS) and monoclonal antibody stains. The muscle fibers of the motor unit were mapped and identified by four myosin heavy-chain (MHC) isoforms: I, IIA, IID, and cardiac-a. In the PAS-stained sections, anatomical parameters of the motor units, affecting the force output, were analyzed: the innervation ratio (IR), motor unit territory area (TA), and relative (R-DENS) and absolute (A-DENS) motor unit fiber densities. The fiber cross-sectional area (F-CSA) was measured for each MHC fiber type. The F-CSA sum of all motor unit fibers, the physiological cross-sectional area (P-CSA), was calculated. The IR ranged between 77 and 720 fibers (mean, 267). The mean TA was 8.71 mm2 (range, 4.45 to 19.58). The mean R-DENS was 10 fibers per 100; the A-DENS was 31 fibers
Chewing requires a low level of muscle activity for jaw movement. Additional muscle activity is required to overcome the resistance of the food. The additional muscle activity consists of two contributions, an anticipating contribution before food contact and a peripherally induced contribution, about 23 ms after food contact. The amounts of both contributions depend on the information about food resistance obtained in preceding chewing cycles. It is not known whether this information is preserved if the resistance is absent during only a limited number of chewing cycles. Our aim was to investigate the extent to which information about food resistance obtained during chewing is used during subsequent cycles to generate anticipating and peripherally induced muscle activity. Subjects made rhythmic open-close movements at their natural chewing frequency, controlled by a metronome. Food resistance was simulated by an external force acting on the jaw in a downward direction during part of the closing movement. Jaw movement and surface EMG of the masseter and suprahyoid muscles were recorded during experiments in which sequences of at least 20 cycles with the force were alternated with a small, random number (from 1 to 10) of cycles without the force. The amount of anticipating muscle activity as well as the peripherally induced muscle activity in the first cycle with the force gradually decreased as a function of the number of preceding forceless cycles. About 30% of the additional muscle activity had an anticipatory origin, whereas the rest of the activity was evoked by the force regardless of the number of preceding forceless cycles.
The existence and nature of parasympathetic nerve fibers in the dental pulp have long been a subject for discussion; indeed, vasodilator responses mediated by such nerve fibers have yet to be conclusively demonstrated in the dental pulp. This study was designed to determine whether parasympathetic vasodilator mechanisms do or do not exist in the cat dental pulp. Dynamic changes in pulpal blood flow (PBF), with mandibular lip blood flow (LBF) recorded as a control, were investigated in cat mandibular canine teeth by means of laser Doppler velocimetry. Peripheral trigeminal afferents (see below) were stimulated electrically to confirm that somato-parasympathetic reflex vasodilatation could be induced. The peripheral cut ends of the facial and glossopharyngeal nerve roots, which have been reported to contain parasympathetic nerve fibers to the oral tissues, were then stimulated intracranially. Electrical stimulation of trigeminal afferents (in the infra-orbital nerve or the maxillary buccal gingiva) caused no change in PBF but did increase ipsilateral LBF. Neither facial nor glossopharyngeal nerve root stimulation caused a PBF increase, though both elicited increases in ipsilateral LBF. The vasodilator responses in the lip were sensitive to ganglion blockade (with hexamethonium), indicating vasodilatation
Urinary catecholamines have been used to measure emotionally stressful states which may affect the development of dental caries. This study investigates the hypothesis that children with and without dental caries do not differ significantly in the mean values of urinary catecholamines such as epinephrine, norepinephrine, and dopamine. As a test of this hypothesis, 314 children, males and females, aged from 6 to 8 years, were included in the study. Dental caries were recorded clinically and radiographically, and oral hygiene was evaluated by the recording of dental plaque. A 24-hour urine sample was collected for each subject, and a representative sample (25 mL) was analyzed by the HPLC technique to assay the catecholamine content. Socio-economic factors such as parental age, education, and profession were recorded by a questionnaire distributed to the parents. Of the examined children, 38 (14 males and 24 females) were free of dental caries and constituted the case group. Two control groups, A and B, of 38 children each (14 males and 24 females) with dental caries were matched by age and gender. Differences in the quantitative and qualitative data were tested by the paired t test and the X2-test, respectively, while a regression analysis was applied to measure the effects of norepinephrine and dopamine on epinephrine. The logistic multiple-regression analysis was used to test, in the entire population, the impact of catecholamines and other related factors on the probability of subjects' developing dental caries. The 95% probability was used. The results showed statistically significant differences in epinephrine values between the case group and control groups A and B. The data suggest, therefore, that children with emotionally stressful states have higher probability of developing dental caries.
Tensile bond strength measurements are commonly used for the evaluation of dentin adhesive systems. Most tests are performed using extracted non-carious human or bovine dentin. However, the adhesion of resins to caries-affected dentin is still unclear. The objectives of this study were to test the hypothesis that bonding to caries-affected dentin is inferior to bonding to normal dentin, and that the quality of the hybrid layer plays a major role in creating good adhesion. We used a micro-tensile bond strength test to compare test bond strengths made to either caries-affected dentin or normal dentin, using three commercial adhesive systems (All Bond 2, Scotchbond Multi-Purpose, and Clearfil Liner Bond II). For scanning electron microscopy, the polished interfaces between the adhesive bond and dentin were subjected to brief exposure to 10% phosphoric acid solution and 5% sodium hypochlorite, so that the quality of the hybrid layers could be observed. Bonding to normal dentin with either All Bond 2 (26.9 ± 8.8 MPa) or Clearfil Liner Bond II (29.5 ± 10.9 MPa) showed tensile bond strengths higher than those to caries-affected dentin (13.0 ± 3.6 MPa and 14.0 ± 4.3 MPa, respectively). The tensile bond strengths obtained with Scotchbond Multi-Purpose were similar in normal and caries-affected dentin (20.3 ± 5.5 MPa and 18.5 ± 4.0 MPa, respectively). The hybrid layers created by All Bond 2 in normal dentin and by Clearfil Liner Bond II in normal or caries-affected dentin showed phosphoric acid and sodium hypochlorite resistance, whereas the hybrid layers created by All Bond 2 in caries-affected dentin and those created by Scotchbond Multi-Purpose to normal and caries-affected dentin showed partial susceptibility to the acid and sodium hypochlorite treatment. The results indicate that the strength of adhesion to dentin depends upon both the adhesive system used and the type of dentin. Moreover, the quality of the hybrid layer may not always contribute significantly to tensile bond strength.
Dental plaque produces not only acids by which underlying enamel is demineralized but also compounds which may inhibit repair of the lesions. The aim of this study was to determine how lipoteichoic acid, a bacterial compound that is abundant in dental plaque and inhibits calcium phosphate precipitation in vitro, affects the remineralization of incipient enamel lesions. Subsurface and surface-softened lesions were made in thin sections of bovine enamel, incubated with various amounts of lipoteichoic acid (isolated from Lactobacillus casei), and remineralized in 1.5 mmol/L CaCl2, 0.9 mmol/L KH 2PO4, 130 mmol/L KC1, and 20 mmol/L Hepes, pH 7.0. Remineralization was followed during several weeks by repeated microradiography of the sections, and characterized by the changes in the integrated mineral loss of the lesions and the differential mineral profiles. The results showed that: (1) the effects of lipoteichoic acid on lesion remineralization were dose-dependent; (2) in subsurface lesions only the highest dose of lipoteichoic acid affected remineralization, which was delayed throughout the lesions; and (3) in surface-softened enamel, lipoteichoic acid did not affect the remineralization of the deeper parts, but remineralization of a surface zone of from 25 to 30 um was increasingly inhibited with increasing doses. These effects were explained by different permeabilities of the surfaces of both types of lesions for the inhibitor: In subsurface lesions, lipoteichoic acid may have mainly clogged the porosities in the surface layer, whereas it could penetrate substantially into surface-softened enamel.
GlucosyltransferaseB, GtfC, and GtfD were purified by hydroxyapatite column chromatography, followed by ultrafiltration from the culture supernatant fluids of three
Studies of the effects of carbon dioxide (CO2) lasers on dental enamel have demonstrated that surface changes can be produced at low fluences (< 10 J/cm2) if wavelengths are used which are efficiently absorbed by the hard tissues. In this study, scanning electron microscopy (SEM) was used to characterize the wavelength dependence of surface changes in dental enamel after exposure to an extensive range of CO2 laser conditions. Bovine and human enamel were irradiated by a tunable, pulsed CO2 laser (9.3, 9.6, 10.3, 10.6 μm), with 5, 25, or 100 pulses, at absorbed fluences of 2, 5, 10, or 20 J/cm2, and pulse widths of 50, 100, 200, 500 us. SEM micrographs revealed evidence of melting, crystal fusion, and exfoliation in a wavelength-dependent manner. Crystal fusion occurred at absorbed fluences as low as 5 J/cm2
The use of a calcium phosphate precipitation method occluded dentin tubules with apatitic mineral and, thus, showed good potential for the treatment of dentin hypersensitivity. The aim of this study was to elucidate the occluding behavior of the precipitate in the oral environment. Dentin disks treated by the calcium phosphate precipitation method, and disks treated with potassium oxalate, NaF, and SrCl2 solutions, were immersed in synthetic saliva, which was regularly replenished so that ionic concentration would be maintained. Treatment of dentin disks by the calcium phosphate precipitation method immediately reduced dentin permeability to 6 ± 8%. When the disk was immersed in synthetic saliva, dentin permeability remained low, even seven days after immersion. Scanning electron microscopic observation showed no distinct boundary line between the precipitate and intertubular dentin; this indicated further mineralization on the precipitate. Potassium oxalate treatment also reduced the dentin permeability to 8 ± 3%. However, the dentin permeability gradually but steadily increased with immersion time, reaching 39 ± 14% at seven days. To elucidate the mechanism underlying dentin permeability changes in synthetic saliva, we immersed the precipitates, i.e., apatitic mineral and calcium oxalate, in a fixed volume of synthetic saliva. When calcium oxalate was immersed in synthetic saliva, there was a large concentration of oxalate ions, indicating dissolution of the calcium oxalate; this phenomenon was ascribed to the increase in dentin permeability. In contrast, calcium and phosphate ions decreased when apatitic powder, the precipitate formed by the calcium phosphate precipitation method, was immersed in synthetic saliva. The decrease in the calcium and phosphate ions in synthetic saliva indicated further precipitation of calcium phosphate on the apatitic precipitate. We concluded, therefore, that the calcium phosphate precipitation method would have a continuous effect in reducing dentin permeability in the oral environment.
The hypotheses to be tested were: (i) that chewing sugar-free gum frequently and for long periods would be associated with higher amounts of supragingival calculus, and (ii) that there would be no site-specificity of calculus deposition on the lingual surfaces of the 6 lower anterior teeth. Subjects, 436 in Glasgow and 191 in Winnipeg, were scored for calculus at mesial, lingual, and distal sites on the lingual surface of each of the 6 lower anterior teeth, by the Volpe-Manhold method. They also answered questions on the time since the last prophylaxis, the frequency of gum chewing, the type of gum chewed, and the length of a typical gum-chewing episode. A subset (233) of the Glasgow subjects were scaled and re-scored for calculus 3 months later. When the data for the logarithmic transformations of the initial calculus scores were subjected to stepwise multiple-regression analysis, the only factor which correlated significantly with initial calculus scores in both cities was the time since the last prophylaxis. In the Glasgow subjects scored 3 months after a prophylaxis, there was a negative correlation between chewing sugar-free gum and calculus scores, whereas in the Winnipeg subjects, age and the chewing of sucrose-containing and sugar-free gum were positively correlated with calculus scores. Thus, the results were contradictory with respect to the first-tested hypothesis. The calculus distribution patterns were very similar in the subset of Glasgow subjects and the Winnipeg subjects, with the amounts on the lateral incisors and canines averaging 70.2% and 44.5%, respectively, of those on the central incisors. Thus, the second hypothesis was disproved.
