Biomedical subjects

R L Kent

Publications and source records attributed to R L Kent.

At least 37 records · Page 2Linked to original sources

PubMed1996

Response to periodontal therapy in patients with high or low levels of P. gingivalis, P. intermedia, P. nigrescens and B. forsythus.

In a previous study, subjects receiving either adjunctive tetracycline or Augmentin showed, on average, more attachment level gain 10 months post-therapy than subjects receiving either Ibuprofen or a placebo, although some subjects in each treatment group showed loss of attachment post-therapy. Since differences in treatment response might have been due to differences in the subgingival microbiota, the response to different therapies in subjects with different pre-therapy subgingival microbiotas was evaluated. 29 subjects exhibiting loss of attachment > 2.5 mm at 1 or more sites during longitudinal monitoring were treated by modified Widman flap surgery at deep sites, subgingival scaling at all other sites and were randomly assigned one of the following agents: Augmentin, tetracycline, ibuprofen or a placebo. Treatment was completed within 30 days, during which time the subject took the assigned agent. Subgingival plaque samples were taken from the mesial surface of each tooth at each visit and evaluated for their content of 14 subgingival species including P. gingivalis, P. nigrescens, P. intermedia and B. forsythus using DNA probes. 18 subjects with mean counts > 10(5) of 2 or more of these 4 species comprised the high test species group; 11 subjects with mean counts > 10(5) of 0 or 1 of the species, the low test species group. Because this was a post-hoc analysis, the number of subjects in some of the treatment/test species groups was small. However, the 8 high test species subjects who received tetracycline showed the most attachment level gain (0.83 +/- 0.20 mm), while the 3 tetracycline-treated, low test species subjects showed minimal gain (0.05 +/- 0.28 mm) 10 months post-therapy. Low test species subjects receiving Augmentin (n = 2) showed a mean gain in attachment of 0.67 (+/- 0.59) mm. The mean % of sites showing either attachment gain or loss > or = 2 mm was computed for each treatment/test species group. High test species subjects receiving tetracycline exhibited the best ratio of gaining to losing sites (16.2), followed by low test species subjects receiving Augmentin (14.1). Periodontal pockets < 7 mm pre-therapy in low test species subjects treated with Augmentin and high test species subjects treated with tetracycline showed attachment gain more frequently than attachment loss. The greatest proportion of gaining sites was seen at pockets > 6 mm, particularly in subjects receiving adjunctive tetracycline. Overall, the data indicated that a gain in mean attachment level post-therapy was significantly associated (p < 0.001) with an increase in C. ochracea accompanied by a decrease in B. forsythus, P. gingivalis, P. intermedia and P. nigrescens. The 4 test species were decreased more in subjects receiving tetracycline. In contrast, Augmentin appeared to be effective in decreasing the % sites colonized by A. actinomycetemcomitans and in increasing the proportion of sites colonized by C. ochracea. Knowledge of the baseline microbiota should improve the choice of an appropriate adjunctive antibiotic for periodontal therapy.

Adolescent↗

PubMed1996

Passive load and angiotensin II evoke differential responses of gene expression and protein synthesis in cardiac myocytes.

This study introduced an improved model of loaded adult cardiocytes to address a proposed requirement for angiotensin II (Ang II) in the transduction pathway between load on the cardiac myocyte and its early anabolic responses of gene expression and acceleration of protein synthesis. The isolated cardiocytes were subjected to passive load by step increments of stretch and responded with proportional acceleration of protein synthesis in both adult and neonatal cardiocytes; this response was unaltered by 1 mumol/L [Sar1, Ile8]Ang II, an antagonist peptide to Ang II. Ang II from 1 nmol/L to 10 mumol/L did not increase protein synthesis after 4 hours in adult cardiocytes nor at 100 nmol/L in neonatal cardiocytes. However, 100 nmol/L Ang II did increase [3H]phenylalanine incorporation into neonatal cardiocyte protein over a 24-hour period by 10%, whereas passive load increased [3H]phenylalanine incorporation into protein by 30%, which was not blocked by [Sar1, Ile8]Ang II. Thus, the anabolic effect of load does not require ANG II to increase either 4-hour protein synthesis in both adult and neonatal cardiocytes or 24-hour [3H]phenylalanine incorporation into protein in neonatal cardiocytes. The genetic response of the cardiocyte to load was examined by assessing c-fos and Na+-Ca2+ exchanger mRNA levels, because there are rapidly expressed at the onset of cardiac pressure overload. The c-fos mRNA was increased fourfold within 1 hour after 100 nmol/L Ang II treatment of either adult or neonatal cardiocytes. This c-fos induction was blocked by [Sar1, Ile8]Ang II. One hour after loading of adult cardiocytes, induction of c-fos expression was increased threefold; this was also blocked by [Sar1, Ile8]Ang II. Thus, load-induced c-fos expression was Ang II dependent in adult cardiocytes. In contrast, exchanger mRNA levels were increased threefold 1 hour after loading of adult cardiocytes, but this increased expression was not blocked by [Sar1, Ile8]Ang II. For additional comparison, c-fos expression was induced by Ang II and phorbol myristate acetate, which did not induce exchanger expression; conversely, exchanger expression was induced by veratridine, which did not increase c-fos expression. Thus, separate c-fos and exchanger expression pathways can be differentiated in adult cardiocytes. This study demonstrated that Ang II is not required for load to initiate the anabolic processes of accelerated protein synthesis or enhanced Na+-Ca2+ exchanger expression pathways can be differentiated in adult cardiocytes. This study demonstrated that Ang II is not required for load to initiate the anabolic processes of accelerated protein synthesis or enhanced Na+-Ca2+ exchanger gene expression in cardiocytes; however, load induced c-fos expression is Ang II dependent.

Angiotensin II↗

PubMed1995

Dietary models for root caries.

A stepwise multiple logistic regression was computed to assess which of the nutritional variables differentiate the healthy and diseased group of participants in the Forsyth Specialized Caries Center (n = 275). Variables considered as candidates for the model included the consumption per week of sugars, starch, cheese, fruits and fruit juices, noncariogenic foods, and dairy products. Two variables--sugars and cheese--were statistically significant by the stepwise procedure. Increased intake of sugar was associated with being in the root caries group, whereas high intake of cheese was negatively associated with root caries. Thus, cheese seems to have a protective effect after sugar intake is controlled for. Odds ratios were computed to quantify the influence of the variables. An increase of two exposures of sugar per day corresponded with an odds ratio of 1.26. The odds ratio continues to increase with sugar intake so that an increase to five exposures per day gives an odds ratio of 1.79. This model is consistent with past in vitro studies suggesting that cheese protects against caries formation when sugar intake is controlled for and that increasing frequency of sugar intake increases the odds of root caries.

Dairy Products↗

PubMed1995

Clinical and microbiological changes associated with the use of 4 adjunctive systemically administered agents in the treatment of periodontal infections.

The purpose of the present investigation was to assess the effects of periodontal surgery and 4 systemically administered agents, Augmentin, tetracycline, ibuprofen or a placebo on clinical and microbiological parameters of periodontal disease. 98 subjects were monitored at 2-month intervals at 6 sites per tooth for clinical parameters. Subgingival plaque samples were taken from the mesial surface of each tooth at each visit and evaluated for their content of 14 subgingival species using DNA probes and a colony lift method. 40 subjects who exhibited loss of attachment > 2.5 mm at 1 or more sites during longitudinal monitoring were treated using modified Widman flap surgery at sites with probing pocket depth > 4 mm, subgingival scaling at all other sites and were randomly assigned 1 of the 4 agents. Treatment was completed within 30 days during which time the subject took the assigned agent. Overall, subjects exhibited a mean attachment level "gain" of 0.34 +/- 0.10 mm (SEM) and a mean pocket depth reduction of 0.62 +/- 0.09 mm 10 +/- 4 months post-therapy. However, certain subjects in each treatment group showed a poor response. Subjects receiving antibiotics exhibited significantly more attachment level "gain" (0.57 +/- 0.15 mm, SEM) than subjects receiving either ibuprofen or a placebo (0.02 +/- 0.10). The differences between Augmentin and tetracycline groups were not significant, nor were the differences between ibuprofen and placebo. 10 months post-therapy, there was a reduction in the number of sites colonized in any subject group by detectable levels (10(3)) of P. gingivalis. Species showing similar reductions were B. forsythus, P. intermedia and P. micros. Subjects receiving systemically administered antibiotics had a significant increase in the proportion of sites colonized by C. ochracea coupled with a greater decrease in the number of sites colonized by P. gingivalis, B. forsythus, P. intermedia and P. micros post-therapy than subjects not receiving antibiotics. The results of this investigation indicate that adjunctive systemic antibiotics increase periodontal attachment "gain" and decrease the levels of some suspected periodontal pathogens in subjects with evidence of current disease progression.

Adolescent↗

PubMed1995

Factors associated with different responses to periodontal therapy.

In a study of the efficacy of modified Widman flap surgery and scaling and root planning accompanied by 1 of 4 systemic adjunctive agents, Augmentin, tetracycline, ibuprofen or placebo, it was observed that subjects differed in their response to therapy. The difference was only partially accounted for by the adjunctive agent employed. The purpose of the present investigation was to examine clinical and microbiological features in subjects who showed different levels of attachment change post-therapy. 40 subjects were subset into 3 groups based on mean attachment level change post-therapy. 10 poor response subjects showed mean attachment loss; 19 moderate response subjects showed mean attachment gain between 0.02-0.5 mm and 11 good response subjects showed a mean gain of attachment > 0.5 mm. Clinical parameters were measured at 6 sites per tooth both pre- and post-therapy. Microbiological samples were taken from the mesial aspect of each tooth and evaluated individually for their content of 14 subgingival taxa using a colony lift method and DNA probes. % of sites colonized by each species was computed for each subject both pre- and post-therapy. Significant differences were observed among treatment response groups for mean probing pocket depth, attachment level and % of sites with plaque pre-therapy. The poor response subjects had the lowest mean probing pocket depth and attachment level, but the highest plaque levels. Post-therapy, the poor response group exhibited the greatest degree of gingival inflammation as assessed by gingival redness and bleeding on probing.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1994

Role of microtubules in contractile dysfunction of hypertrophied cardiocytes.

Cardiac hypertrophy in response to systolic pressure overloading frequently results in contractile dysfunction, the cause for which has been unknown. Since, in contrast, the same degree and duration of hypertrophy in response to systolic volume overloading does not result in contractile dysfunction, we postulated that the contractile dysfunction of pressure hypertrophied myocardium might result from a direct effect of stress as opposed to strain loading on an intracellular structure of the hypertrophied cardiocyte. The specific hypothesis tested here is that the microtubule component of the cytoskeleton is such an intracellular structure, which, forming in excess, impedes sarcomere motion. The feline right ventricle was either pressure overloaded by pulmonary artery banding or volume overloaded by atrial septotomy. The quantity of microtubules was estimated from immunoblots and immunofluorescent micrographs, and their mechanical effects were assessed by measuring sarcomere motion during microtubule depolymerization. We show here that stress loading increases the microtubule component of the cardiac muscle cell cytoskeleton; this apparently is responsible for the entirety of the cellular contractile dysfunction seen in our model of pressure-hypertrophied myocardium. No such effects were seen in right ventricular cardiocytes from normal or volume-overloaded cats or in left ventricular cardiocytes from any group of cats. Importantly, the linked microtubule and contractile abnormalities are persistent and thus may be found to have significance for the deterioration of initially compensatory cardiac hypertrophy into the congestive heart failure state.

Animals↗

PubMed1994

Electrical stimulation of contractile activity accelerates growth of cultured neonatal cardiocytes.

An electrical stimulation system was designed to regulate synchronized contractile activity of neonatal rat cardiocytes and to examine the effects of mechanical contraction on cardiocyte growth. Continuous electrical stimulation at a pulse duration of 5 milliseconds and frequency of 3 Hz resulted in a time-dependent accumulation of cell protein that reached 34% above initial values, as measured by the protein-to-DNA ratio. The growth response did not occur using voltage amplitudes that were subthreshold for contraction and was independent of contraction frequencies set at > or = 0.5 Hz. The RNA-to-DNA ratio increased in parallel to cell protein, indicating that the capacity for protein synthesis was enhanced by contraction. Rates of 28S rRNA synthesis were accelerated twofold in contracting cardiocytes. By comparison, protein and RNA accumulation did not occur in electrically stimulated cardiocytes in which contraction was blocked by either 10 mumol/L verapamil or by 5 mmol/L 2,3-butanedione monoxime, an inhibitor of actomyosin crossbridge cycling. Electrical stimulation of cardiocyte contraction did not enhance alpha-cardiac actin or myosin heavy chain (alpha+beta) mRNA transcript levels relative to 28S rRNA during the period of rapid growth that occurred over the first 48 hours. It is concluded that (1) electrical stimulation of contraction accelerates cardiocyte growth and RNA accumulation, (2) mechanical contraction is involved in regulating the growth of electrically stimulated cardiocytes, and (3) the levels of alpha-actin and myosin heavy chain mRNA increase in proportion to rRNA during the growth of contracting cardiocytes.

Animals↗

PubMed1994

Acute changes in myosin heavy chain synthesis rate in pressure versus volume overload.

The left ventricular hypertrophy that develops with the volume overload of mitral regurgitation is relatively less than that which develops with the pressure overload of aortic stenosis even when both lesions are severe. The hypertrophy that develops must be the sum of changes in the rate of myocardial protein synthesis and degradation. In the present canine study, we explored early changes in the synthesis rate of myosin heavy chain in response to severe acute pressure overload versus that of the severe acute volume overload of mitral regurgitation. We tested the hypothesis that in acute overload, the rate of protein synthesis would increase less in the volume-overload model than in the pressure-overload model, a potential partial mechanism for the discrepancy in the eventual total amount of hypertrophy that develops in these two lesions. Acute pressure overload was produced by inflating a balloon in the descending aorta, and acute volume overload was produced by using our closed-chest mitral chordal rupture technique. In both models, the hemodynamic lesion that was created was severe. In eight dogs with pressure overload, the average gradient across the balloon was 119.8 +/- 6.1 mm Hg. In six dogs with volume overload, the average regurgitant fraction was 0.67 +/- 0.06. Six other dogs served as controls. The average rate of myosin heavy chain synthesis in control dogs was 2.7 +/- 0.2% per day, virtually identical to the rate we found in the severe volume-overload model. In contrast, the rate was increased in the pressure-overload model by 30% to 3.5 +/- 0.3% per day (P < .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗

PubMed1994

Gingival recession: intra-oral distribution and associated factors.

This study assesses the role of poor oral hygiene and forceful toothbrushing as risk factors for recession. As part of a cross-sectional root surface caries study, 298 subjects, 42 to 67 years of age, with at least one exposed root surface, were examined. Since 66% of the root surface exposure and practically all the abrasion was on buccal surfaces, the analyses focused only on the buccal surface. Analysis of variance on subject means for buccal recession showed both calculus and presence of buccal root surfaces with abrasion to be significantly associated with recession after adjusting for age and gender. Root surface abrasion was considered a surrogate variable for forceful brushing. An additional analysis utilized means for each tooth, aggregating across subjects. For each of the 32 tooth types mean buccal recession, percent of exposed root surfaces with abrasion (%ra), and mean debris and calculus scores were calculated. Partial correlation coefficients across tooth types between recession and calculus, adjusting for abrasion, and for recession and abrasion adjusting for calculus, were 0.55. Interpretation of the %ra as a crude measure of forceful brushing is supported by its strong negative correlation across tooth types, with mean debris (r = -0.8) and mean calculus (r = -0.7). Separate analyses on premolars and on molars suggested that recession on premolars may be primarily due to brushing force and on the molars may be primarily due to debris and calculus. The findings suggest that recession is positively associated with percent abrasion (reflecting forceful brushing) and with poor oral hygiene.

Adult↗

PubMed1993

Cardiocyte contractile performance in experimental biventricular volume-overload hypertrophy.

Previous studies have shown that the right ventricle (RV) appears to tolerate volume overloading better than does the left ventricle (LV). To determine whether this dichotomous response is due to intrinsic differences in the contractile performance of volume hypertrophied RV vs. LV cardiac muscle cells, or cardiocytes, we characterized the contractile performance of cardiocytes isolated from an experimental feline model of biventricular volume overload (n = 7 cats), wherein a peripheral arteriovenous fistula (AVF) produced an identical duration and degree of volume overload for both ventricles; sham-operated cats served as the appropriate controls (n = 7). Cardiocyte contractile function was defined by laser diffraction measurement of sarcomere motion. For the AVF cats, there was a 2.4-fold increase in cardiac output, a significant increase in the RV and LV weight-to-body weight ratios, and a significant increase in cell surface area for the RV and LV cardiocytes. Despite this, cardiocyte contractile function in the AVF cats was entirely normal. Thus there was no significant difference between RV and LV cardiocytes from control cats in the extent or velocity of sarcomere shortening either in 1 cP superfusate or in higher viscosity superfusates, and comparison of RV and LV cells from the AVF cats to those from sham-operated cats again revealed no significant differences. Furthermore, cardiocyte relengthening properties showed no significant differences between AVF and control groups. In summary, this study shows that contractile dysfunction is not an inherent property of either RV or LV cardiac muscle cells hypertrophying in response to substantial volume overloading when preload is increased but afterload is normal.

Animals↗

PubMed1993

Electrically stimulated contraction accelerates protein synthesis rates in adult feline cardiocytes.

Cardiocytes were induced to contract via electrical field stimulation with an 8 V/cm electrical square-wave pulse of 5 ms at 0.125-2.0 Hz for up to 6 h. Protein synthesis rates were measured as rate of incorporation of [3H]-phenylalanine into total cell protein. Rates of protein synthesis were accelerated 43 +/- 4%, P < 0.001, by 4 h. The acceleration of total protein synthesis showed a frequency dependence between 0.125 and 0.5 Hz. In addition to accelerating rates of total protein synthesis, electrical stimulation of contraction accelerated fractional rates of synthesis of myosin heavy chain by 42 +/- 8%, P < 0.05. Protein synthesis rates were not accelerated upon electrical stimulation using subthreshold voltages. Addition of 100 ng/ml of actinomycin D had no effect on the ability of electrical stimulation of contraction to accelerate protein synthesis. To uncouple excitation-contraction coupling, 2,3-butanedione monoxime (BDM) was used to block actin-myosin cross-bridge interactions. BDM significantly decreased the ability of electrical stimulation to accelerate protein synthesis rates.

Animals↗

PubMed1993

Rapid expression of the Na(+)-Ca2+ exchanger in response to cardiac pressure overload.

This report identifies a rapid increase in the expression of cardiac Na(+)-Ca2+ exchanger mRNA in response to an acute pressure overload. This enhanced exchanger expression appeared within 1 h after the onset of right ventricular pressure overload in the cat and was sustained during cardiac overloading for at least 4 h. Maintenance of this right ventricular pressure overload for 48 h evoked an increase in the production of exchanger protein. Because of our previous finding that load imposition on the heart initiates cell growth and our hypothesis that this is in response to the enhanced entry of cellular cations, we then examined the effect of Na+ influx into cultured adult cardiac myocytes, or cardiocytes, in terms of early anabolic responses. Pressure overload of the heart and cardiocyte Na+ influx were found to produce a common, rapid result in terms of both enhanced Na(+)-Ca2+ exchanger expression and accelerated synthesis of general and contractile proteins, the hallmarks of cardiac hypertrophy.

Animals↗

PubMed1993

Evidence for cigarette smoking as a major risk factor for periodontitis.

The role of smoking as a risk factor for periodontitis was assessed separately in diabetic and nondiabetic study groups. Subject listings stratified for age (19 to 40 years) and sex were obtained for subjects with insulin-dependent diabetes mellitus (IDDM) and nondiabetic subjects. For both the IDDM group (n = 132) and the nondiabetic group (n = 95), age and sex stratified samples were constructed by random selection of subjects from each subject listing. Patients were recruited by phone, examined, and their medical and dental histories obtained. Among nondiabetic subjects, the prevalence of periodontitis was markedly higher among current smokers compared with never smokers (P < or = 0.005) in both the 19 to 30 year-old (46% vs. 12%) and 31 to 40 year-old groups (88% vs. 33%). The subject mean percent of sites with gingival pocket depth > or = 4 mm was higher among current smokers than never smokers (P = 0.001) in the 19 to 30 (8.2% vs. 3.4%) and 31 to 40 (14.3% vs. 4.3%) age groups. The effects of smoking among IDDM subjects were similar to that observed in the nondiabetic population. There were no differences between current and never smokers in the proportion of sites positive for plaque. Attributable risk percents from prevalence data suggest that among nondiabetic subjects, a large proportion, perhaps as much as 51% of the periodontitis in the 19 to 30 year old group and 32% of the periodontitis in the 31 to 40 year old group, is associated with smoking.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1992

Adrenergic effects on the biology of the adult mammalian cardiocyte.

BACKGROUND: To delineate the mechanism(s) of catecholamine-mediated cardiac toxicity, we exposed cultures of adult cardiac muscle cells, or cardiocytes, to a broad range of norepinephrine concentrations. METHODS AND RESULTS: Norepinephrine stimulation resulted in a concentration-dependent decrease in cardiocyte viability, as demonstrated by a significant decrease in viable rod-shaped cells and a significant release of creatine kinase from cells in norepinephrine-treated cultures. Norepinephrine-mediated cell toxicity was attenuated significantly by beta-adrenoceptor blockade and mimicked by selective stimulation of the beta-adrenoceptor, whereas the effects mediated by the alpha-adrenoceptor were relatively less apparent. When norepinephrine stimulation was examined in terms of cardiocyte anabolic activity, there was a concentration-dependent decrease in the incorporation of [3H]phenylalanine and [3H]uridine into cytoplasmic protein and nuclear RNA, respectively. The decrease in cytoplasmic labeling was largely attenuated by beta-adrenoceptor blockade and mimicked by selective stimulation of the beta-adrenoceptor, but alpha-adrenoceptor stimulation resulted in relatively minor decreases in cytoplasmic labeling. The norepinephrine-induced toxic effect appeared to be the result of cyclic AMP-mediated calcium overload of the cell, as suggested by studies in which pharmacological strategies that increased intracellular cyclic AMP led to decreased cell viability, as well as studies that showed that influx of extracellular calcium through the verapamil-sensitive calcium channel was necessary for the induction of cell lethality. Additional time-course studies showed that norepinephrine caused a rapid, fourfold increase in intracellular cyclic AMP, followed by a 3.2-fold increase in intracellular calcium [( Ca2+]i). CONCLUSIONS: These results constitute the initial demonstration at the cellular level that adrenergic stimulation leads to cyclic AMP-mediated calcium overload of the cell, with a resultant decrease in synthetic activity and/or viability.

Animals↗

PubMed1992

Cellular and ventricular contractile dysfunction in experimental canine mitral regurgitation.

This study was designed to answer two questions. First, does the left ventricular contractile dysfunction resulting from mitral regurgitation (MR) reflect a primary defect in the cardiac muscle cell? Second, what is the basis for any change in cellular contractile function that might be observed? Left ventricular volume overload was produced in 10 dogs by catheter transection of mitral chordae tendineae. Three months later in these and in seven control dogs, left ventricular contractile function was characterized by the end-ejection stress-volume relation (EESVR). Investigators who were blinded to these results then characterized the contractile performance of cardiac muscle cells, or cardiocytes, from these same left ventricles in terms of the viscosity (graded external load)-velocity relation. Finally, the tissue and cellular components of these same left ventricles were analyzed morphometrically. Both the left ventricles from the MR group and their constituent cardiocytes showed marked contractile abnormalities. By matching ventricles with cells from the same MR dogs, ventricular EESVR was correlated with cardiocyte peak sarcomere shortening velocity (SSV). The correlation coefficient between EESVR and SSV was 0.63, but between a size-independent measure of active ventricular stiffness and SSV, it was 0.88. No change in left ventricular interstitial volume fraction was found in MR dogs, but both ventricular and cellular contractile dysfunction strongly correlated with a decreased volume fraction of cardiocyte myofibrils. Last, in an attempt to relate the degree of contractile dysfunction to the hypertrophic response, left ventricular mass in the MR dogs was correlated with both cellular and ventricular contractile indexes; no significant correlation was found. Three conclusions are warranted by these studies. First, chronic left ventricular volume overload from mitral regurgitation leads to contractile defects at both the ventricular and cellular levels, the extent of which correlates well in individual animals. Second, no quantitative interstitial change resulted from MR. Taken together, these two findings strongly suggest that the contractile defect is intrinsic to the cardiocyte. Third, while the contractile abnormality in MR remains undefined, the most basic defects appear to be a combination of myofibrillar loss with the failure of compensatory hypertrophy to occur in response to progressive decrements in cellular and ventricular function.

Animals↗

PubMed1992

Cigarette smoking in a periodontal practice.

This case-control study compares the prevalence of cigarette smoking among patients in a periodontal practice (cases) with that of patients in referring general dental practices (controls). Smoking histories of patients (age greater than or equal to 25 years) in a periodontal practice and five general dental practices were obtained by questionnaire. From the general practices, only patients reporting negative histories for periodontitis were studied. Periodontal status of the periodontal practice patients was based on bone loss from full mouth radiographic surveys and gingival pocket depths. Patients were stratified by age (25 to 40, 41 to 55, and greater than 55 years) and sex. The combined frequency of current or former cigarette smoking reported by 196 periodontal practice patients with moderate or advanced periodontitis (M-A perio group) was higher than that reported by 209 general dental practice patients (gen prac group) in all age and sex categories. The age and sex adjusted summary odds ratio for a positive smoking history among M-A perio subjects relative to gen prac subjects was 2.6 (P less than 0.001). Separate corresponding odds ratios (age and sex adjusted) for current smoking versus never smoking in the two groups were 3.3 (P less than 0.001) and for former smoking versus never smoking 2.1 (P less than 0.004). Among current smokers, patients in the M-A perio group reported heavy smoking (greater than 10 cigarettes/day) relatively more often than control subjects (adjusted R.O. = 5.7; P less than 0.001). In the M-A perio group the frequency of current smoking increased with disease severity.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1991

Signals for cardiac muscle hypertrophy in hypertension.

Hypertension is associated with a rise in arterial pressure and a compensatory increase in cardiac mass, which if not treated effectively, progresses to decompensated congestive heart failure. This decompensation of an initially compensatory hypertrophy has intensified interest in the factors that initiate and maintain the development of cardiac hypertrophy. The potential signals that induce the development of cardiac hypertrophy are grouped as hemodynamic, growth-promoting hormonal, vasoconstriction-promoting hormonal, and genetic factors. Growth-promoting hormones such as insulin and thyroxine appear to play a permissive, but essential, role in the development and maintenance of cardiac hypertrophy. However, changes in cardiac load, both above and below normal, result in parallel changes in cardiac mass, which will return to normal when a normal load is restored. This adaptive response of the myocardium in direct response to elevated and depressed loads demonstrates that cardiac structure, composition, and function are not fixed postneonatal cardiac properties, but instead are regulated dynamically by the cardiocyte loading environment. This adaptive response is subject to modulation by vasoconstriction-promoting hormones and genetic factors. The current thrust in this research area is to elucidate the cellular signals that transduce the physical stimulus for hypertrophy into biochemical events underlying hypertrophic cardiac growth. To remove complex systemic interactions in vivo from the experimental paradigm, several in vitro models have been used to examine three general, but distinct, cellular pathways involving protein kinase C activation, cyclic AMP formation, and increased ion fluxes. Each pathway demonstrated a stimulatory effect on general protein synthesis, which is necessary for growth in all cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1991

Clinical risk indicators for periodontal attachment loss.

The purpose of the present investigation was to evaluate the association of baseline clinical parameters of periodontal disease with disease progression in the following year. 271 randomly selected subjects from Ushiku Japan were monitored for overt gingivitis and plaque accumulation at 4 sites per tooth and probing pocket depth, probing attachment level and bleeding on probing at 6 sites per tooth for all teeth at baseline and 1 year. A subject was considered to exhibit additional attachment loss if one or more sites increased 3 mm or more in a probing attachment level measurement in one year. The clinical variables included age, sex, number of missing teeth, mean pocket depth and attachment level. In addition, the % of sites which exhibited overt gingivitis, visible plaque, pocket depths, attachment levels or gingival recession over certain mm thresholds or bled on probing were determined. Chi 2 analysis was used to seek significant associations between the baseline clinical variables and subsequent attachment loss in a subject. Only 74 of the 271 subjects (27.3%) exhibited additional attachment loss of 3 mm or more at 1 or more sites after 1 year. Older subjects had a greater risk of disease progression than younger subjects. There were no significant differences in % of individuals exhibiting additional attachment loss when divided on the basis of sex, number of missing teeth or % of sites with overt gingivitis. However, the greater the % of sites with visible plaque or which bled on probing, the greater was the likelihood of subsequent attachment loss. Increasing mean levels of pocket depth or attachment level or increasing %s of sites exhibiting prior attachment loss were strongly related to the proportion of individuals with subsequent attachment loss. Gingival recession exhibited similar but weaker relationships. Log-linear analysis suggested that the association between bleeding on probing, age, or plaque levels with additional attachment loss may be explained by the association of these variables with baseline attachment loss. The analyses were repeated with a positive subject defined as having only 1 active site or 2 or more active sites. 37 subjects fit the 1st criterion and the remaining 37 the 2nd criterion. The associations observed were almost identical to those found when subjects were considered positive on the basis of 1 or more changing sites. Discriminant analysis was used to classify subjects as active or inactive using up to 11 predictor variables.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗