Evidence suggests that brushing with a toothpaste may slow plaque reformation over 24 h. This study measured the effect of toothpaste alone on plaque regrowth over a 96 h period and compared the effect with water and the known antiplaque agent chlorhexidine. At 9 a.m. at the beginning of 7,4‐day no oral hygiene periods, 10 volunteers were scaled and polished. Al 5 p.m. subjects brushed their own teeth with water until plaque free. Each subject rinsed for I min with 10 ml of a randomly allocated rinse. Rinsing was repeated at 10 a.m. and 10 p.m. on subsequent days. The rinses were water, chlorhexidine 0.2% or 3 g/10 ml slurries of toothpastes containing (1) monofluorophosphate(MFP), (2) monofluorophosphate + sodium fluoride (MFP+NaF) (3) monofluorophosphate + zinc citrate (MFP+ZCT) (4) stannous fluoride (SnF2) (5) sodium fluoride (NaF). At 16, 24, 48 and 72 h plaque on the buccal surface of the upper and lower premolars, canines and incisors was scored by the Gingival Margin Plaque Index (GMPI) and gram films of plaque samples made. At 96 h plaque was recorded diagraromatically and areas of coverage measured visually (Debris Index) and by planimetry. Progressive plaque formation to a Gingival Margin Plaque Index of 100% at 72 h was observed for toothpaste and water rinses. For chlorhexidine the Gingival Margin Plaque Index at 72 h was 6%, At 96 h plaque areas were significantly less with toothpaste rinses compared with water. Chlorhexidine very significantly reduced plaque areas compared with toothpaste and water. The bacteriological assessment of smears revealed essentially similar plaque development during toothpaste and water rinses and was consistent with previous reports. However, with chlorhexidine the densities of organisms in the smears were greatly reduced. It was concluded that the small effect of toothpaste rinses on plaque accumulation compared with chlorhexidine would not alone represent a true antiplaque effect resulting in therapeutic benefit.
As a result of the low yield of cartilage from primary patient harvests and a high demand for autologous cartilage for reconstructive surgery and structural repair, primary explant cartilage must be augmented by tissue engineering techniques. In this study, chondrocytes seeded on PLLA/PGA scaffolds in static culture and a direct perfusion bioreactor were biochemically and histologically analyzed to determine the effects of fluid flow and media pH on matrix assembly. A gradual media pH change was maintained in the bioreactor within 7.4-6.96 over 2 weeks compared to a more rapid decrease from 7.4 to 6.58 in static culture over 3 days. Seeded scaffolds subjected to 1 microm/s flow demonstrated a 118% increase (p < 0.05) in DNA content, a 184% increase (p < 0.05) in GAG content, and a 155% (p < 0.05) increase in hydroxyproline content compared to static culture. Distinct differences were noted in tissue morphology, including more intense staining for proteoglycans by safranin-O and alignment of cells in the direction of media flow. Culture of chondrocyte seeded matrices thus offers the possibility of rapid in vitro expansion of donor cartilage for the repair of structural defects, tracheal injury, and vascularized tissue damage.
The objective of this study was to determine the effects of scaffold composition on the physical properties, adhesion, and growth of bovine articular chondrocytes on polylactic acid (PLA)/polyglycolic acid (PGA) composites. Nonwoven meshes of PGA were coated with PLA, using a solvent evaporation technique that resulted in composites with fractional PLA contents ranging from 0 to 68%. The compressive modulus of scaffolds increased linearly with the addition of PLA, ranging from less than 1 kPa for PGA to approximately 20 kPa for scaffolds with 68% PLA content. The characteristic degradation time of these scaffolds also increased from approximately 5 days for 0% PLA to 45 days for 68% PLA. Addition of PLA decreased cell seeding efficiency from 48% for 0% PLA scaffolds to 27% for 68% PLA scaffolds. Cells seeded onto 27% PLA scaffolds increased 3-fold in number over 4 weeks in culture, whereas cells seeded onto 68% PLA increased only 2-fold in number. Scanning electron microscopy indicated that cells attached to PGA appeared flat with many small processes, whereas those attached to PLA were more rounded. These studies provide important information for the design of scaffolds for cartilage tissue engineering.
Much has been written on the subject of extrinsic tooth discoloration, but, except when the pigment is intentionally applied, the etiologies and mechanisms are poorly understood. Extrinsic stains have been classified as non-metallic or metallic. The pigment usually lies not on or in the dental tissues, but in surface deposits, particularly the acquired pellicle layer and at sites receiving limited cleaning. Whether pigments absorb, adsorb, or chemically interact with dental surfaces is unclear. Some stains merely seem to reflect the color of the apparent source, whereas others have been ascribed to a secondary chemical alteration of a substance at the tooth or pellicle surface. Theories of chromogenic bacteria and formation of metal sulfides are frequently propounded but without clear supportive evidence. Staining by cationic antiseptics and, to a lesser extent, metal salts has attracted research interest. Chlorhexidine and other cationic antiseptics, it is hypothesized, may catalyze browning reactions or facilitate metal sulfide formation in pellicle. Controlled clinical studies have repeatedly shown that dental and mucosal staining associated with the use of chlorhexidine and some metal salts is dependent upon volunteers' imbibing reasonable quantities of chromogenic beverages, such as tea. However, it must be appreciated that cationic antiseptics and polyvalent metals can precipitate chromogenic material from a large range of dietary compounds. The control of dental staining, at least that associated with chlorhexidine, can be achieved both in vitro and in vivo by the use of oxidizing agents which appear to remove the stain physically from the surfaces.
C Co om mp pa ar ri is so on n o of f c ce er rv vi ic ca al l m ma ag gn ne et ti ic c s st ti im mu ul la at ti io on n a an nd d b bi il la at te er ra al l p pe er rc cu ut ta an ne eo ou us s e el le ec ct tr ri ic ca al l s st ti im mu ul la at ti io on n o of f t th he e p ph hr re en ni ic c n ne er rv ve es s i in n n no or rm ma al l s su ub bj je ec ct ts s We compared cervical magnetic stimulation with conventional supramaximal bilateral percutaneous electrical stimulation in nine normal subjects. We measured oesophageal pressure (Poes), gastric pressure (Pgas) and transdiaphragmatic pressure (Pdi). The maximal relaxation rate (MRR) was also measured. The mean magnetic twitch Pdi was 36.5 cmH 2 O (range 27-48 cmH 2 O), significantly larger than electrical twitch Pdi, mean 29.7 cmH 2 O (range 22-40 cmH 2 O).The difference in twitch Pdi was explained entirely by twitch Poes, and it is possible that the magnetic technique stimulates some of the nerves to the upper chest wall muscles as well as the phrenic nerves. We compared bilateral, rectified, integrated, diaphragm surface electromyographic (EMG) responses in three subjects and found results within 10% in each subject, indicating similar diaphragmatic activation. The within occasion coefficient of variation, i.e. same subject/same session, was 6.7% both for magnetic and electrical twitch Pdi. The between occasion coefficient of variation, i.e. same subject/different days, was 6.6% for magnetic stimulation and 8.8% for electrical. There was no difference between relaxation rates measured with either technique.We conclude that magnetic stimulation is a reproducible and acceptable technique for stimulating the phrenic nerves, and that it provides a potentially useful alternative to conventional electrical stimulation as a nonvolitional test of diaphragm strength.
Background -Skeletal muscle twitch responses may be transiently increased by previous contractions, a phenomenon termed twitch potentiation. The aim of this study was to examine the extent and time course of diaphragmatic twitch potentiation and its relationship to both the magnitude and duration of the preceding voluntary diaphragmatic contraction. Methods -Twitch transdiaphragmatic pressure (PDI) was measured in six normal subjects, before and after voluntary diaphragm contractions of 100%, 75%, 50%, and 25% of maximum PDI (PDImax) sustained for five and 10 seconds. Results -Twitch PDI was significantly increased after 100%, 75%, and 50% contractions. Following maximal contractions sustained for 10 seconds the mean increase in twitch PDI was 52%. Following 50% contractions sustained for five seconds the mean increase in twitch height was 28%. In all runs twitch PDI returned to rested levels within 20 minutes. Conclusions -Twitch potentiation can be substantial, even following submaximal contractions, and must be taken into account when twitch pressure is used to assess diaphragm contractility.
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