, 2000[28] Hili et al ,1997[29] and Nzeako et al , 2006[30] thyme

, 2000[28] Hili et al.,1997[29] and Nzeako et al., 2006[30] thyme and clove oil possessed antimicrobial activity against S. aureus, E. coli and C. albicans at various concentration of the extracts. In our study, antimicrobial susceptibility in order of sequence for thyme oil was E. coli with MIC: 2 ��l/ml, selleckchem MBC: 8 ��l/ml, C. albicans with MIC, MFC: 16 ��l/ml, E. faecalis with MIC, MBC: 32 ��l/ml and S. aureus with MIC, MBC: 32 ��l/ml respectively. Essential oil of peppermint (Mentha piperita-Lamiaceae/Labiatae) is cultivated on a wide scale in Europe, USA and Japan. It is extensively used in toiletry, food and pharmaceutical industries. A variety of products ranging from toothpastes, mouthwashes and digestive tablets to sweets, ice cream and liquors are flavored with peppermint.

Essential oil of peppermint is obtained from the leaves by steam distillation method. Its principal constituents include monoterpinic alcohols mainly menthol (38-48%), ketones mainly menthones (20-30%), some monoterpens and oxides. It is a good antiseptic, antibacterial and antiviral. It has light, clean, refreshing aroma and is a good insect repellant. It has stimulating and strengthening effect; in treatment of shock, helpful for neuralgia and relief of general debility, headaches and migraines. It has antiseptic and anti-spasmodic effect; in reducing mucus and relieving coughs, sinusitis, throat infections, colds, flu, asthma and bronchitis. It is also used in inhalations, baths or applications. It has got cooling and cleansing effect; soothes itchy skin, relieves inflammation.

It has soothing and anti-spasmodic effect; relieves acidity, heartburn, diarrhea, indigestion and flatulence, also effective for travel sickness and nausea. It has cooling effect in case of varicose veins and hemorrhoids.[20] Peppermint oil makes the mouth feel fresh and of course, makes the formula taste good. Peppermint oil can also increase salivation, which is useful because dry mouth may result in halitosis.[31] In our study, antimicrobial effect was achieved at the concentration of 0.5 ��l/ml for C. albicans and at the concentration of 32 ��l/ml for E. coli, S. aureus, E. faecalis (32 ��l/ml). The clove plant grows in warm climates and is cultivated commercially in Tanzania, Sumatra, the Maluku (Molucca) Islands and South America. The tall evergreen plant grows up to 20 m and has leathery leaves.

The clove spice is the dried flower bud of Eugenia caryophyllata species. Essential oils are obtained Cilengitide from the buds, stems and leaves by steam distillation. The buds or cloves are strongly aromatic. Clove buds yield approximately 15-20% of a volatile oil that is responsible for the characteristic smell and flavor. The bud also contains a tannin complex, a gum and resin and a number of glucosides of sterols. The principal constituent of distilled clove bud oil (60-90%) is eugenol (4-allyl-2-methoxyphenol).

[24] All of the teeth in this study exhibiting dentine hypersensi

[24] All of the teeth in this study exhibiting dentine hypersensitivity also had some degree of gingival recession. Most teeth had at least 1-3 mm of gingival recession (n = 15), which is similar to the average recession of 2.5 mm reported by Addy et al. in their sample of sensitive teeth.[25] The teeth most often affected by dentine selleck inhibitor hypersensitivity were the lower incisors, followed by the premolars, then the canines, and then the upper molars. This distribution is reminiscent of the reports of Rees et al.[16] Taani and Awartani studies,[13] but dissimilar to Rees and Addy,[15] and Rees,[3] and earlier studies that reported the upper premolars most affected. Since the lower incisors are the teeth most affected by calculus accumulation followed by non-surgical periodontal therapy and because of the esthetic impact of these teeth, the lower incisors are more likely to be retained, even when severely compromised.

[26] The mean number of sensitive teeth per patient peaked at about 8 in the 50-59 year group, which is higher than the values reported in several of the studies mentioned above.[2,27] It has been hypothesized that dentine hypersensitivity might be more common among smokers, as they are more prone to gingival recession. However, the data from this study found no association between dentine hypersensitivity and smoking. A recent report by M��ller et al. suggested that smokers are not at risk for gingival recession,[26] but other studies, including those of Al-Wahadni and Linden,[28] and Rees and Addy,[15] have found more gingival recession and sensitivity among smokers.

The previous studies (Fischer et al.[8] Orchardson and Collins;[7] Addy et al.[25] Flynn et al.[6] Cunha et al.[29] Oyama and Matsumoto;[30] Taani and Awartani;[31] Rees;[3] Rees and Addy,[15]) reported a higher incidence of dentine hypersensitivity in females than in males. In this study, the ratio of females to males with hypersensitivity was 1.3:1; this difference is not likely to be statistically significant. About 11% of patients in the current study reported avoiding hypersensitive teeth most of the time. This figure is similar to that reported by Taani and Awartani.[31] Approximately, 34% of patients in this study were treated for dentine hypersensitivity by dentists, and 55% had tried treatment with desensitizing dentifrice.

These figures are higher than those reported by Taani and Awartani,[31] Liu et al.[12] and Fischer et al.[8] It is the author’s clinical impression, supported by some data, (Absi et al.),[32] that dentine hypersensitivity is more prevalent among patients who have good oral hygiene practices as tends to be the case in higher socioeconomic groups. To investigate this further, the patients with dentine hypersensitivity were divided into social groups using the Registrar General’s Classification Drug_discovery of Occupations as used in the recent UK Adult Dental Health Survey.

In addition, according to previous studies, propolis prevents den

In addition, according to previous studies, propolis prevents dental caries and periodontal disease, since it demonstrated significant antimicrobial activity selleck bio against the microorganisms involved in such diseases. These results give hope to us that propolis, a natural product, can be used for oral rehabilitation of patients for various purposes.
The extraction of a tooth requires that the surrounding alveolar bone be expanded to allow an unimpeded pathway for tooth removal. However, in generally the small bone parts are removed with the tooth instead of expanding.1�C4 Fracture of a large portion of bone in the maxillary tuberosity area is a situation of special concern. The maxillary tuberosity is especially important for the stability of maxillary denture.

2,3 Large fractures of the maxillary tuberosity should be viewed as a grave complication. The major therapeutic goal of management is to salvage the fractured bone in place and to provide the best possible environment for healing.3 Routine treatment of the large maxillary tuberosity fractures is to stabilize the mobile part(s) of bone with one of rigid fixation techniques for 4 to 6 weeks. Following adequate healing, a surgical extraction procedure may be attempted. However, if the tooth is infected or symptomatic at the time of the tuberosity fracture, the extraction should be continued by loosening the gingival cuff and removing as little bone as possible while attempting to avoid separation of the tuberosity from the periosteum.

If the attempt to remove the attached bone is unsuccessful and the infected tooth is delivered with the attached tuberosity, the tissues should be closed with watertight sutures because there may not be a clinical oroantral communication. The surgeon may elect to graft the area after 4 to 6 weeks of healing and postoperative antibiotic therapy. If the tooth is symptomatic but there is no frank sign of purulence or infection, the surgeon may elect to attempt to use the attached bone as an autogenous graft.5 There are many reports about complication of the tooth extraction in the literature, but only a few cases are about maxillary tuberosity fractures. The purpose of this paper is to present a case of maxillary tuberosity large fracture during extraction of first maxillary molar tooth, because of high possibility in dental practice but being rare in literature.

CASE REPORT A 28-year-old Caucasian male was referred to our clinic by the patient��s general dental practitioner (GDP) after the practitioner attempted to extract the patient��s upper right first molar tooth with forceps. He was a healthy young man with no history of significant medical problems. In dental examination; the maxillary right first, second and third Entinostat molars were elevated and mobile, so the patient was unable to close his mouth (Figure 1). An oroantral communication and bleeding from right nostril were present.

[24] All of the teeth in this study exhibiting dentine hypersensi

[24] All of the teeth in this study exhibiting dentine hypersensitivity also had some degree of gingival recession. Most teeth had at least 1-3 mm of gingival recession (n = 15), which is similar to the average recession of 2.5 mm reported by Addy et al. in their sample of sensitive teeth.[25] The teeth most often affected by dentine selleck catalog hypersensitivity were the lower incisors, followed by the premolars, then the canines, and then the upper molars. This distribution is reminiscent of the reports of Rees et al.[16] Taani and Awartani studies,[13] but dissimilar to Rees and Addy,[15] and Rees,[3] and earlier studies that reported the upper premolars most affected. Since the lower incisors are the teeth most affected by calculus accumulation followed by non-surgical periodontal therapy and because of the esthetic impact of these teeth, the lower incisors are more likely to be retained, even when severely compromised.

[26] The mean number of sensitive teeth per patient peaked at about 8 in the 50-59 year group, which is higher than the values reported in several of the studies mentioned above.[2,27] It has been hypothesized that dentine hypersensitivity might be more common among smokers, as they are more prone to gingival recession. However, the data from this study found no association between dentine hypersensitivity and smoking. A recent report by M��ller et al. suggested that smokers are not at risk for gingival recession,[26] but other studies, including those of Al-Wahadni and Linden,[28] and Rees and Addy,[15] have found more gingival recession and sensitivity among smokers.

The previous studies (Fischer et al.[8] Orchardson and Collins;[7] Addy et al.[25] Flynn et al.[6] Cunha et al.[29] Oyama and Matsumoto;[30] Taani and Awartani;[31] Rees;[3] Rees and Addy,[15]) reported a higher incidence of dentine hypersensitivity in females than in males. In this study, the ratio of females to males with hypersensitivity was 1.3:1; this difference is not likely to be statistically significant. About 11% of patients in the current study reported avoiding hypersensitive teeth most of the time. This figure is similar to that reported by Taani and Awartani.[31] Approximately, 34% of patients in this study were treated for dentine hypersensitivity by dentists, and 55% had tried treatment with desensitizing dentifrice.

These figures are higher than those reported by Taani and Awartani,[31] Liu et al.[12] and Fischer et al.[8] It is the author’s clinical impression, supported by some data, (Absi et al.),[32] that dentine hypersensitivity is more prevalent among patients who have good oral hygiene practices as tends to be the case in higher socioeconomic groups. To investigate this further, the patients with dentine hypersensitivity were divided into social groups using the Registrar General’s Classification AV-951 of Occupations as used in the recent UK Adult Dental Health Survey.

These complexity-based rules were interpreted as those that gover

These complexity-based rules were interpreted as those that govern how genes are organized into functional groups, taking into account the full content (and limitations) of the analyzed data set. This was contrasted with the pathway analysis of genetic Nutlin-3a 675576-98-4 interactions, in which the rules are interpreted in terms of information flow through individual gene pairs. Thus, we conclude that the most fruitful application of the complexity-based algorithm is the identification of gene modules rather than linear gene pathways. As a corollary, we conclude that methods designed to order genes into molecular-interaction sequences (pathways) are not ideal for the discovery of modules. In this work, we further demonstrate that these modular structures are optimally defined using the set complexity method described previously15 in a way that best balances general and specific information within a network.

We show that na?ve clustering measures are often not functionally informative, particularly as networks become very dense and involve multiple modes of interaction between nodes. Since genetic interaction networks can become very dense, especially when one considers many genes involved in a given function, a clustering measure that reflects functional modularity is necessary. We provide evidence that set complexity maximizes nontrivial, functional modularity. MODULARITY IN GENETIC INTERACTION DATA Genetic interaction is a general term to describe phenotypic nonindependence of two or more genetic perturbations. However, it is generally unclear how to define this independence.

2, 13, 19 Therefore, it is useful to consider a general approach to the analysis of genetic interaction. We have developed a method to systematically encode genetic interactions in terms of phenotype inequalities.2 This allows the modes of genetic interaction to be systematically analyzed and formally classified. Consider a genotype X and its cognate observed phenotype PX. The phenotype could be a quantitative measurement or any other observation that can be clearly compared across mutant genotypes (e.g., slow versus standard versus fast growth, or color or shape of colony, or invasiveness of growth on agar, etc.). The genotype is usually labeled by the mutation of one or more genes, which could be gene deletions, high-copy amplifications, single-nucleotide polymorphisms, or other allele forms.

With genotypes labeled by mutant alleles, a set of four phenotype observations can be assembled which defines Carfilzomib a genetic interaction: PA and PB for gene A and gene B mutant alleles, PAB for the AB double mutant, and PWT for the wild type or reference genotype. The relationship among these four measurements defines a genetic interaction. For example, if we follow the classic genetic definitions described above, PAB=PA

mutans colony count levels from the tongue surface in the first s

mutans colony count levels from the tongue surface in the first sample (P = 0.110) [Table 4]. The comparison of the S. mutans colony count levels from the tongue surface of the second samples of the Ondrohexidine?, Listerine? and control groups did reveal statistically significant differences (P = 0.017). The two-group comparison revealed that the S. mutans colony find more info count level of the control group was significantly higher than those of the MC?, Listerine? and Ondrohexidine? groups, whereas the comparisons between other groups did not reveal any statistically significant differences (P > 0.05), [Table 5].

Table 2 Streptococcus mutans colony count levels from the teeth surface on the first day after professional cleaning (first sample) and after 4th day (second sample): Results (P values) of Kruskal Wallis test * for comparison of mouth rinses Table 3 Post hoc Dunn’s multiple comparison tests to compare the differences between the teeth surface second sample values of the mouth rinses Table 4 Streptococcus mutans colony counts levels from the tongue surface on the 1st day after professional cleaning (first sample) and after 4th day (second sample): Results (P values) of Kruskal Wallis test * for comparison of mouth rinses Table 5 Post hoc Dunn’s multiple comparison tests to compare the differences between the second tongue sample values of the mouth rinses DISCUSSION During fixed orthodontic therapy, braces, bands, wires, and other attachments make it difficult for the patient to perform mechanical oral hygiene procedures; this difficulty results in plaque accumulation, which is the main cause of demineralization.

[1] Following the placement of fixed appliances, plaque volume, and S. mutans colony counts were shown to increase; after the removal of the appliances, S. mutans counts decreased to normal values.[19,20] Soet et al.[21] concluded that the most notable etiologic factor contributing to decay formation was S. mutans because this bacterium produced more acid than sobrius and mitis. There is double risk with respect to caries formation for orthodontic patients; besides the problem of cleaning of the tooth surfaces, S. mutans also exhibit high adhesion to the surfaces of brackets.[22] Antimicrobial mouth rinses are easy to use with fixed orthodontic appliances, and their ability to access most areas, including embrasures and around the appliances, makes them useful.

[9,23] Based on current Drug_discovery practices daily rinsing with a 0.05% sodium fluoride mouth rinse[24,25] is recommended for these patients. However patients�� compliance with these directions is often unsatisfactory.[26] There are some undesirable side effects[16] related to the continuous use of antimicrobial mouth rinses; which is why patients are advised to use these mouth rinses on a short-term basis. Also, the clinicians are prompted to seek alternative mouth rinses that could be used for long spans of time.