text:
NEW YORK (CNN) -- Bank of America's chief executive officer spent four hours Thursday testifying in an investigation into the $3.6 billion in bonuses that Merrill Lynch paid out just before it was acquired by the bank last year, but still refused to give out the details of those payments.
Kenneth Lewis prepares to enter the offices of Attorney General Andrew Cuomo on Thursday in New York City.
The New York Attorney General's Office served a subpoena on Bank of America during chief executive Kenneth Lewis' testimony Thursday evening, seeking the full list of individual bonus recipients at Merrill Lynch, according to Benjamin M. Lawsky, a special assistant to Attorney General Andrew Cuomo.
"We obviously wanted to question Mr. Lewis about this list and are very disappointed that Bank of America has chosen not to produce it. As a result, during the testimony this evening, we served a subpoena on Bank of America for the list, which we intend to obtain," Lawsky said in a written statement.
Lewis, speaking to reporters as he left the attorney general's office after his testimony, said that he had come to "deliver clarity" and that he answered the questions that were asked to the best of his knowledge, but refused to take any questions about the details of the deposition.
Bank of America has been allocated $45 billion of federal bailout funds, and the Treasury has guaranteed to protect Bank of American against potentially billions of dollars in losses from investments Merrill Lynch made in real estate loans.
Former Merrill Lynch Chief Executive John Thain told investigators last week that Lewis was aware Merrill employees would be awarded billions of dollars in bonuses before Bank of America's takeover of Merrill became effective January 1, according to sources familiar with the investigation.
In testimony before the House Financial Services Committee on February 11, Lewis said he had little involvement in the Merrill bonus plan.
"They were a public company until the first of the year, they had a separate board, separate compensation committee and we had no authority to tell them what to do, just urged them what to do," Lewis said.
But Cuomo's staff obtained a document, negotiated between Bank of America and Merrill during their takeover negotiations, that set a cap for Merrill Lynch's bonus pool at about $5 billion, said sources with knowledge of the investigation. Bank of America confirmed there was a cap set.
Cuomo has accused Merrill Lynch of trying to hide lavish bonus payments.
"Merrill Lynch secretly moved up the planned date to allocate bonuses and then richly rewarded their failed executives," Cuomo wrote in a letter to House Financial Services Committee Chairman Rep. Barney Frank, D-Massachusetts.
Cuomo found Merrill paid its four top bonus recipients $121 million and doled out bonuses of $1 million or more to 696 employees, as the firm lost $15 billion in the fourth quarter.
"I don't want to see the taxpayers being taken advantage of. And I don't want to see the taxpayers paying performance bonuses that shouldn't be paid," Cuomo said.
Cuomo is investigating to see whether failure to disclose the bonus payments to investors violated New York's Martin Act, a powerful securities law that empowers the attorney general to bring not only civil but also criminal charges.
CNN's Allan Chernoff contributed to this report.
All About Bank of America Corporation • Merrill Lynch & Co. Inc. • Kenneth D. Lewis • John Thain • Andrew Cuomo


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Caries - Related Links
Open Access Articles- Top Results for Caries
Oral Health and Dental ManagementPrevalence of Dental Caries among Smokeless Tobacco Chewers in Dakshina Kannada District Population: A Cross Sectional Study
Oral Health and Dental ManagementDiagnostic Challange: Instances Mimicking a Proximal Carious Lesion Detected by Bitewing Radiography
Research & Reviews: Journal of Dental SciencesScrew Impacted in a Deciduous Tooth
Research & Reviews: Journal of Dental SciencesAnalysis of Salivary Flow Rate, Buffering Capacity and Isolation Of Streptococcus mutans Using Selective MSKB Media in Caries Active and Caries Free
Pediatric Dental CareBlack Stains in Primary Teeth: Overview
Dental caries
|Dental caries
Destruction of a tooth by dental caries. This type of decay is also known as root decay.
|Classification and external resources
|Dental caries
|Patient UK
|Dental caries
Dental caries (caries is Latin for "rottenness"[1]), also known as tooth decay, cavities, or caries, is breakdown of teeth due to the activities of bacteria.[2] The cavities may be a number of different colors from yellow to black.[3] Symptoms may include pain and difficulty with eating.[3][4] Complications may include inflammation of the tissue around the tooth, tooth loss, and infection or abscess formation.[1][3]
The bacteria break down the hard tissues of the teeth (enamel, dentin and cementum) by making acid from food debris or sugar on the tooth surface.[5] Simple sugars in food are these bacteria's primary energy source and thus a diet high in simple sugar is a risk factor.[5] If mineral breakdown is greater than build up from sources such as saliva, caries results.[5] Risk factors include conditions that result in less saliva such as: diabetes mellitus, Sjogren's syndrome and some medications.[5] Medications that decrease saliva production include antihistamines and antidepressants among others.[5] Caries are also associated with poverty, poor cleaning of the mouth, and receding gums resulting in exposure of the roots of the teeth.[2][6]
Prevention includes: regular cleaning of the teeth, a diet low in sugar and small amounts of fluoride.[4][5] Brushing the teeth two times per day and flossing between the teeth once a day is recommended by many.[2][5] Fluoride may be from water, salt or toothpaste among other sources.[4] Treating a mother's dental caries may decrease the risk in her children by decreasing the numbers of certain bacteria.[5] Screening can result in earlier detection.[2] Depending on the extent of destruction, various treatments can be used to restore the tooth to proper function or the tooth may be removed.[2] There is no known method to grow back large amounts of tooth.[7] The availability of treatment is often poor in the developing world.[4] Paracetamol (acetaminophen) or ibuprofen may be taken for pain.[2]
Worldwide, approximately 2.43 billion people (36% of the population) have dental caries in their permanent teeth.[8] The World Health Organizations estimates that nearly all adults have dental caries at some point in time.[4] In baby teeth it affects about 620 million people or 9% of the population.[8] They have become more common in both children and adults in recent years.[9] The disease is most common in the developed world and less common in the developing world due to greater simple sugar consumption.[2]
- 1 Signs and symptoms
- 2 Cause
- 3 Pathophysiology
- 4 Diagnosis
- 5 Prevention
- 6 Treatment
- 7 Epidemiology
- 8 History
- 9 Research
- 10 Other animals
- 11 References
- 12 External links
Signs and symptoms
A person experiencing caries may not be aware of the disease.[10] The earliest sign of a new carious lesion is the appearance of a chalky white spot on the surface of the tooth, indicating an area of demineralization of enamel. This is referred to as a white spot lesion, an incipient carious lesion or a "microcavity".[11] As the lesion continues to demineralize, it can turn brown but will eventually turn into a cavitation ("cavity"). Before the cavity forms, the process is reversible, but once a cavity forms, the lost tooth structure cannot be regenerated. A lesion that appears dark brown and shiny suggests dental caries were once present but the demineralization process has stopped, leaving a stain. Active decay is lighter in color and dull in appearance.[12]
As the enamel and dentin are destroyed, the cavity becomes more noticeable. The affected areas of the tooth change color and become soft to the touch. Once the decay passes through enamel, the dentinal tubules, which have passages to the nerve of the tooth, become exposed, resulting in pain that can be transient, temporarily worsening with exposure to heat, cold, or sweet foods and drinks.[13] A tooth weakened by extensive internal decay can sometimes suddenly fracture under normal chewing forces. When the decay has progressed enough to allow the bacteria to overwhelm the pulp tissue in the center of the tooth a toothache can result and the pain will become more constant. Death of the pulp tissue and infection are common consequences. The tooth will no longer be sensitive to hot or cold, but can be very tender to pressure.
Dental caries can also cause bad breath and foul tastes.[14] In highly progressed cases, infection can spread from the tooth to the surrounding soft tissues. Complications such as cavernous sinus thrombosis and Ludwig angina can be life-threatening.[15][16][17]
There are four main criteria required for caries formation: a tooth surface (enamel or dentin), caries-causing bacteria, fermentable carbohydrates (such as sucrose), and time.[18] However, it is also known that these four criteria are not always enough to cause the disease and a sheltered environment promoting development of a cariogenic biofilm is required. The caries process does not have an inevitable outcome, and different individuals will be susceptible to different degrees depending on the shape of their teeth, oral hygiene habits, and the buffering capacity of their saliva. Dental caries can occur on any surface of a tooth that is exposed to the oral cavity, but not the structures that are retained within the bone.[19]
The bacteria most responsible for dental cavities are the mutans streptococci, most prominently Streptococcus mutans and Streptococcus sobrinus, and lactobacilli. If left untreated, the disease can lead to pain, tooth loss and infection.[20]
Tooth decay disease is caused by specific types of bacteria that produce acid in the presence of fermentable carbohydrates such as sucrose, fructose, and glucose.[21][22] The mineral content of teeth is sensitive to increases in acidity from the production of lactic acid. To be specific, a tooth (which is primarily mineral in content) is in a constant state of back-and-forth demineralization and remineralization between the tooth and surrounding saliva. For people with little saliva, especially due to radiation therapies and autoimmune disorders, such as Sjögren's syndrome, that may destroy the salivary glands, there also exists therapies such as saliva substitutes and remineralization products. These patients may be susceptible to dental caries. When the pH at the surface of the tooth drops below 5.5, demineralization proceeds faster than remineralization (meaning that there is a net loss of mineral structure on the tooth's surface).
All caries occur from bacterial acid demineralization that exceeds saliva and fluoride remineralization, and acid demineralization occurs where bacterial plaque is left on teeth. Because most plaque-retentive areas are between teeth and inside pits and fissures on chewing surfaces where brushing is difficult, over 80% of cavities occur inside pits and fissures. Areas that are easily cleansed with a toothbrush, such as the front and back surfaces (facial and lingual), develop fewer cavities.
Some foods have an acidic pH of 5.5 or lower which can result in demineralisation in the absence of bacteria. This is known as erosion, rather than caries, because the acid is not bacterial in origin. Attack by acid from systemic complications such as bulimia and stomach difficulties as well as vomiting can cause tooth erosion.
There are certain diseases and disorders affecting teeth that may leave an individual at a greater risk for cavities.. Amelogenesis imperfecta, which occurs between 1 in 718 and 1 in 14,000 individuals, is a disease in which the enamel does not fully form or forms in insufficient amounts and can fall off a tooth.[23] In both cases, teeth may be left more vulnerable to decay because the enamel is not able to protect the tooth.[24]
In most people, disorders or diseases affecting teeth are not the primary cause of dental caries. Approximately 96% of tooth enamel is composed of minerals.[25] These minerals, especially hydroxyapatite, will become soluble when exposed to acidic environments. Enamel begins to demineralize at a pH of 5.5.[26] Dentin and cementum are more susceptible to caries than enamel because they have lower mineral content.[27] Thus, when root surfaces of teeth are exposed from gingival recession or periodontal disease, caries can develop more readily. Even in a healthy oral environment, however, the tooth is susceptible to dental caries.
The evidence for linking malocclusion and/or crowding to the dental caries is weak;[28][29] however, the anatomy of teeth may affect the likelihood of caries formation. Where the deep developmental grooves of teeth are more numerous and exaggerated, pit and fissure caries are more likely to develop (see next section). Also, caries are more likely to develop when food is trapped between teeth.
The mouth contains a wide variety of oral bacteria, but only a few specific species of bacteria are believed to cause dental caries: Streptococcus mutans and Lactobacillus species among them. These organisms can produce high levels of lactic acid following fermentation of dietary sugars, and are resistant to the adverse effects of low pH, properties essential for cariogenic bacteria.[21] As the cementum of root surfaces is more easily demineralized than enamel surfaces, a wider variety of bacteria can cause root caries including Lactobacillus acidophilus, Actinomyces spp., Nocardia spp., and Streptococcus mutans. Bacteria collect around the teeth and gums in a sticky, creamy-coloured mass called plaque, which serves as a biofilm. Some sites collect plaque more commonly than others, for example sites with a low rate of salivary flow (molar fissures). Grooves on the occlusal surfaces of molar and premolar teeth provide microscopic retention sites for plaque bacteria, as do the interproximal sites. Plaque may also collect above or below the gingiva where it is referred to as supra- or sub-gingival plaque, respectively.
These bacterial strains, most notably S. mutans can be inherited by a child from a caretaker's kiss or through feeding premasticated food.[30]
Fermentable carbohydrates
Bacteria in a person's mouth convert glucose, fructose, and most commonly sucrose (table sugar) into acids such as lactic acid through a glycolytic process called fermentation.[22] If left in contact with the tooth, these acids may cause demineralization, which is the dissolution of its mineral content. The process is dynamic, however, as remineralization can also occur if the acid is neutralized by saliva or mouthwash. Fluoride toothpaste or dental varnish may aid remineralization.[31] If demineralization continues over time, enough mineral content may be lost so that the soft organic material left behind disintegrates, forming a cavity or hole. The impact such sugars have on the progress of dental caries is called cariogenicity. Sucrose, although a bound glucose and fructose unit, is in fact more cariogenic than a mixture of equal parts of glucose and fructose. This is due to the bacteria utilising the energy in the saccharide bond between the glucose and fructose subunits. S.mutans adheres to the biofilm on the tooth by converting sucrose into an extremely adhesive substance called dextran polysaccharide by the enzyme dextransucranase.[32]
The frequency of which teeth are exposed to cariogenic (acidic) environments affects the likelihood of caries development.[33] After meals or snacks, the bacteria in the mouth metabolize sugar, resulting in an acidic by-product that decreases pH. As time progresses, the pH returns to normal due to the buffering capacity of saliva and the dissolved mineral content of tooth surfaces. During every exposure to the acidic environment, portions of the inorganic mineral content at the surface of teeth dissolves and can remain dissolved for two hours.[34] Since teeth are vulnerable during these acidic periods, the development of dental caries relies heavily on the frequency of acid exposure.
The carious process can begin within days of a tooth's erupting into the mouth if the diet is sufficiently rich in suitable carbohydrates. Evidence suggests that the introduction of fluoride treatments have slowed the process.[35] Proximal caries take an average of four years to pass through enamel in permanent teeth. Because the cementum enveloping the root surface is not nearly as durable as the enamel encasing the crown, root caries tends to progress much more rapidly than decay on other surfaces. The progression and loss of mineralization on the root surface is 2.5 times faster than caries in enamel. In very severe cases where oral hygiene is very poor and where the diet is very rich in fermentable carbohydrates, caries may cause cavities within months of tooth eruption. This can occur, for example, when children continuously drink sugary drinks from baby bottles (see later discussion).
Other factors
Reduced salivary flow rate is associated with increased caries since the buffering capability of saliva is not present to counterbalance the acidic environment created by certain foods. As a result, medical conditions that reduce the amount of saliva produced by salivary glands, in particular the submandibular gland and parotid gland, are likely to dry mouth and thus to widespread tooth decay. Examples include Sjögren's syndrome, diabetes mellitus, diabetes insipidus, and sarcoidosis.[36] Medications, such as antihistamines and antidepressants, can also impair salivary flow. Stimulants, most notoriously methylamphetamine ("meth mouth"), also occlude the flow of saliva to an extreme degree. Tetrahydrocannabinol, the active chemical substance in cannabis, also causes a nearly complete occlusion of salivation, known in colloquial terms as "cotton mouth". Moreover, 63% of the most commonly prescribed medications in the United States list dry mouth as a known side-effect.[36] Radiation therapy of the head and neck may also damage the cells in salivary glands, somewhat increasing the likelihood of caries formation.[37][38]
Susceptibility to caries can be related to altered metabolism in the tooth, in particular to fluid flow in the dentin. Experiments on rats have shown that a high-sucrose, cariogenic diet "significantly suppresses the rate of fluid motion" in dentin.[39]
The use of tobacco may also increase the risk for caries formation. Some brands of smokeless tobacco contain high sugar content, increasing susceptibility to caries.[40] Tobacco use is a significant risk factor for periodontal disease, which can cause the gingiva to recede.[41] As the gingiva loses attachment to the teeth due to gingival recession, the root surface becomes more visible in the mouth. If this occurs, root caries is a concern since the cementum covering the roots of teeth is more easily demineralized by acids than enamel.[42] Currently, there is not enough evidence to support a causal relationship between smoking and coronal caries, but evidence does suggest a relationship between smoking and root-surface caries.[43]
Intrauterine and neonatal lead exposure promote tooth decay.[44][45][46][47][48][49][50] Besides lead, all atoms with electrical charge and ionic radius similar to bivalent calcium,[51] such as cadmium, mimic the calcium ion and therefore exposure may promote tooth decay.[52]
Poverty is also a significant social determinant for oral health.[53] Dental caries have been linked with lower socio-economic status and can be considered a disease of poverty.[54]
Forms are available for risk assessment for caries when treating dental cases; this system using the evidence-based Caries Management by Risk Assessment (CAMBRA).[55] It is still unknown if the identification of high-risk individuals can lead to more effective long-term patient management that prevents caries initiation and arrests or reverses the progression of lesions.[56]
Enamel is a highly mineralized acellular tissue, and caries act upon it through a chemical process brought on by the acidic environment produced by bacteria. As the bacteria consume the sugar and use it for their own energy, they produce lactic acid. The effects of this process include the demineralization of crystals in the enamel, caused by acids, over time until the bacteria physically penetrate the dentin. Enamel rods, which are the basic unit of the enamel structure, run perpendicularly from the surface of the tooth to the dentin. Since demineralization of enamel by caries, in general, follows the direction of the enamel rods, the different triangular patterns between pit and fissure and smooth-surface caries develop in the enamel because the orientation of enamel rods are different in the two areas of the tooth.[57]
As the enamel loses minerals, and dental caries progresses, the enamel develop several distinct zones, visible under a light microscope. From the deepest layer of the enamel to the enamel surface, the identified areas are the: translucent zone, dark zones, body of the lesion, and surface zone.[58] The translucent zone is the first visible sign of caries and coincides with a one to two percent loss of minerals.[59] A slight remineralization of enamel occurs in the dark zone, which serves as an example of how the development of dental caries is an active process with alternating changes.[60] The area of greatest demineralization and destruction is in the body of the lesion itself. The surface zone remains relatively mineralized and is present until the loss of tooth structure results in a cavitation.
Unlike enamel, the dentin reacts to the progression of dental caries. After tooth formation, the ameloblasts, which produce enamel, are destroyed once enamel formation is complete and thus cannot later regenerate enamel after its destruction. On the other hand, dentin is produced continuously throughout life by odontoblasts, which reside at the border between the pulp and dentin. Since odontoblasts are present, a stimulus, such as caries, can trigger a biologic response. These defense mechanisms include the formation of sclerotic and tertiary dentin.[61]
In dentin from the deepest layer to the enamel, the distinct areas affected by caries are the advancing front, the zone of bacterial penetration, and the zone of destruction.[57] The advancing front represents a zone of demineralised dentine due to acid and has no bacteria present. The zones of bacterial penetration and destruction are the locations of invading bacteria and ultimately the decomposition of dentin. The zone of destruction has a more mixed bacterial population where proteolytic enzymes have destroyed the organic matrix. The innermost dentine caries has been reversibly attacked because the collage matrix is not severely damaged, giving it potential for repair. The outer more superficial zone is highly infected with proteolytic degradation of the collagen matrix and as a result the dentine is irreversibly demineralised.
Sclerotic dentin
The structure of dentin is an arrangement of microscopic channels, called dentinal tubules, which radiate outward from the pulp chamber to the exterior cementum or enamel border.[62] The diameter of the dentinal tubules is largest near the pulp (about 2.5 μm) and smallest (about 900 nm) at the junction of dentin and enamel.[63] The carious process continues through the dentinal tubules, which are responsible for the triangular patterns resulting from the progression of caries deep into the tooth. The tubules also allow caries to progress faster.
In response, the fluid inside the tubules bring immunoglobulins from the immune system to fight the bacterial infection. At the same time, there is an increase of mineralization of the surrounding tubules.[64] This results in a constriction of the tubules, which is an attempt to slow the bacterial progression. In addition, as the acid from the bacteria demineralizes the hydroxyapatite crystals, calcium and phosphorus are released, allowing for the precipitation of more crystals which fall deeper into the dentinal tubule. These crystals form a barrier and slow the advancement of caries. After these protective responses, the dentin is considered sclerotic.
According to hydrodynamic theory, fluids within dentinal tubules are believed to be the mechanism by which pain receptors are triggered within the pulp of the tooth.[65] Since sclerotic dentin prevents the passage of such fluids, pain that would otherwise serve as a warning of the invading bacteria may not develop at first. Consequently, dental caries may progress for a long period of time without any sensitivity of the tooth, allowing for greater loss of tooth structure.[citation needed]
Tertiary dentin
In response to dental caries, there may be production of more dentin toward the direction of the pulp. This new dentin is referred to as tertiary dentin.[63] Tertiary dentin is produced to protect the pulp for as long as possible from the advancing bacteria. As more tertiary dentin is produced, the size of the pulp decreases. This type of dentin has been subdivided according to the presence or absence of the original odontoblasts.[66] If the odontoblasts survive long enough to react to the dental caries, then the dentin produced is called "reactionary" dentin. If the odontoblasts are killed, the dentin produced is called "reparative" dentin.
In the case of reparative dentin, other cells are needed to assume the role of the destroyed odontoblasts. Growth factors, especially TGF-β,[66] are thought to initiate the production of reparative dentin by fibroblasts and mesenchymal cells of the pulp.[67] Reparative dentin is produced at an average of 1.5 μm/day, but can be increased to 3.5 μm/day. The resulting dentin contains irregularly shaped dentinal tubules that may not line up with existing dentinal tubules. This diminishes the ability for dental caries to progress within the dentinal tubules.
The incidence of cemental caries increases in older adults as gingival recession occurs from either trauma or periodontal disease. It is a chronic condition that forms a large, shallow lesion and slowly invades first the root's cementum and then dentin to cause a chronic infection of the pulp (see further discussion under classification by affected hard tissue). Because dental pain is a late finding, many lesions are not detected early, resulting in restorative challenges and increased tooth loss.[68]
The presentation of caries is highly variable. However, the risk factors and stages of development are similar. Initially it may appear as a small chalky area (smooth surface caries), which may eventually develop into a large cavitation. Sometimes caries may be directly visible. However other methods of detection such as X-rays are used for less visible areas of teeth and to judge the extent of destruction. Lasers for detecting caries allow detection without ionizing radiation and are now used for detection of interproximal decay (between the teeth). Disclosing solutions are also used during tooth restoration to minimize the chance of recurrence.[citation needed]
Primary diagnosis involves inspection of all visible tooth surfaces using a good light source, dental mirror and explorer. Dental radiographs (X-rays) may show dental caries before it is otherwise visible, in particular caries between the teeth. Large dental caries are often apparent to the naked eye, but smaller lesions can be difficult to identify. Visual and tactile inspection along with radiographs are employed frequently among dentists, in particular to diagnose pit and fissure caries.[69] Early, uncavitated caries is often diagnosed by blowing air across the suspect surface, which removes moisture and changes the optical properties of the unmineralized enamel.
Some dental researchers have cautioned against the use of dental explorers to find caries,[70] in particular sharp ended explorers. In cases where a small area of tooth has begun demineralizing but has not yet cavitated, the pressure from the dental explorer could cause a cavity. Since the carious process is reversible before a cavity is present, it may be possible to arrest the caries with fluoride and remineralize the tooth surface. When a cavity is present, a restoration will be needed to replace the lost tooth structure.
At times, pit and fissure caries may be difficult to detect. Bacteria can penetrate the enamel to reach dentin, but then the outer surface may remineralize, especially if fluoride is present.[71] These caries, sometimes referred to as "hidden caries", will still be visible on x-ray radiographs, but visual examination of the tooth would show the enamel intact or minimally perforated.
The differential diagnosis for dental caries includes dental fluorosis and developmental defects of the tooth including hypomineralization of the tooth and hypoplasia of the tooth.[72]
Caries can be classified by location, etiology, rate of progression, and affected hard tissues.[73] These forms of classification can be used to characterize a particular case of tooth decay in order to more accurately represent the condition to others and also indicate the severity of tooth destruction. In some instances, caries are described in other ways that might indicate the cause. G.V. Black classification:
- Class I - occlusal surfaces of posterior teeth, buccal or lingual pits on molars, lingual pit near cingulum of maxillary incisors
- Class II - proximal surfaces of posterior teeth
- Class III - interproximal surfaces of anterior teeth without incisal edge involvement
- Class IV - interproximal surfaces of anterior teeth with incisal edge involvement
- Class V - cervical third of facial or lingual surface of tooth
- Class VI - incisal or occlusal edge worn away due to abrasion
Early childhood caries
Early childhood caries (ECC) or "Baby bottle caries," "baby bottle tooth decay," or "Bottle Rot" is a pattern of decay found in young children with their deciduous (baby) teeth. The teeth most likely affected are the maxillary anterior teeth, but all teeth can be affected.[74] The name for this type of caries comes from the fact that the decay usually is a result of allowing children to fall asleep with sweetened liquids in their bottles or feeding children sweetened liquids multiple times during the day.[75]
Another pattern of decay is "rampant caries", which signifies advanced or severe decay on multiple surfaces of many teeth.[76] Rampant caries may be seen in individuals with xerostomia, poor oral hygiene, stimulant use (due to drug-induced dry mouth[77]), and/or large sugar intake. If rampant caries is a result of previous radiation to the head and neck, it may be described as radiation-induced caries. Problems can also be caused by the self-destruction of roots and whole tooth resorption when new teeth erupt or later from unknown causes.
Rate of progression
Temporal descriptions can be applied to caries to indicate the progression rate and previous history. "Acute" signifies a quickly developing condition, whereas "chronic" describes a condition that has taken an extended time to develop, in which thousands of meals and snacks, many causing some acid demineralization that is not remineralized, eventually results in cavities.
Recurrent caries, also described as secondary, are caries that appears at a location with a previous history of caries. This is frequently found on the margins of fillings and other dental restorations. On the other hand, incipient caries describes decay at a location that has not experienced previous decay. Arrested caries describes a lesion on a tooth that was previously demineralized but was remineralized before causing a cavitation. Fluoride treatment can help recalcification of tooth enamel as well as use of Amorphous calcium phosphate.
Affected hard tissue
Depending on which hard tissues are affected, it is possible to describe caries as involving enamel, dentin, or cementum. Early in its development, caries may affect only enamel. Once the extent of decay reaches the deeper layer of dentin, "dentinal caries" is used. Since cementum is the hard tissue that covers the roots of teeth, it is not often affected by decay unless the roots of teeth are exposed to the mouth. Although the term "cementum caries" may be used to describe the decay on roots of teeth, very rarely does caries affect the cementum alone. Roots have a very thin layer of cementum over a large layer of dentin, and thus most caries affecting cementum also affects dentin.
Oral hygiene
Personal hygiene care consists of proper brushing and flossing daily. The purpose of oral hygiene is to minimize any etiologic agents of disease in the mouth. The primary focus of brushing and flossing is to remove and prevent the formation of plaque or dental biofilm. Plaque consists mostly of bacteria.[78] As the amount of bacterial plaque increases, the tooth is more vulnerable to dental caries when carbohydrates in the food are left on teeth after every meal or snack. A toothbrush can be used to remove plaque on accessible surfaces, but not between teeth or inside pits and fissures on chewing surfaces. When used correctly, dental floss removes plaque from areas that could otherwise develop proximal caries but only if the depth of sulcus has not been compromised. Other adjunct oral hygiene aids include interdental brushes, water picks, and mouthwashes.
However oral hygiene is probably more effective at preventing gum disease (periodontal disease) than tooth decay. Food is forced inside pits and fissures under chewing pressure, leading to carbohydrate-fueled acid demineralisation where the brush, fluoride toothpaste, and saliva have no access to remove trapped food, neutralise acid, or remineralise demineralised tooth like on other more accessible tooth surfaces food to be trapped. (Occlusal caries accounts for between 80 and 90% of caries in children (Weintraub, 2001).) Chewing fibre like celery after eating forces saliva inside trapped food to dilute any carbohydrate like sugar, neutralise acid and remineralise demineralised tooth. The teeth at highest risk for carious lesions are the permanent first and second molars due to length of time in oral cavity and presence of complex surface anatomy.
Professional hygiene care consists of regular dental examinations and professional prophylaxis (cleaning). Sometimes, complete plaque removal is difficult, and a dentist or dental hygienist may be needed. Along with oral hygiene, radiographs may be taken at dental visits to detect possible dental caries development in high risk areas of the mouth (e.g. "bitewing" x-rays which visualize the crowns of the back teeth).
Dietary modification
For dental health, frequency of sugar intake is more important than the amount of sugar consumed.[33] In the presence of sugar and other carbohydrates, bacteria in the mouth produce acids that can demineralize enamel, dentin, and cementum. The more frequently teeth are exposed to this environment the more likely dental caries are to occur. Therefore, minimizing snacking is recommended, since snacking creates a continuous supply of nutrition for acid-creating bacteria in the mouth. Also, chewy and sticky foods (such as dried fruit or candy) tend to adhere to teeth longer, and, as a consequence, are best eaten as part of a meal. For children, the American Dental Association and the European Academy of Paediatric Dentistry recommend limiting the frequency of consumption of drinks with sugar, and not giving baby bottles to infants during sleep (see earlier discussion).[79][80] Mothers are also recommended to avoid sharing utensils and cups with their infants to prevent transferring bacteria from the mother's mouth.[81]
It has been found that milk and certain kinds of cheese like cheddar cheese can help counter tooth decay if eaten soon after the consumption of foods potentially harmful to teeth.[33] Also, chewing gum containing xylitol (a sugar alcohol) is widely used to protect teeth in many countries now. Xylitol's effect on reducing dental biofilm is, it is presumed, due to bacteria's inability to utilize it like other sugars.[82] Chewing and stimulation of flavor receptors on the tongue are also known to increase the production and release of saliva, which contains natural buffers to prevent the lowering of pH in the mouth to the point where enamel may become demineralized.[83]
Other measures
The use of dental sealants is a means of prevention.[84] A sealant is a thin plastic-like coating applied to the chewing surfaces of the molars to prevent food from being trapped inside pits and fissures. This deprives resident plaque bacteria carbohydrate preventing the formation of pit and fissure caries. Sealants are usually applied on the teeth of children, as soon as the tooth erupt but adults are receiving them if not previously performed. Sealants can wear out and fail to prevent access of food and plaque bacteria inside pits and fissures and need to be replaced so they must be checked regularly by dental professionals.
Calcium, as found in food such as milk and green vegetables, is often recommended to protect against dental caries. Fluoride helps prevent decay of a tooth by binding to the hydroxyapatite crystals in enamel.[85] The incorporated calcium makes enamel more resistant to demineralization and, thus, resistant to decay.[86] Topical fluoride is now more highly recommended than systemic intake such as by tablets or drops to protect the surface of the teeth. This may include a fluoride toothpaste or mouthwash or varnish.[87] After brushing with fluoride toothpaste, rinsing should be avoided and the excess spat out instead.[88] This leaves a greater concentration of fluoride residue on the teeth. Many dental professionals include application of topical fluoride solutions as part of routine visits and recommend the use of xylitol and amorphous calcium phosphate products.
Vaccines are also under development.[89]
|No carious lesion
|No treatment
|Carious lesion
|Inactive lesion
|No treatment
|Active lesion
|Non-cavitated lesion
|Non-operative treatment
|Cavitated lesion
|Operative treatment
|Existing filling
|No defect
|No replacement
|Defective filling
|Ditching, overhang
|No replacement
|Fracture or food impaction
|Repair or replacement of filling
|Inactive lesion
|No treatment
|Active lesion
|Non-cavitated lesion
|Non-operative treatment
|Cavitated lesion
|Repair or replacement of filling
Most importantly, whether the carious lesion is cavitated or noncavitated dictates the management. Clinical assessment of whether the lesion is active or arrested is also important. Noncavitated lesions can be arrested and remineralization can occur under the right conditions. However, this may require extensive changes to the diet (reduction in frequency of refined sugars), improved oral hygiene (toothbrushing twice per day with fluoride toothpaste and daily flossing), and regular application of topical fluoride. Such management of a carious lesion is termed "non-operative" since no drilling is carried out on the tooth. Non-operative treatment requires excellent understanding and motivation from the individual, otherwise the decay will continue.
Once a lesion has cavitated, especially if dentin is involved, remineralization is much more difficult and a dental restoration is usually indicated ("operative treatment"). Before a restoration can be placed, all of the decay must be removed otherwise it will continue to progress underneath the filling. Sometimes a small amount of decay can be left if it is entombed and the there is a seal which isolates the bacteria from their substrate. This can be likened to placing a glass container over a candle, which burns itself out once the oxygen is used up. Techniques such as stepwise caries removal are designed to avoid exposure of the dental pulp and overall reduction of the amount of tooth substance which requires removal before the final filling is placed. Often enamel which overlies decayed dentin must also be removed as it is unsupported and susceptible to fracture. The modern decision-making process with regards the activity of the lesion, and whether it is cavitated, is summarized in the table.[90]
Destroyed tooth structure does not fully regenerate, although remineralization of very small carious lesions may occur if dental hygiene is kept at optimal level.[13] For the small lesions, topical fluoride is sometimes used to encourage remineralization. For larger lesions, the progression of dental caries can be stopped by treatment. The goal of treatment is to preserve tooth structures and prevent further destruction of the tooth. Aggressive treatment, by filling, of incipient carious lesions, places where there is superficial damage to the enamel, is controversial as they may heal themselves, while once a filling is performed it will eventually have to be redone and the site serves as a vulnerable site for further decay.[11]
In general, early treatment is quicker and less expensive than treatment of extensive decay. Local anesthetics, nitrous oxide ("laughing gas"), or other prescription medications may be required in some cases to relieve pain during or following treatment or to relieve anxiety during treatment.[91] A dental handpiece ("drill") is used to remove large portions of decayed material from a tooth. A spoon, a dental instrument used to carefully remove decay, is sometimes employed when the decay in dentin reaches near the pulp.[92] Once the decay is removed, the missing tooth structure requires a dental restoration of some sort to return the tooth to function and aesthetic condition.
Restorative materials include dental amalgam, composite resin, porcelain, and gold.[93] Composite resin and porcelain can be made to match the color of a patient's natural teeth and are thus used more frequently when aesthetics are a concern. Composite restorations are not as strong as dental amalgam and gold; some dentists consider the latter as the only advisable restoration for posterior areas where chewing forces are great.[94] When the decay is too extensive, there may not be enough tooth structure remaining to allow a restorative material to be placed within the tooth. Thus, a crown may be needed. This restoration appears similar to a cap and is fitted over the remainder of the natural crown of the tooth. Crowns are often made of gold, porcelain, or porcelain fused to metal.
In certain cases, endodontic therapy may be necessary for the restoration of a tooth.[95] Endodontic therapy, also known as a "root canal", is recommended if the pulp in a tooth dies from infection by decay-causing bacteria or from trauma. During a root canal, the pulp of the tooth, including the nerve and vascular tissues, is removed along with decayed portions of the tooth. The canals are instrumented with endodontic files to clean and shape them, and they are then usually filled with a rubber-like material called gutta percha.[96] The tooth is filled and a crown can be placed. Upon completion of a root canal, the tooth is now non-vital, as it is devoid of any living tissue.
An extraction can also serve as treatment for dental caries. The removal of the decayed tooth is performed if the tooth is too far destroyed from the decay process to effectively restore the tooth. Extractions are sometimes considered if the tooth lacks an opposing tooth or will probably cause further problems in the future, as may be the case for wisdom teeth.[97] Extractions may also be preferred by patients unable or unwilling to undergo the expense or difficulties in restoring the tooth.
Worldwide, approximately 2.43 billion people (36% of the population) have dental caries in their permanent teeth.[8] In baby teeth it affects about 620 million people or 9% of the population.[8] The disease is most common in Latin American countries, countries in the Middle East, and South Asia, and least prevalent in China.[99] In the United States, dental caries is the most common chronic childhood disease, being at least five times more common than asthma.[100] It is the primary pathological cause of tooth loss in children.[101] Between 29% and 59% of adults over the age of fifty experience caries.[102]
The number of cases has decreased in some developed countries, and this decline is usually attributed to increasingly better oral hygiene practices and preventive measures such as fluoride treatment.[103] Nonetheless, countries that have experienced an overall decrease in cases of tooth decay continue to have a disparity in the distribution of the disease.[102] Among children in the United States and Europe, twenty percent of the population endures sixty to eighty percent of cases of dental caries.[104] A similarly skewed distribution of the disease is found throughout the world with some children having none or very few caries and others having a high number.[102] Australia, Nepal, and Sweden (where children receive dental care paid for by the government) have a low incidence of cases of dental caries among children, whereas cases are more numerous in Costa Rica and Slovakia.[105]
The classic DMF (decay/missing/filled) index is one of the most common methods for assessing caries prevalence as well as dental treatment needs among populations. This index is based on in-field clinical examination of individuals by using a probe, mirror and cotton rolls. Because the DMF index is done without X-ray imaging, it underestimates real caries prevalence and treatment needs.[71]
Bacteria typically associated with dental caries have been isolated from vaginal samples who have bacterial vaginosis.[106]
There is a long history of dental caries. Over a million years ago, hominids such as Australopithecus suffered from cavities.[107] The largest increases in the prevalence of caries have been associated with dietary changes.[107][108] Archaeological evidence shows that tooth decay is an ancient disease dating far into prehistory. Skulls dating from a million years ago through the neolithic period show signs of caries, including those from the Paleolithic and Mesolithic ages.[109] The increase of caries during the neolithic period may be attributed to the increased consumption of plant foods containing carbohydrates.[110] The beginning of rice cultivation in South Asia is also believed to have caused an increase in caries. Although there is also some evidence from sites in Thailand, such as Khok Phanom Di, that shows a decrease in overall percentage of dental caries with the increase in dependence on rice agriculture.[111]
A Sumerian text from 5000 BC describes a "tooth worm" as the cause of caries.[112] Evidence of this belief has also been found in India, Egypt, Japan, and China.[108] Unearthed ancient skulls show evidence of primitive dental work. In Pakistan, teeth dating from around 5500 BC to 7000 BC show nearly perfect holes from primitive dental drills.[113] The Ebers Papyrus, an Egyptian text from 1550 BC, mentions diseases of teeth.[112] During the Sargonid dynasty of Assyria during 668 to 626 BC, writings from the king's physician specify the need to extract a tooth due to spreading inflammation.[108] In the Roman Empire, wider consumption of cooked foods led to a small increase in caries prevalence.[104] The Greco-Roman civilization, in addition to the Egyptian, had treatments for pain resulting from caries.[108]
The rate of caries remained low through the Bronze Age and Iron Age, but sharply increased during the Middle Ages.[107] Periodic increases in caries prevalence had been small in comparison to the 1000 AD increase, when sugar cane became more accessible to the Western world. Treatment consisted mainly of herbal remedies and charms, but sometimes also included bloodletting.[114] The barber surgeons of the time provided services that included tooth extractions.[108] Learning their training from apprenticeships, these health providers were quite successful in ending tooth pain and likely prevented systemic spread of infections in many cases. Among Roman Catholics, prayers to Saint Apollonia, the patroness of dentistry, were meant to heal pain derived from tooth infection.[115]
There is also evidence of caries increase in North American Indians after contact with colonizing Europeans. Before colonization, North American Indians subsisted on hunter-gatherer diets, but afterwards there was a greater reliance on maize agriculture, which made these groups more susceptible to caries.[107]
During the European Age of Enlightenment, the belief that a "tooth worm" caused caries was also no longer accepted in the European medical community.[116] Pierre Fauchard, known as the father of modern dentistry, was one of the first to reject the idea that worms caused tooth decay and noted that sugar was detrimental to the teeth and gingiva.[117] In 1850, another sharp increase in the prevalence of caries occurred and is believed to be a result of widespread diet changes.[108] Prior to this time, cervical caries was the most frequent type of caries, but increased availability of sugar cane, refined flour, bread, and sweetened tea corresponded with a greater number of pit and fissure caries.
In the 1890s, W.D. Miller conducted a series of studies that led him to propose an explanation for dental caries that was influential for current theories. He found that bacteria inhabited the mouth and that they produced acids that dissolved tooth structures when in the presence of fermentable carbohydrates.[118] This explanation is known as the chemoparasitic caries theory.[119] Miller's contribution, along with the research on plaque by G.V. Black and J.L. Williams, served as the foundation for the current explanation of the etiology of caries.[108] Several of the specific strains of lactobacilli were identified in 1921 by Fernando E. Rodriguez Vargas.
In 1924 in London, Killian Clarke described a spherical bacterium in chains isolated from carious lesions which he called Streptococcus mutans. Although Clarke proposed this organism was the cause of caries the discovery was not followed up. Later, in the 1950s in the USA, Keyes and Fitzgerald working with hamsters showed that caries was transmissible and caused by an acid-producing Streptococcus. It was not until the late 1960s that it became generally accepted that the Streptococcus isolated from hamster caries was the same as S. mutans described by Clarke.[120]
Tooth decay has been present throughout human history, from early hominids millions of years ago, to modern humans.[121] The prevalence of caries increased dramatically in the 19th century, as the Industrial Revolution made certain items, such as refined sugar and flour, readily available.[108] The diet of the "newly industrialized English working class"[108] then became centered on bread, jam, and sweetened tea, greatly increasing both sugar consumption and caries.
Etymology and usage
Naturalized from Latin into English (a loanword), caries in its English form originated as a mass noun that means "rottenness",[1][122] that is, "decay". When used in that sense, it takes singular verb inflections (just like the word decay does). Thus caries was not traditionally a plural word synonymous with holes or cavities; that is, it was not the plural form of any singular form cary meaning hole or cavity. Nonetheless, the idea that it is such a plural is a reanalysis that naturally occurs to most English speakers, and the reanalyzed sense is common enough to be entered in various dictionaries and to exist in respectable usage. It still shows a hint of its reanalyzed origins in that it remains idiomatically limited to a plurale tantum sense—that is, like scissors or glasses, one speaks of plural caries obligately in the plural—not of one scissor, glass, or cary. (This is why one can look for a singular count-noun form of dental cary in any of a dozen major medical and general dictionaries and not find it listed.) Many still use it in the traditional sense (mass, singular), which is why they speak of carious lesions rather than just caries when they intend the plural count sense.
Cariology is the study of dental caries.
Other animals
Dental caries is uncommon among companion animals.[123]
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- ^ "Aspects of Treatment of Cavities and of Caries Disease" from the Disease Control Priorities Project. Page accessed August 15, 2006.
- ^ Oral Health Topics: Dental Filling Options, hosted on the American Dental Association website. Page accessed August 16, 2006.
- ^ What is a Root Canal?, hosted by the Academy of General Dentistry. Page accessed August 16, 2006.
- ^ FAQs About Root Canal Treatment, hosted on the American Association of Endodontists website. Page accessed August 16, 2006.
- ^ Wisdom Teeth, packet in pdf format hosted by the American Association of Oral and Maxillofacial Surgeons. Page accessed August 16, 2006.
- ^ "WHO Disease and injury country estimates". World Health Organization. 2009. Retrieved Nov 11, 2009.
- ^ The World Oral Health Report 2003: Continuous improvement of oral health in the 21st century – the approach of the WHO Global Oral Health Programme, released by the World Health Organization. (File in pdf format.) Page accessed August 15, 2006.
- ^ Healthy People: 2010. Html version hosted on Healthy People.gov website. Page accessed August 13, 2006.
- ^ Frequently Asked Questions, hosted on the American Dental Hygiene Association website. Page accessed August 15, 2006.
- ^ a b c "Dental caries", from the Disease Control Priorities Project. Page accessed August 15, 2006.
- ^ World Health Organization website, "World Water Day 2001: Oral health", p. 2. Page accessed August 14, 2006.
- ^ a b Touger-Decker R, van Loveren C (October 2003). "Sugars and dental caries". The American Journal of Clinical Nutrition 78 (4): 881S–892S. PMID 14522753.
- ^ "Table 38.1. Mean DMFT and SiC Index of 12-Year-Olds for Some Countries, by Ascending Order of DMFT", from the Disease Control Priorities Project. Page accessed January 8, 2007.
- ^ Africa, Charlene; Nel, Janske; Stemmet, Megan (2014). "Anaerobes and Bacterial Vaginosis in Pregnancy: Virulence Factors Contributing to Vaginal Colonisation". International Journal of Environmental Research and Public Health 11 (7): 6979–7000. ISSN 1660-4601. doi:10.3390/ijerph110706979.
- ^ a b c d Epidemiology of Dental Disease, hosted on the University of Illinois at Chicago website. Page accessed January 9, 2007.
- ^ a b c d e f g h i Suddick RP, Harris NO (1990). "Historical perspectives of oral biology: a series". Critical Reviews in Oral Biology and Medicine 1 (2): 135–51. PMID 2129621. doi:10.1177/10454411900010020301.
- ^ Caries Through Time: An Anthropological Overview; Luis Pezo Lanfranco and Sabine Eggers; Laboratório de Antropologia Biológica, Depto. de Genética e Biologia Evolutiva, Instituto de Biociências, Universidade de São Paulo, Brazil
- ^ Richards MP (December 2002). "A brief review of the archaeological evidence for Palaeolithic and Neolithic subsistence". European Journal of Clinical Nutrition 56 (12): 16 p following 1262. PMID 12494313. doi:10.1038/sj.ejcn.1601646.
- ^ Tayles, N., Domett, K., & Nelsen, K. (2000). Agriculture and dental caries? The case of rice in prehistoric Southeast Asia. World Archaeology, 32(1), 68-83.
- ^ a b History of Dentistry: Ancient Origins, hosted on the American Dental Association website. Page accessed January 9, 2007.
- ^ Coppa A, Bondioli L, Cucina A et al. (April 2006). "Palaeontology: early Neolithic tradition of dentistry". Nature 440 (7085): 755–6. PMID 16598247. doi:10.1038/440755a. Lay summary – Associated Press (April 5, 2006).
- ^ Anderson T (October 2004). "Dental treatment in Medieval England". British Dental Journal 197 (7): 419–25. PMID 15475905. doi:10.1038/sj.bdj.4811723.
- ^ Elliott, Jane. Medieval teeth 'better than Baldrick's', hosted on the BBC news website. October 8, 2004. Page accessed January 11, 2007.
- ^ Gerabek WE (March 1999). "The tooth-worm: historical aspects of a popular medical belief". Clinical Oral Investigations 3 (1): 1–6. PMID 10522185. doi:10.1007/s007840050070.
- ^ McCauley, H. Berton. Pierre Fauchard (1678-1761), hosted on the Pierre Fauchard Academy website. The excerpt comes from a speech given at a Maryland PFA Meeting on March 13, 2001. Page accessed January 17, 2007.
- ^ Kleinberg I (1 March 2002). "A mixed-bacteria ecological approach to understanding the role of the oral bacteria in dental caries causation: an alternative to Streptococcus mutans and the specific-plaque hypothesis". Crit Rev Oral Biol Med. 13 (2): 108–25. PMID 12097354. doi:10.1177/154411130201300202.
- ^ Baehni PC, Guggenheim B (1996). "Potential of diagnostic microbiology for treatment and prognosis of dental caries and periodontal diseases" (PDF). Crit Rev Oral Biol Med. 7 (3): 259–77. PMID 8909881. doi:10.1177/10454411960070030401.
- ^ Newbrun, E. 1989 Cariology. Quintessence Books, Chicago[page needed]
- ^ Selwitz RH, Ismail AI, Pitts NB (January 2007). "Dental caries". Lancet 369 (9555): 51–9. PMID 17208642. doi:10.1016/S0140-6736(07)60031-2.
- ^ Elsevier, Dorland's Illustrated Medical Dictionary.
- ^ "AVDS Cavities information page — Dog Tooth Health — Cat Tooth Health". American Veterinary Dental Society. Retrieved 10 November 2013.
External links
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- Dental caries at DMOZ
- Centers for Disease Control, Dental Caries at http://www.cdc.gov/healthywater/hygiene/disease/dental_caries.html

subset: commoncrawl


text:
5 Reasons Why You Should Enter This Competition
I've just seen David Mackay's blog highlighting a competition where you can win money and software tools. Each day, starting on June 14 through the following 20 work days, a question will be posted here. You can win by correctly answering a question.
Here's my five reasons why I think you should enter:
- The competition is free.
- I can't enter (Intel employees are barred) -- but you can. If you win, I'm sure my circle of friends will increase :-)
- There's $500 prize money and Intel Parallel Studio just waiting to be won. (There are other prizes as well).
- Intel Parallel Studio is a great productivity tool for writing applications.
- Maybe you can win, impress your boss, and get that well deserved pay rise.
You can find more information in the FAQ.
If you are wondering what you can do with Intel Parallel Studio, then look here.
Best of luck, and let me know how you get on.


text:
Hot Lotto Ft. Fat Trel - Juiced (Video Trailer) [Xpensive Ent Submitted]
Official Video Trailer for Hot Lotto's Hit single Juiced Featuring Fat Trel. Watch out for the Full Video dropping soon.
Produced By @SuperstaarBeats
Directed By @1st_Impressions
Follow on Twitter: @HotLotto @FatTrel @XpensiveEnt
For bookings and features contact email@example.com
Please click the "Report" button below if the video on this page is not working properly.
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text:
Hi all,
I've discovered MrDeity.
I've seen them all and I want more.
I can't get that damn tune out of my head and I want the ringtone.
I've infected several other people with the same itch that needs scratching.......is this what a born again Christians feel?
Today I tricked a Catholic friend into watching one...priceless!
So, the thing is, as you know, they need money to make more shows (more shows = good). I wanted to help but I'm doing the Mummy thing and not actually bringing in any money at the moment. I made a small donation today and my plan is to see how my husband reacts when he sees it on his credit card statement, if he sees it. :-) If nothing happens I'll try a bigger one next month. He is a new viewer too so it should be ok. Maybe. Definitely maybe ok.
So, click donate and then send me your thoughts. No thoughts without donation and we're on the honour system here.
Views: 251
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text:
Definition of larine
a. - Of or pertaining to the Gull family (Laridae). 2
The word "larine" uses 6 letters: A E I L N R.
Direct anagrams of larine:
aliner linear nailer renail
Words formed by adding one letter before or after larine (in bold), or to aeilnr in any order:
c - carline e - aliener g - aligner engrail nargile realign reginal h - hernial inhaler i - airline k - lankier l - ralline m - manlier marline mineral o - aileron alienor p - plainer praline s - aliners nailers renails t - latrine ratline reliant retinal trenail v - ravelin x - relaxin y - inlayer
Shorter words found within larine:
ae ai ail ain air airn al ale alien aline an ane ani anil anile ar are ariel aril ear earl earn el elain elan en er era ern ilea in ire la lain lair lane lar lari lea lean lear learn lei li liane liar lie lien lier lin line liner lira lire na nae nail ne near nil rail rain rale ran rani re real rei rein renal ria rial riel rile rin
List shorter words within larine, sorted by length
Words formed from any letters in larine, plus an optional blank or existing letter
List all words starting with larine, words containing larine or words ending with larine
All words formed from larine by changing one letter
Other words with the same letter pairs: la ar ri in ne
Browse words starting with larine by next letter
Previous word in list: lariats
Next word in list: laris
Some random words: cuif mo oeillade kludge eerie peavy hoecake
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text:
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H&R Block
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WASHINGTON — For the first time since 1999, American employers have added more than 200,000 jobs a month for four straight months, offering more evidence that the U.S. economy is steadily growing while much of Europe and Asia struggle.
Last month's gain of 217,000 jobs means the economy has finally recovered all the jobs lost to the Great Recession. And it coincides with indications that American consumers have grown more confident. Auto sales have surged. Manufacturers and service companies are expanding.
"I don't think we have a boom, but we have a good economy growing at about 3 percent," said John Silvia, chief economist at Wells Fargo. "We're pulling away from the rest of the world."
Still, Friday's report from the Labor Department showed that pay remains subpar for many workers, millions who want full-time work are still stuck in part-time jobs, and the number of people out of work for more than six months remains historically high.
Monthly job growth has averaged 234,000 for the past three months, up sharply from 150,000 in the previous three. The unemployment rate, which is derived from a separate survey, matched April's 6.3 percent, the lowest in more than five years.
Investors seemed pleased. The Dow Jones industrial average closed up 88 points.
Though the economy has regained the nearly 9 million jobs lost to the recession, more hiring is needed because the working-age U.S. population has grown nearly 7 percent since the recession began. Economists at the liberal Economic Policy Institute estimate that 7 million more jobs would have been needed to keep up with population growth.
In addition, average wages have grown only about 2 percent a year since the recession ended, well below the long-run average annual growth of about 3.5 percent.
And unemployment has fallen from a 10 percent peak in 2009 partly for an unfortunate reason: Fewer people are working or seeking work. The percentage of adults who either have a job or are looking for one remained at a 35-year low in May.
Yet the United States is faring far better than most other major industrial nations.
Overall unemployment for the 18 countries that use the euro was 11.7 percent in April, though some European nations, such as Germany and Denmark, have much lower rates. On Thursday, Europe's central bank cut interest rates and took other extraordinary steps to try to boost ultra-low inflation, encourage more lending and jump-start growth.
Japan is struggling to emerge from more than a decade of sluggish growth and deflation. And China has been undergoing a prolonged slowdown from explosive expansion and is at risk of slowing too sharply.
"The U.S. was incredibly aggressive" after the financial crisis and Great Recession, said Daniel Drezner, a professor of international politics at Tufts University. "Compared to Europe in particular, we did much more."
The U.S. government approved stimulus spending and tax cuts, Drezner noted, while many European nations cut spending. The Federal Reserve slashed rates further than the European Central Bank did and launched bond purchases to ease long-term loan rates. Central banks in Japan and Europe have only recently considered the types of unconventional steps the Fed launched in 2008.
The solid U.S. hiring gains in May might be expected to lower the unemployment rate. But the two figures come from separate surveys. The job gains are derived from a survey of businesses, the unemployment rate from a survey of households.
The two surveys sometimes diverge but usually paint a similar picture over time. For May, the survey of businesses found a bigger job gain than the survey of households did.
Average hourly pay rose 5 cents in May to $24.38. That's up 2.1 percent from 12 months ago and barely ahead of inflation, which was 2 percent.
Weak pay gains have limited Americans' ability to spend and held back growth, because consumer spending drives about 70 percent of the economy.
"The sluggishness in wages is the weak link that is preventing the U.S. economy from fully expanding its wings," said Gregory Daco, U.S. economist at Oxford Economics.
One reason pay has lagged: The jobs added since the recession have been more likely to be part time and in lower-paying industries. That pattern was evident in May: Hotels, restaurants and entertainment companies added 39,000 jobs. Retailers gained 12,500, temporary services 14,300.
By contrast, construction firms added just 6,000, manufacturers 10,000. Those industries tend to be higher-paying.
There are still 2.9 million fewer people working in full-time jobs than when the recession began. And nearly 2.5 million more are working in part-time positions. Those trends have eased somewhat in the past year or so, as the number of part-time workers has fallen 500,000 in the last 12 months.
The number of long-term unemployed fell 78,000 to 3.37 million last month, down from 4.4 million a year ago. That's still nearly three times as many as when the recession began.
The U.S. economy actually shrank in the first three months of this year as a blast of cold weather shut down factories and kept consumers away from shopping malls and car dealerships.
The economy contracted at a 1 percent annual rate, its first decline in three years.
2019 Lee Auto Malls Sustainability Champion Award
Go East, young man (and woman)
Letter to the editor: Maine voters should throw off yoke of party domination
Jim Fossel: Maine's Green New Deal as substance-free as the federal version
Letter to the editor: Maine should ban use of devices by motorists


text:
Big K.R.I.T. "Live From The Underground" Part 2
"Chapter II of the Live From The Underground video diary follows Big K.R.I.T. as he keeps on touring the country in support of his debut album Live From
The Underground released this June 5th with Def Jam. From Denver to LA, Vancouver to Seattle, and plenty other cities in between, the video captures
K.R.I.T. going from place to place converting one fan at a time with each stop. Sold-out shows and huge lines offer a backdrop to this intimate look at a
star on the rise who always puts an emphasis on connecting with his fans no matter what. From live interviews to performance footage and fan shout-
outs, this video shows viewers a day in the life of one of hip hop's most compelling new stars." - BIGKRITtv
Please click the "Report" button below if the video on this page is not working properly.


text:
California State University, Fresno
Commitment to Accessibility for Events and Activities
at Fresno State
In accordance with the Americans with Disabilities Act (ADA) and the Rehabilitation Act of 1973, section 504, no qualified person will be denied access to, participation in, or the benefits of, any program or activity operated by the University because of disability.
Fresno State is an equal opportunity, affirmative action institution. The University does not discriminate on the basis of race, color, religion, sex, national origin, age, disability, veteran status, sexual orientation, or gender identity in its admissions, programs and activities. Our commitment to creating an inclusive campus for people with disabilities includes removing policy, attitudinal, program, and structural barriers and, when necessary, providing reasonable accommodations. These commitments are supported by the University's administration and by federal law.
Fresno State's obligation to consider the needs of participants with disabilities extends to any event sponsored by the University, student organizations, departments, or groups whether held on or off campus and whether members of the public are invited to attend.
- Standard 1. Promotion and Communications – Fresno State shall communicate information about event and activities that will promote the inclusiveness of all attendees by including a standard accessibility contact statement on all publicity materials.
- Standard 2. Service Delivery - Fresno State shall seek to ensure that services provided through events and activities
are inclusive and appropriate and that the environment is welcoming to all constituents.
In addition, every effort will be made to respond to requests for accommodations made
within time frame identified by event sponsor.
- Standard 3. Physical Access – Fresno State shall assure that the facilities for events and activities hosted on and off campus will be fully accessible.
- Standard 4. Disability Awareness - Fresno State is committed to supporting efforts to promote a general understanding of disability awareness.


text:
About a week ago I upgraded from Vista to Windows 7 on my T400. I did a completely clean reinstall with a new hard drive and then downloaded all the drivers.
Befrore switching to Windows 7 my 9 cell battery had no problems at all and lasted 4 hours easily.
The first time I ran the computer on Windows 7 everything was going fine and I Think Pad Power Manager said I had 35% battery and an hour left on it. Then, it suddenly turned itself off. I turned it back on and Power Manager then said I had 3% battery and 6 minutes. I plugged it in and it charged fully. However it did the same thing several more times. I checked that battery tab and it said the battery condition was "Good."
Then, last night, I was working on some work stuff. The Power Manager said I had 45% battery left. Suddenly the computer turned off and would not turn back on. I plugged it in and the battery icon on the front started blinking orange on and off. The computer turned back on, but now it says "The battery has failed due to normal wear. The battery cannot be charged. Replace the battery." The battery will not charge and I cannot run the comptuer unless it is plugged in. The cycle count currently is 443 and it says the condition is "Poor."
So here is my question: Did this happen because of Windows 7? I realize I have to in all likelihood get a new battery, but the battery was fine and never did anything like this when I was running Vista. It was working well and lasted a good 4 hours before needing to be plugged in. It was in great condition until I switched to Windows 7. I do not want to pay a bunch of money for a new battery just to install it and have the same thing happen. Is there something I need to install with Windows 7 that I somehow missed? Is there a way I can figure that out before I put a new battery in and risk the same thing happening?
Thank you!
Solved! Go to Solution.
Hello and welcome,
No way to know for sure, but I have to vote for coincidence. That's a lot of cycles on the battery, and maybe it was just due to go.
Based on the first part of your description, I would have suggested a battery reset, but that would probably have triggered the total shutdown that you've seen. These batteries have internal protective logic, and once they think that battery is unusable or unsafe to charge it's game over.
To back up my guess that it's just an unfortunate coincidence, I have a T400 that I switched from Vista to Win 7 and the 3+ year old battery didn't change status. (Apart from some issues with the switchable graphics driver causing somewhat increased power consumption - fixed at last...)
Good luck,
The large print: please read the Community Participation Rules before posting. Include as much information as possible: model, machine type, operating system, and a descriptive subject line. Do not include personal information: serial number, telephone number, email address, etc.
The fine print: I do not work for, nor do I speak for Lenovo. Unsolicited private messages will be ignored - questions and answers belong in the forum so that others may contribute and benefit. ... GeezBlog
@leelu11mb wrote:
The cycle count currently is 443 and it says the condition is "Poor."
That's a quite remarkable cycle count for LiON battery, you are extremely fortunate that it has lasted this long.
Yes, all the drivers were installed to my knowledge.
I just re-downloaded all the Think Pad Power ones just in case.
Okay, so get a new battery and I should be fine then?
Thank you for all your responses! I appreciate it!
Well, the cycles were much much better before it decided to fail. Unfortunately I did not write down that number last week and don't remember off the top of my head.
Is it normal for a battery to go from functioning well and the status being "good" to completely dying and the status being "poor."
I just ordered my new battery. I am hoping it was a coincidence and the same thing does not happen with the new one!
Yes, it is very possible for a battery to fail with that many cycles. Batteries are very sensitive and if the system detected even the smallest fault it can shut down the battery completely from use. You should give your battery some props, 400+ cycles is above average. Most laptop lithium ions are rated for around 300 charge cycles. Do not worry with your new battery, if you bought it from Lenovo it will come with a new one year warranty.
|Kudos Count


text:
Molson Coors Brewing Co reported higher quarterly profit on Wednesday helped by the acquisition of operations in Eastern Europe.
Coors, the maker of Coors Light and Blue Moon beers, said third-quarter net income rose to $198.4 million, or $1.09 per share, from $197.4 million, or $1.06 per share, a year earlier.
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Net sales increased to $1.20 billion from $954.4 million.