<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Tooth decay and can you explain it in depth? [/INST] Tooth decay, also known as cavities or caries, is the breakdown of teeth due to acids produced by bacteria. The cavities may be a number of different colors from yellow to black. Symptoms may include pain and difficulty with eating. Complications may include inflammation of the tissue around the tooth, tooth loss and infection or abscess formation.The cause of cavities is acid from bacteria dissolving the hard tissues of the teeth (enamel, dentin and cementum). The acid is produced by the bacteria when they break down food debris or sugar on the tooth surface. Simple sugars in food are these bacterias primary energy source and thus a diet high in simple sugar is a risk factor. If mineral breakdown is greater than build up from sources such as saliva, caries results. Risk factors include conditions that result in less saliva such as: diabetes mellitus, Sjögren syndrome and some medications. Medications that decrease saliva production include antihistamines and antidepressants. Dental caries are also associated with poverty, poor cleaning of the mouth, and receding gums resulting in exposure of the roots of the teeth.Prevention of dental caries includes regular cleaning of the teeth, a diet low in sugar, and small amounts of fluoride. Brushing ones teeth twice per day and flossing between the teeth once a day is recommended. Fluoride may be acquired from water, salt or toothpaste among other sources. Treating a mothers dental caries may decrease the risk in her children by decreasing the number of certain bacteria she may spread to them. Screening can result in earlier detection. Depending on the extent of destruction, various treatments can be used to restore the tooth to proper function or the tooth may be removed. There is no known method to grow back large amounts of tooth. The availability of treatment is often poor in the developing world. Paracetamol (acetaminophen) or ibuprofen may be taken for pain.Worldwide, approximately 3.6 billion people (48% of the population) have dental caries in their permanent teeth as of 2016. The World Health Organization estimates that nearly all adults have dental caries at some point in time. In baby teeth it affects about 620 million people or 9% of the population. They have become more common in both children and adults in recent years. The disease is most common in the developed world due to greater simple sugar consumption and less common in the developing world. Caries is Latin for "rottenness".

Signs and symptoms
A person experiencing caries may not be aware of the disease.  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 "micro-cavity".   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.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 the 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. 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. In highly progressed cases, an infection can spread from the tooth to the surrounding soft tissues. Complications such as cavernous sinus thrombosis and Ludwig angina can be life-threatening.

Cause
Four things are required for caries to form: a tooth surface (enamel or dentin), caries-causing bacteria, fermentable carbohydrates (such as sucrose), and time. This involves adherence of food to the teeth and acid creation by the bacteria that makes up the dental plaque.  However, 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 disease 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.Tooth decay is caused by biofilm (dental plaque) lying on the teeth and maturing to become cariogenic (causing decay).  Certain bacteria in the biofilm produce acid in the presence of fermentable carbohydrates such as sucrose, fructose, and glucose.Caries occur more often in people from the lower end of the socio-economic scale than people from the upper end of the socio-economic scale, due to lack of education about dental care, and lack of access to professional dental care which may be expensive.

Bacteria
The most common bacteria associated with dental cavities are the mutans streptococci, most prominently Streptococcus mutans and Streptococcus sobrinus, and lactobacilli. However, cariogenic bacteria (the ones that can cause the disease) are present in dental plaque, but they are usually in too low concentrations to cause problems unless there is a shift in the balance. This is driven by local environmental change, such as frequent sugar intake or inadequate biofilm removal (toothbrushing).  If left untreated, the disease can lead to pain, tooth loss and infection.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. Streptococcus mutans are gram-positive bacteria which constitute biofilms on the surface of teeth. 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.  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 caretakers kiss or through feeding pre-masticated food.

Dietary sugars
Bacteria in a persons mouth convert glucose, fructose, and most commonly sucrose (table sugar) into acids such as lactic acid through a glycolytic process called fermentation. 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.  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 dextran sucranase.

Exposure
The frequency with which teeth are exposed to cariogenic (acidic) environments affects the likelihood of caries development.  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 dissolve and can remain dissolved for two hours.  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 tooths erupting into the mouth if the diet is sufficiently rich in suitable carbohydrates. Evidence suggests that the introduction of fluoride treatments has slowed the process.  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 tend 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).

Teeth
There are certain diseases and disorders affecting teeth that may leave an individual at a greater risk for cavities.
Molar incisor hypo-mineralization, which seems to be increasingly common. While the cause is unknown it is thought to be a combination of genetic and environmental factors. Possible contributing factors that have been investigated include systemic factors such as high levels of dioxins or polychlorinated biphenyl (PCB) in the mothers milk, premature birth and oxygen deprivation at birth, and certain disorders during the childs first 3 years such as mumps, diphtheria, scarlet fever, measles, hypoparathyroidism, malnutrition, malabsorption, hypo-vitaminosis D, chronic respiratory diseases, or undiagnosed and untreated coeliac disease, which usually presents with mild or absent gastrointestinal symptoms.Amelogenesis imperfecta, which occurs in 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. In both cases, teeth may be left more vulnerable to decay because the enamel is not able to protect the tooth.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.  These minerals, especially hydroxyapatite, will become soluble when exposed to acidic environments.  Enamel begins to demineralize at a pH of 5.5.  Dentin and cementum are more susceptible to caries than enamel because they have lower mineral content.  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 dental caries is weak; 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 is more likely to develop (see next section).  Also, caries is more likely to develop when food is trapped between teeth.

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 lead to dry mouth and thus to widespread tooth decay. Examples include Sjögren syndrome, diabetes mellitus, diabetes insipidus, and sarcoidosis. Medications, such as antihistamines and antidepressants, can also impair salivary flow. Stimulants, most notoriously methylamphetamine, also occlude the flow of saliva to an extreme degree. This is known as meth mouth. Tetrahydrocannabinol (THC), 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. Radiation therapy of the head and neck may also damage the cells in salivary glands, somewhat increasing the likelihood of caries formation.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.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.  Tobacco use is a significant risk factor for periodontal disease, which can cause the gingiva to recede.  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.  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.
Exposure of children to secondhand tobacco smoke is associated with tooth decay.Intrauterine and neonatal lead exposure promote tooth decay. Besides lead, all atoms with electrical charge and ionic radius similar to bivalent calcium,
such as cadmium, mimic the calcium ion and therefore exposure to them may promote tooth decay.Poverty is also a significant social determinant for oral health. Dental caries have been linked with lower socio-economic status and can be considered a disease of poverty.Forms are available for risk assessment for caries when treating dental cases; this system using the evidence-based Caries Management by Risk Assessment (CAMBRA). 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.Saliva also contains iodine and EGF. EGF results effective in cellular proliferation, differentiation and survival. Salivary EGF, which seems also regulated by dietary inorganic iodine, plays an important physiological role in the maintenance of oral (and gastro-oesophageal) tissue integrity, and, on the other hand, iodine is effective in prevention of dental caries and oral health.

Pathophysiology
Teeth are bathed in saliva and have a coating of bacteria on them (biofilm) that continually forms. The development of biofilm begins with pellicle formation. Pellicle is an acellular proteinaceous film which covers the teeth. Bacteria colonize on the teeth by adhering to the pellicle-coated surface. Over time, a mature biofilm is formed and this create a cariogenic environment on the tooth surface. The minerals in the hard tissues of the teeth (enamel, dentin and cementum) are constantly undergoing processes of demineralization and remineralization. Dental caries results when the demineralization rate is faster than the remineralization and there is net mineral loss. This happens when there is an ecologic shift within the dental biofilm, from a balanced population of micro-organisms to a population that produce acids and can survive in an acid environment.

Enamel
Tooth 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.As the enamel loses minerals,  and dental caries progresses, the enamel develops 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. The translucent zone is the first visible sign of caries and coincides with a one to two percent loss of minerals. 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. 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.

Dentin
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.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. The advancing front represents a zone of demineralized dentin 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 dentin caries has been reversibly attacked because the collagen matrix is not severely damaged, giving it potential for repair.

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. 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. 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 brings immunoglobulins from the immune system to fight the bacterial infection. At the same time, there is an increase of mineralization of the surrounding tubules.  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. 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.

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. 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.  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, are thought to initiate the production of reparative dentin by fibroblasts and mesenchymal cells of the pulp. 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.

Cementum
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 roots 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.

Diagnosis
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).
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 areas of 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.  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, 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 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. 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.The early carious lesion is characterized by demineralization of the tooth surface, altering the tooths optical properties. Technology utilizing laser speckle image (LSI) techniques may provide a diagnostic aid to detect early carious lesions.

Classification
Caries can be classified by location, etiology, rate of progression, and affected hard tissues. 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 is described in other ways that might indicate the cause. The G. V. Black classification is as follows:

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 is worn away due to attrition

Early childhood caries
Early childhood caries (ECC), also known as "baby bottle caries," "baby bottle tooth decay" or "bottle rot," is a pattern of decay found in young children with their deciduous (baby) teeth. This must include the presence of at least one carious lesion on a primary tooth in a child under the age of 6 years. The teeth most likely affected are the maxillary anterior teeth, but all teeth can be affected.  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.Another pattern of decay is "rampant caries", which signifies advanced or severe decay on multiple surfaces of many teeth. Rampant caries may be seen in individuals with xerostomia, poor oral hygiene, stimulant use (due to drug-induced dry mouth), 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.
Children at 6–12 months are at increased risk of developing dental caries. For other children aged 12–18 months, dental caries develop on primary teeth and approximately twice yearly for permanent teeth.A range of studies have reported that there is a correlation between caries in primary teeth and caries in permanent teeth.

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 result in cavities.
Recurrent caries, also described as secondary, are caries that appear 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 the use of amorphous calcium phosphate.
Micro-invasive interventions (such as dental sealant or resin infiltration) have been shown to slow down the progression of proximal decay.

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, the term "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.

Prevention
Oral hygiene
The primary approach to dental hygiene care consists of tooth-brushing and flossing. The purpose of oral hygiene is to remove and prevent the formation of plaque or dental biofilm, although studies have shown this effect on caries is limited. While there is no evidence that flossing prevents tooth decay, the practice is still generally recommended.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. Additional aids include interdental brushes, water picks, and mouthwashes. The use of rotational electric toothbrushes might reduce the risk of plaque and gingivitis, though it is unclear whether they are of clinical importance.However, oral hygiene is effective at preventing gum disease (gingivitis / periodontal disease). Food is forced inside pits and fissures under chewing pressure, leading to carbohydrate-fuelled acid demineralisation where the brush, fluoride toothpaste, and saliva have no access to remove trapped food, neutralise acid, or remineralise tooth enamel. (Occlusal caries accounts for between 80 and 90% of caries in children (Weintraub, 2001).)  Unlike brushing, fluoride leads to proven reduction in caries incidence by approximately 25%; higher concentrations of fluoride (>1,000 ppm) in toothpaste also helps prevents tooth decay, with the effect increasing with concentration up to a plateau. A randomized clinical trial demonstrated that toothpastes that contain arginine have greater protection against tooth cavitation than the regular fluoride toothpastes containing 1450 ppm alone. A Cochrane review has confirmed that the use of fluoride gels, normally applied by a dental professional from once to several times a year, assists in the prevention of tooth decay in children and adolescents, reiterating the importance of fluoride as the principal means of caries prevention. Another review concluded that the supervised regular use of a fluoride mouthwash greatly reduced the onset of decay in the permanent teeth of children.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).
Alternative methods of oral hygiene also exist around the world, such as the use of teeth cleaning twigs such as miswaks in some Middle Eastern and African cultures. There is some limited evidence demonstrating the efficacy of these alternative methods of oral hygiene.

Dietary modification
People who eat more free sugars get more cavities, with cavities increasing exponentially with increasing sugar intake. Populations with less sugar intake have fewer cavities. In one population, in Nigeria, where sugar consumption was about 2g/day, only two percent of the population, of any age, had had a cavity.Chewy and sticky foods (such as candy, cookies, potato chips, and crackers) tend to adhere to teeth longer. However, dried fruits such as raisins and fresh fruit such as apples and bananas disappear from the mouth quickly, and do not appear to be a risk factor. Consumers are not good at guessing which foods stick around in the mouth.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).  Parents are also recommended to avoid sharing utensils and cups with their infants to prevent transferring bacteria from the parents mouth.Xylitol is a naturally occurring sugar alcohol that is used in different products as an alternative to sucrose (table sugar). As of 2015 the evidence concerning the use of xylitol in chewing gum was insufficient to determine if it is effective at preventing caries.

Other measures
The use of dental sealants is a means of prevention. 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 of carbohydrate, preventing the formation of pit and fissure caries. Sealants are usually applied on the teeth of children, as soon as the teeth 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. Dental sealants have been shown to be more effective at preventing occlusal decay when compared to fluoride varnish applications.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. Streptococcus mutans is the leading cause of tooth decay. Low concentration fluoride ions act as bacteriostatic therapeutic agent and high concentration fluoride ions are bactericidal. The incorporated fluorine makes enamel more resistant to demineralization and, thus, resistant to decay. Fluoride can be found in either topical or systemic form. Topical fluoride is more highly recommended than systemic intake to protect the surface of the teeth. Topical fluoride is used in toothpaste, mouthwash and fluoride varnish. Standard fluoride toothpaste (1,000–1,500 ppm) is more effective than low fluoride toothpaste (< 600ppm) to prevent dental caries. It is recommended that all adult patients to use fluoridated toothpaste with at least 1350ppm fluoride content, brushing at least 2 times per day and brush right before bed. For children and young adults, use fluoridated toothpaste with 1350ppm to 1500ppm fluoride content, brushing 2 times per day and also brush right before bed. American Dental Association Council suggest that for children <3 years old, caregivers should begin brushing their teeth by using fluoridated toothpaste with an amount no more than a smear. Supervised toothbrushing must also be done to children below 8 years of age to prevent swallowing of toothpaste. After brushing with fluoride toothpaste, rinsing should be avoided and the excess spat out. 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. Silver diamine fluoride may work better than fluoride varnish to prevent cavities. Systemic fluoride is found as lozenges, tablets, drops and water fluoridation. These are ingested orally to provide fluoride systemically. Water fluoridation has been shown to be beneficial to prevent tooth decay, especially in low social economical areas, where other forms of fluoride is not available. However, a Cochrane systematic review found no evidence to suggest that taking fluoride systemically daily in pregnant women was effective in preventing dental decay in their offspring. While some products containing chlorhexidine have been shown to limit the progression of existing tooth decay; there is currently no evidence suggesting that chlorhexidine gels and varnishes can prevent dental caries or reduce the population of Streptococcus mutans in the mouth.An oral health assessment carried out before a child reaches the age of one may help with management of caries. The oral health assessment should include checking the childs history, a clinical examination, checking the risk of caries in the child including the state of their occlusion and assessing how well equipped the childs parent or carer is to help the child prevent caries. In order to further increase a childs cooperation in caries management, good communication by the dentist and the rest of the staff of a dental practice should be used. This communication can be improved by calling the child by their name, using eye contact and including them in any conversation about their treatment.Vaccines are also under development.

Treatment
Most importantly, whether the carious lesion is cavitated or non-cavitated 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. More recently,  Immunoglobulin Y specific to Streptococcus mutans has been used to suppress growth of S mutans. 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 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.Destroyed tooth structure does not fully regenerate, although remineralization of very small carious lesions may occur if dental hygiene is kept at optimal level.  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.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. 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. Some dentists remove dental caries using a laser rather than the traditional dental drill. A Cochrane review of this technique looked at Er:YAG (erbium-doped yttrium aluminium garnet), Er,Cr:YSGG (erbium, chromium: yttrium-scandium-gallium-garnet) and Nd:YAG (neodymium-doped yttrium aluminium garnet) lasers and found that although people treated with lasers (compared to a conventional dental "drill") experienced less pain and had a lesser need for dental anaesthesia, that overall there was little difference in caries removal. Another alternative to drilling or lasers for small caries is the use of air abrasion, in which small abrasive particles are blasted at decay using pressurized air (similar to sand blasting). Once the cary 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, glass ionomer cement, porcelain, and gold. Composite resin and porcelain can be made to match the color of a patients 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.  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.
For children, preformed crowns are available to place over the tooth. These are usually made of metal (usually stainless steel but increasingly there are aesthetic materials). Traditionally teeth are shaved down to make room for the crown but, more recently, stainless steel crowns have been used to seal decay into the tooth and stop it progressing. This is known as the Hall Technique and works by depriving the bacteria in the decay of nutrients and making their environment less favorable for them. It is a minimally invasive method of managing decay in children and does not require local anesthetic injections in the mouth.

In certain cases, endodontic therapy may be necessary for the restoration of a tooth.  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.  In root canal therapy, 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.  The tooth is filled and a crown can be placed. Upon completion of root canal therapy, the tooth is 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. Extractions may also be preferred by people unable or unwilling to undergo the expense or difficulties in restoring the tooth.

Epidemiology
Worldwide, approximately 3.6 billion people have dental caries in their permanent teeth. In baby teeth it affects about 620 million people or 9% of the population. The disease is most common in Latin American countries, countries in the Middle East, and South Asia, and least prevalent in China. In the United States, dental caries is the most common chronic childhood disease, being at least five times more common than asthma.  It is the primary pathological cause of tooth loss in children. Between 29% and 59% of adults over the age of 50 experience caries.Treating dental cavities costs 5–10% of health-care budgets in industrialized countries, and can easily exceed budgets in lower-income countries.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.  Nonetheless, countries that have experienced an overall decrease in cases of tooth decay continue to have a disparity in the distribution of the disease.  Among children in the United States and Europe, twenty percent of the population endures sixty to eighty percent of cases of dental caries.  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.  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.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.Bacteria typically associated with dental caries have been isolated from vaginal samples from females who have bacterial vaginosis.

History
There is a long history of dental caries. Over a million years ago, hominins such as Paranthropus had cavities. The largest increases in the prevalence of caries have been associated with dietary changes.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.  The increase of caries during the neolithic period may be attributed to the increased consumption of plant foods containing carbohydrates.  The beginning of rice cultivation in South Asia is also believed to have caused an increase in caries especially for women, 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.A Sumerian text from 5000 BC describes a "tooth worm" as the cause of caries.  Evidence of this belief has also been found in India, Egypt, Japan, and China. 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. The Ebers Papyrus, an Egyptian text from 1550 BC, mentions diseases of teeth.  During the Sargonid dynasty of Assyria during 668 to 626 BC, writings from the kings physician specify the need to extract a tooth due to spreading inflammation.  In the Roman Empire, wider consumption of cooked foods led to a small increase in caries prevalence. The Greco-Roman civilization, in addition to the Egyptian civilization, had treatments for pain resulting from caries.The rate of caries remained low through the Bronze Age and Iron Age, but sharply increased during the Middle Ages.  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.  The barber surgeons of the time provided services that included tooth extractions.  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.There is also evidence of caries increase when Indigenous people in North America changed from a strictly hunter-gatherer diet to a diet with maize. Rates also increased after contact with colonizing Europeans, implying an even greater dependence on maize.During the European Age of Enlightenment, the belief that a "tooth worm" caused caries was also no longer accepted in the European medical community.   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.  In 1850, another sharp increase in the prevalence of caries occurred and is believed to be a result of widespread diet changes. 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.  This explanation is known as the chemoparasitic caries theory.  Millers 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.  Several of the specific strains of lactobacilli were identified in 1921 by Fernando E. Rodríguez 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 that this organism was the cause of caries, the discovery was not followed up </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Molar incisor hypomineralisation and can you explain it in depth? [/INST] Molar incisor hypomineralisation (MIH) is a type of enamel defect affecting, as the name suggests, the first molars and incisors in the permanent dentition. MIH is considered a worldwide problem and usually occurs in children under 10 years old. This developmental condition is caused by the lack of mineralisation of enamel during its maturation phase, due to interruption to the function of ameloblasts. Many factors have been suggested, such as genetics and medical problems during pregnancy, but only childhood illness, fever in particular, seems to be associated with MIH. However, further studies on the aetiology of MIH are required because it is believed to be multifactorial.MIH often presents as discolouration on one to four affected permanent molars and the associated incisors. The enamel of the affected teeth appears yellow, brown, cream or white and thus are sometimes referred to as ‘cheese molars’. These teeth are deemed less aesthetically pleasing, hence causing distress in children with MIH and their parents. It is important to note that although there is difference in enamel translucency in the affected teeth, there should not be any changes to the enamel thickness, unlike in enamel hypoplasia.As a consequence, children with MIH are more likely to experience tooth decay compared to those without the condition. Moreover, the development of tooth decay is very rapid due to the less mineralised enamel. MIH only becomes visible once the permanent molars start to erupt and that is when opacities on the tooth can be observed if it is affected. It will be useful for the children who are suspected to suffer from MIH to visit their dentist more frequently during the eruption of their first permanent molars to prevent any further complications affecting their oral health.

Signs and symptoms
The distribution of disease in those affected with MIH can vary greatly. It can be common for the enamel of one molar to be affected while the enamel of the contralateral molar is clinically unaffected, or with minor defects only.

Lesions
The lesions that appear in teeth affected with MIH can present as opacities that vary from white to yellow-brown. They are usually asymmetrical in appearance, with a sharp demarcation that distinguishes between normal and affected enamel. The lesions usually do not involve the cervical third of affected teeth.

Post-eruptive breakdown
Post-eruptive breakdown (PEB) is a clinical feature, often observed in the majority of severely affected cases.  The rate of PEB may be increased by the loading of masticatory forces on enamel weakened by MIH. The lesions resulting from PEB are irregularly shaped, with rough margins from the shearing of the enamel.  PEB is more likely to occur in MIH affected teeth with yellow or brown opacities rather than those with white opacities, as darker lesions reflect a greater deficit in mineral content.

Atypical caries
Teeth affected with MIH are at an increased risk of acquiring dental caries. This is because the properties of the enamel are altered by increased porosity and decreased hardness. Essentially, the balance between mineralisation and demineralisation shifts to favour demineralisation of enamel, giving the tooth less resilience in structure, thereby making it vulnerable to caries.The poor structural properties of the enamel in teeth with MIH also increase the likelihood of cavitation of any lesions, thereby causing the lesion to progress at a faster rate. Progression of the carious lesion is also more rapid in teeth with MIH as patients may experience tooth sensitivity while carrying out oral hygiene, causing them to avoid doing so and consequentially accelerating the decay.

Hypersensitivity
Teeth affected by MIH are often affected by hypersensitivity due to changes in temperature or toothbrushing. A study has suggested that a possible cause of hypersensitivity in MIH is the inflammatory reactions in the pulp due to oral bacteria penetrating through the hypomineralised enamel into the dentinal tubules.

Difficult to anaesthetise
It has been reported that MIH-affected teeth were more difficult to anaesthetise. Difficulty achieving anaesthesia in MIH-affected teeth may be caused by the chronic inflammation of the pulp due to the penetration of bacteria as the presence of inflammation can reduce the efficacy of local anaesthetics  which may then result in more anaesthetic being given to achieve anaesthesia. Some dental treatment has been undertaken without local anaesthesia which could result in a child becoming more fearful and anxious when receiving dental treatment. This can be especially challenging in paediatric dentistry thus more specialised methods may be needed to increase the efficiency of anaesthetising teeth.Opacities due to MIH can be quite visible especially on anterior teeth which could present as a problem aesthetically. Patients frequently claim aesthetic discomfort when anterior teeth are involved. The discoloured appearance of the anterior teeth could also have negative effects on a child’s psychological development and self-esteem.

Tooth breakdown and restoration problems
MIH-affected teeth are more prone to breakdown as they are hypomineralised which weakens the enamel structure. Restorations placed on MIH-affected teeth were found to be more prone to failure due to both loss of tooth structure and material loss. The enamel can also fracture more easily due to chewing forces.

Causes
The exact cause of MIH is unknown but thought to be multifactorial.Pre-natally: risks, such as infection, maternal psychological stress and frequent exposure to ultrasonic scans were all correlated with increased risks of MIH.
During the perinatal stage, Pitiphat found that cesarean section and complications during vaginal delivery could contribute to an increased chance of MIH. Children born preterm and those with poor general health or systemic conditions in their first 3 years of development also run a higher risk of developing MIH.  It has also been proposed that developmental dental defects were associated with long-term breastfeeding due to exposure to dioxin.
More recent evidence has suggested a relationship between respiratory diseases and oxygen shortage of the ameloblasts and MIH. Lastly oxygen shortage combined with low birth weight is suspected to be a contributing factor

Diagnosis
Differential diagnosis
It is essential to exclude other causes of enamel opacities, differentiating MIH from them, to ensure an appropriate treatment plan is made. These conditions include:

Dental caries, which is the most common cause of destruction of dental hard tissues. This is more unlikely in a patient with a previously intact primary dentition. White spot lesions are also uncommon on incisors, hence ruling out dental caries.
Fluorosis, which can result from an intake of a high fluoride concentration while the tooth is still undergoing mineralisation. Fluorosis presents as irregular, diffuse enamel opacities which affect more than 1 tooth, in contrast to the well-demarcated borders of hypomineralised enamel seen in MIH.
Amelogenesis imperfecta, a genetic condition, and thus there may be a history of similar defects in other family members. This condition affects both the primary and permanent dentition, and all surfaces tend to be equally affected, differentiating it from MIH.
Trauma to primary incisors resulting in discolouration of permanent incisors.
Administration of tetracycline during pregnancy and to children under 6 resulting in tooth staining (grey or yellow).
Enamel hypoplasia, caused by defective enamel matrix formation, is a quantitative defect which presents as a localised reduction in enamel thickness. This differs from hypomineralisation, which is a qualitative defect affecting the translucency of enamel.

Classification
MIH examination should be carried out on clean, wet teeth. The ideal age for examination is when the child is 8 years old - the age where all permanent first molars and most of the incisors are erupted. The permanent first molar will also still be in a comparatively sound condition without excessive post-eruption breakdown. Judgements of each individual teeth should be recorded, aiding the correct diagnosis of the condition.
There is currently a lack of standardisation in the scoring system and severity indices used to record the diagnosis of MIH. Various systems commonly employed in studies include:

Modified Defect of Dental Enamel (DDE) Index: This set of criteria allows for enamel defects to be detected, enabling a distinction between demarcated and diffused opacities.
European Academy of Paediatric Dentistry (EAPD) judgement criteria: This set of criteria was developed in 2003 to standardise classifications for use in epidemiological studies. However, while it allows the categorisation of the enamel condition, it does not address the severity of the enamel condition.
Molar Hypomineralisation Severity Index (MHSI): This set of criteria has been developed to address deficiencies in indices concerning the severity of hypomineralisation. It is based on both the clinical characteristics of hypomineralised defects and the EAPD judgement criteria. It was found to be effective in guiding the clinical management of children by predicting treatment undertaken for affected permanent first molars.
Ghanim et al index: The index combines principles of the EAPD judgement criteria and DDE index in order to grade the clinical status, amount of tooth surface area affected, and other enamel defects comparable to MIH. The index has been validated  and a training manual was developed to assist researchers in implementing the index in a standardised manner.

Prevention
Prevention is of prior importance at an early developmental age as the defective tooth is more likely to have caries and post-eruptive breakdown due to its increased porosity.  Appropriate dietary advice and toothpaste with a fluoride level of at least 1,000 ppm F should be recommended. For treating spontaneous hypersensitivity professional applications of fluoride varnish (e.g. Duraphat 22,600ppm F) or 0.4% stannous fluoride gel may be helpful.Casein Phosphopepetide-Amorphus Calcium Phosphate (CPP-ACP) provides a supersaturated environment of calcium and phosphate on the enamel surface to enhance remineralisation in the form of toothpaste or sugar free chewing gum. Its clinical effectiveness is still debatable but may benefit those patients who complain of mild pain to external stimuli.

Treatment
The frequency of first permanent molar treatment for children with MIH is nearly 10 times greater compared to children without MIH. The available treatment modalities for MIH is extensive but the decision on which treatment should be used is complex and multi-factorial. Factors may include: condition severity, the patient’s dental age, the child/parent’s social background and expectations. There are treatment modalities available to manage children affected by MIH; however, the evidence supporting these modalities are still weak.

Anterior teeth
Etch-bleach-seal technique
Involves repeated cycles of etching with 37% phosphoric acid followed by applying 5% sodium hypochlorite until improvement of discolouration is achieved. Clear resin composite or resin infiltrate can be used to seal the lesion after the technique.

Microabrasion
The aesthetics of a child’s anterior teeth is a concern for both children and their parents alike.
Yellow or brownish-yellow defects are of full thickness, and therefore may respond to bleaching with carbamide peroxide. However, careful consideration should be made of the risks including hypersensitivity, mucosal irritation and enamel surface alterations.Creamy-yellow or whitish-creamy defects are less porous and variable in depth, and may respond to microabrasion with 18% hydrochloric acid or 37.5% phosphoric acid and abrasive paste. Again, this should be undertaken cautiously as microabrasion may result in loss of enamel.

Veneers
Direct or indirect composite veneers can be effective in improving aesthetics with minimal tooth tissue removal. Ceramic veneers as a treatment option should be delayed due to the risks of resulting in a short clinical crown height, immature tooth pulp irritation and also the instability of the gingival margins during the eruption of teeth.

Posterior teeth
Fissure sealants
The placement of fissure sealants on permanent molars without post-eruptive breakdown should be undertaken. Use of a 5th generation bonding adhesive prior to fissure sealant application may improve retention rates of fissure sealants.For partially erupted molars with inadequate moisture control, glass ionomer cements (GIC) can be considered as an interim treatment option. As the retention rate of GIC is often poor, replacement with a resin-based fissure sealant is recommended following tooth eruption.Resin-based fissure sealants can be beneficial to patients affected with mild MIH where the first permanent molars have fully erupted, although the degree of hypomineralization affects the bond strength of said sealants.  The bond strength of resin based fissure sealants to affected MIH can be enhanced by pre-treating with 5% sodium hypochlorite for one minute after etching, and applying a bonding agent. However, more evidence is needed from clinical based studies.

Direct restorations
Cavity design
There is still much debate of whether margin extension should include removal of all defective enamel or only the porous enamel. The former provides sound enamel for bonding but leads to excessive tooth tissue loss. The latter is less invasive, but the margins may have a high risk of breakdown due to defective bonding. Yet, it is agreed that adhesive restorations should be used as opposed to those reliant upon mechanical retention (such as amalgam).

Composite resin restorations
Composite resin material has been shown to have longer-term stability in MIH teeth, with a median survival rate of 5.2 years and a success rate of 74%-100%  during a 4-year follow-up period. Self-etching adhesive was found to have better bond strength to enamel affected by MIH compared to total etch single-bottle adhesive. The use of composite should be considered both for permanent molars affected by MIH, as well as incisors. Furthermore, composite veneers may achieve a better aesthetic result where deep lesions are seen in incisors.

Glass ionomer cement (GIC) restorations
GIC materials have adhesive capabilities with both enamel and dentine, long-term fluoride release and hydrophilicity when there is inadequate moisture control intra-orally, during early post-eruptive stages. However, GIC’s poorer mechanical properties suggest avoidance in stress-bearing areas. In later post-eruptive stages GIC may be valuable as sub-layer beneath composite restorations.

Indirect restorations
Preformed metal crowns
Pre-formed metal crowns (PMC), also known as stainless steel crowns, can be used to reduce the risk of marginal breakdown, coronal leakage and has a good longevity. The use of preformed metal crowns on MIH-affected molars can prevent further tooth loss, control hypersensitivity and aim to establish correct interproximal and occlusal contact. They are relatively inexpensive and require little preparation.To prevent further tooth preparation and tissue loss, use of the Hall Technique should also be considered. There advantage is use during any stage of post-eruptive breakdown, but evidence of their efficacy is limited. Although the PMC has evidence to show that it is well accepted, a few of the children and their carers expressed their concerns about the metallic appearances of the restoration.

Cast restorations
Cast restorations may include full coverage crowns for MIH-affected permanent teeth. Generally cast restorations requiring tooth preparation are not recommended in young children due to large pulp size, short crown height and potential difficulties in obtaining a good impression for subgingival crown margins.

Extractions
A list of considerations can affect the final decision on whether extraction of the affected teeth should be carried out or should it be retained such as: severity of MIH; patient’s aesthetic expectations; whether the patient is suitable to undergo orthodontic treatment; orthodontic concerns (e.g. crowding, facial profile, missing or supernumerary teeth, presence of third molars).Timely extractions are often the preferred treatment plan for first permanent molars that are severely affected and symptomatic. The facilitation of eruption of the second permanent molars to the space of the first permanent molar removes the burden of continuous restorative treatment.A favourable occlusion may be acquired following a well-planned treatment and this eliminates the need for fixed orthodontic appliances therapy. However, a comprehensive discussion of the possible need of orthodontic sequelae and treatment is important.Favorable eruption position of the second permanent molar may result if the first permanent molar is extracted when the child is at the age of between 8–10 years old </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Heavy chain disease and can you explain it in depth? [/INST] Heavy chain disease is a form of paraproteinemia and plasma cell dyscrasia that involves the proliferation of cells producing immunoglobulin heavy chains.This disease is characterized by an excessive production of heavy chains that are short and truncated. These heavy chain disease proteins have various deletions, mainly in their amino-terminal part, which causes the heavy chains to lose the ability to form disulfide bonds with the light chains. The defect in the immunoglobulins presumably arises during somatic hypermutation. Deletion of the N-terminal part of the heavy chain disease protein leads to aggregation and signaling of the B cell receptor, presumably due to the loss of the anti-aggregating properties of the light chain.

Classification
There are four forms:

alpha chain disease (Seligmanns disease)
gamma chain disease (Franklins disease)
mu chain disease
delta chain disease

IgA/αHCD
The most common type of heavy chain disease is the IgA type, known as αHCD. The most common type of αHCD is the gastrointestinal form (known as immunoproliferative small intestine disease or IPSID), but it has also been reported in the respiratory tract, and other areas of the body.

IgG/γHCD
Franklins disease (gamma heavy chain disease)
It is a very rare B-cell lymphoplasma cell proliferative disorder which may be associated with autoimmune diseases and infection is a common characteristic of the disease </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Focal facial dermal dysplasia and can you explain it in depth? [/INST] Focal facial dermal dysplasia  is a rare genetically heterogeneous group of disorders that are characterized by congenital bilateral scar like facial lesions, with or without associated facial anomalies. It is characterized by hairless lesions with fingerprint like puckering of the skin, especially at the temples, due to alternating bands of dermal and epidermal atrophy.
This condition is also known as Brauer syndrome (hereditary symmetrical aplastic nevi of temples, bitemporal aplasia cutis congenita, bitemporal aplasia cutis congenita: OMIM  136500) and Setleis syndrome (facial ectodermal dysplasia: OMIM  227260).

Presentation
This condition is characterised by symmetrical lesions on the temples resembling forceps marks. It is characterized a puckered skin due to a virtual absence of subcutaneous fat </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Ventricular outflow tract obstruction and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Bunion and can you explain it in depth? [/INST] A bunion, also known as hallux valgus, is a deformity of the joint connecting the big toe to the foot. The big toe often bends towards the other toes and the joint becomes red and painful. The onset of bunions is typically gradual. Complications may include bursitis or arthritis.The exact cause is unclear. Proposed factors include wearing overly tight shoes, high-heeled shoes, family history, and rheumatoid arthritis. Diagnosis is generally based on symptoms and supported by X-rays. A similar condition of the little toe is referred to as a bunionette.Treatment may include proper shoes, orthotics, or NSAIDs. If this is not effective for improving symptoms, surgery may be performed. It affects about 23% of adults. Females are affected more often than males. Usual age of onset is between 20 and 50 years old. The condition also becomes more common with age. It was first clearly described in 1870. Archaeologists have found a high incidence of bunions in skeletons from 14th- and 15th-century England, coinciding with a fashion for pointy shoes.

Signs and symptoms
Symptoms may include irritation of the skin around the bunion, and blisters may form more easily at the site. Pain may be worse when walking.
Bunions can lead to difficulties finding properly fitting footwear and may force a person to buy a larger size shoe to accommodate the width of the bunion. If the bunion deformity becomes severe enough, the foot can hurt in different places even without the constriction of shoes. It is then considered as being a mechanical function problem of the forefoot.

Cause
The exact cause is unclear. It may be due to a combination of internal and external causes. Proposed factors include wearing overly tight shoes, high-heeled shoes, family history  and rheumatoid arthritis. The American College of Foot and Ankle Surgeons states that footwear only worsens a problem caused by genetics.Excessive pronation of the foot causes increased pressure on the inside of the big toe that can result in a deformation of the medial capsular structures of the joint, subsequently increasing the risk of developing bunions.

Pathophysiology
The bump itself is partly due to the swollen bursal sac or an osseous (bony) anomaly on the metatarsophalangeal joint. The larger part of the bump is a normal part of the head of the first metatarsal bone that has tilted sideways to stick out at its distal (far) end (metatarsus primus varus).
Bunions are commonly associated with a deviated position of the big toe toward the second toe, and the deviation in the angle between the first and second metatarsal bones of the foot.  The small sesamoid bones found beneath the first metatarsal (which help the flexor tendon bend the big toe downwards) may also become deviated over time as the first metatarsal bone drifts away from its normal position. Osteoarthritis of the first metatarsophalangeal joint, diminished and/or altered range of motion, and discomfort with pressure applied to the bump or with motion of the joint, may all accompany bunion development. Atop of the first metatarsal head either medially or dorso-medially, there can also arise a bursa that when inflamed (bursitis), can be the most painful aspect of the process.

Diagnosis
Bunion can be diagnosed and analyzed with a  simple x-ray, which should be taken with the weight on the foot. The hallux valgus angle (HVA) is the angle between the long axes of the proximal phalanx and the first metatarsal bone of the big toe. It is considered abnormal if greater than 15–18°. The following HV angles can also be used to grade the severity of hallux valgus:
Mild: 15–20°
Moderate: 21–39°
Severe: ≥ 40°The intermetatarsal angle (IMA) is the angle between the longitudinal axes of the first and second metatarsal bones, and is normally less than 9°. The IM angle can also grade the severity of hallux valgus as:
Mild: 9–11°
Moderate: 12–17°
Severe: ≥ 18°

Treatment
Conservative treatment for bunions include changes in footwear, the use of orthotics (accommodative padding and shielding), rest, ice, and pain medications such as acetaminophen or nonsteroidal anti-inflammatory drugs. These treatments address symptoms but do not correct the actual deformity </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Acral fibrokeratoma and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Schwannoma and can you explain it in depth? [/INST] A schwannoma (or neurilemmoma) is a usually benign nerve sheath tumor composed of Schwann cells, which normally produce the insulating myelin sheath covering peripheral nerves.
Schwannomas are homogeneous tumors, consisting only of Schwann cells. The tumor cells always stay on the outside of the nerve, but the tumor itself may either push the nerve aside and/or up against a bony structure (thereby possibly causing damage). Schwannomas are relatively slow-growing. For reasons not yet understood, schwannomas are mostly benign and less than 1% become malignant, degenerating into a form of cancer known as neurofibrosarcoma. These masses are generally contained within a capsule, so surgical removal is often successful.Schwannomas can be associated with neurofibromatosis type II, which may be due to a loss-of-function mutation in the protein merlin.  They are universally S-100 positive, which is a marker for cells of neural crest cell origin.
Schwannomas of the head and neck are a fairly common occurrence and can be found incidentally in 3–4% of patients at autopsy. Most common of these is a vestibular schwannoma, a tumor of the vestibulocochlear nerve that may lead to tinnitus and hearing loss on the affected side </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Subacute lymphocytic thyroiditis and can you explain it in depth? [/INST] Subacute lymphocytic thyroiditis is a form of thyroiditis </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Hyperacusis and can you explain it in depth? [/INST] Hyperacusis is the increased sensitivity to sound and a low tolerance for environmental noise. Definitions of hyperacusis can vary significantly; it can refer to normal noises being perceived as: loud, annoying, painful, fear-inducing, or a combination of those, and is often categorized into four subtypes: loudness, pain, annoyance, and fear.It can be a highly debilitating hearing disorder. Hyperacusis is often coincident with tinnitus. The latter is more common and there are important differences between their involved mechanisms.Little is known about the prevalence of hyperacusis, in part due to the degree of variation in the terms definition. Reported prevalence in children and adolescents ranges from 3% to 17%.

Signs and symptoms
In hyperacusis, the symptoms are ear pain, annoyance, distortions, and general intolerance to many sounds that most people are unaffected by. Crying spells or panic attacks may result from the experience of hyperacusis. It may affect only one or both ears.  Hyperacusis can also be accompanied by tinnitus. Hyperacusis can result in anxiety, stress and phonophobia. Avoidant behavior is often a response to prevent the effects of hyperacusis and this can include avoiding social situations.

Loudness Hyperacusis
Hyperacusis is most often characterized by a sensitivity to sound, where the perception of loudness is much greater than for a typical person; it is often associated with certain volumes and/or frequencies.  Hyperacusis can occur in children and adults, and can be either "short-term" in a duration of weeks to less than a year before recovery, or, less-commonly, "long-term", spanning years and in some cases becoming permanent.  Sensitivity is often different between ears.

Noxacusis (Pain Hyperacusis)
In some instances, hyperacusis is accompanied by pain, which is known as noxacusis.  Noxacusis is characterized by pain resulting from sounds, often initiated at certain volumes or frequencies; pain can be immediate or delayed, and sometimes persists for an extended period of time following exposure.  Pain can be acute or chronic, and is often described as stabbing, burning, acid, or nerve pain, and is sometimes equated with the pain of a root canal or a broken tooth.

Loudness Discomfort Level (LDL)
The threshold of sound at which discomfort is initially experienced; measured in decibels (dB).

Setback
After a period of some relief from symptoms, discomfort resumes; often resulting from exposure to sound, or, in some cases, ototoxic medications or injuries.  Setback prevention is an important focus among those affected.

Associated conditions
Some conditions that are associated with hyperacusis include:

Causes
The most common cause of hyperacusis is overexposure to excessively high decibel (sound pressure) levels.Some affected people acquire hyperacusis suddenly as a result of taking ear sensitizing drugs, Lyme disease, Ménières disease, head injury, or surgery. Others are born with sound sensitivity, develop superior canal dehiscence syndrome, have had a history of ear infections, or come from a family that has had hearing problems. Bells palsy can trigger hyperacusis if the associated flaccid paralysis affects the tensor tympani, and stapedius, two small muscles of the middle ear. Paralysis of the stapedius muscle prevents its function in dampening the oscillations of the ossicles, causing sound to be abnormally loud on the affected side. Age may also be a significant factor.
Some psychoactive drugs such as LSD, methaqualone, or phencyclidine can cause hyperacusis. An antibiotic, ciprofloxacin, has also been seen to be a cause, known as ciprofloxacin-related hyperacusis. Benzodiazepine withdrawal syndrome is also a possible cause.

Neurophysiological mechanisms
As one important mechanism, adaptation processes in the auditory brain that influence the dynamic range of neural responses, are assumed to be distorted by irregular input from the inner ear. This is mainly caused by hearing loss related damage in the inner ear. The mechanism behind hyperacusis is not currently known, but it is suspected to be caused by damage to the inner ear and cochlea. It is theorized that type II afferent fibers become excited after damage to hair cells and synapses, triggering  a release of ATP in response </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Lassa fever and can you explain it in depth? [/INST] Lassa fever, also known as Lassa hemorrhagic fever (LHF), is a type of viral hemorrhagic fever caused by the Lassa virus. Many of those infected by the virus do not develop symptoms. When symptoms occur they typically include fever, weakness, headaches, vomiting, and muscle pains. Less commonly there may be bleeding from the mouth or gastrointestinal tract. The risk of death once infected is about one percent and frequently occurs within two weeks of the onset of symptoms. Of those who survive, about a quarter have hearing loss, which improves within three months in about half of these cases.The disease is usually initially spread to people via contact with the urine or feces of an infected multimammate mouse. Spread can then occur via direct contact between people. Diagnosis based on symptoms is difficult. Confirmation is by laboratory testing to detect the viruss RNA, antibodies for the virus, or the virus itself in cell culture. Other conditions that may present similarly include Ebola, malaria, typhoid fever, and yellow fever. The Lassa virus is a member of the Arenaviridae family of viruses.There is no vaccine. Prevention requires isolating those who are infected and decreasing contact with the mice. Other efforts to control the spread of disease include having a cat to hunt vermin, and storing food in sealed containers. Treatment is directed at addressing dehydration and improving symptoms. The antiviral medication ribavirin has been recommended, but evidence to support its use is weak.Descriptions of the disease date from the 1950s. The virus was first described in 1969 from a case in the town of Lassa, in Borno State, Nigeria. Lassa fever is relatively common in West Africa including the countries of Nigeria, Liberia, Sierra Leone, Guinea, and Ghana. There are about 300,000 to 500,000 cases which result in 5,000 deaths a year.

Signs and symptoms
Onset of symptoms is typically 7 to 21 days after exposure. In 80% of those who are infected few or no symptoms occur. These mild symptoms may include fever, tiredness, weakness, and headache. In 20% of people more severe symptoms such as bleeding gums, breathing problems, vomiting, chest pain, or dangerously low blood pressure may occur. Long term complications may include hearing loss. In those who are pregnant, miscarriage may occur in 95% of child-bearing women. Lassa fever can be difficult to distinguish clinically from other viral hemorrhagic fevers, such as Ebola virus disease. A combination of pharyngitis, pain behind the sternum, presence of excess protein in the urine and fever can indicate Lassa fever with higher specificity.In cases in which death occurs, this typically occurs within 14 days of onset. About 1% of all Lassa virus infections result in death. Approximately 15%-20% of those who have required hospitalization for Lassa fever die. The risk of death is greater in those who are pregnant. A "Swollen baby syndrome" may occur in newborns, infants and toddlers with pitting edema, abdominal distension and bleeding.

Cause
Virology
Lassa virus is a member of the Arenaviridae, a family of negative-sense, single-stranded RNA viruses. Specifically it is an old world arenavirus, which is enveloped, single-stranded, and bi-segmented RNA. This virus has both a large and a small genome section, with four lineages identified to date: Josiah (Sierra Leone), GA391 (Nigeria), LP (Nigeria) and strain AV.

Spread
Lassa virus commonly spreads to humans from other animals, specifically the Natal multimammate mouse or African rat, also called the Natal multimammate rat (Mastomys natalensis). This is probably the most common mouse in equatorial Africa, common in human households and eaten as a delicacy in some areas.The multimammate mouse can quickly produce a large number of offspring, tends to colonize human settlements, increasing the risk of rodent-human contact, and is found throughout the west, central and eastern parts of the African continent.Once the mouse has become a carrier, it will excrete the virus throughout the rest of its lifetime through feces and urine creating ample opportunity for exposure. The virus is probably transmitted by contact with the feces or urine of animals accessing grain stores in residences. No study has proven presence in breast milk, but the high level of viremia suggests it may be possible.Individuals who are at a higher risk of contracting the infection are those who live in rural areas where Mastomys are discovered, and where sanitation is not prevalent. Infection typically occurs by direct or indirect exposure to animal excrement through the respiratory or gastrointestinal tracts. Inhalation of tiny particles of infectious material (aerosol) is believed to be the most significant means of exposure. It is possible to acquire the infection through broken skin or mucous membranes that are directly exposed to infectious material. Transmission from person to person has been established, presenting a disease risk for healthcare workers. The virus is present in urine for between three and nine weeks after infection, and it can be transmitted in semen for up to three months after becoming infected.

Diagnosis
A range of laboratory investigations are performed, where possible, to diagnose the disease and assess its course and complications. The confidence of a diagnosis can be compromised if laboratory tests are not available. One comprising factor is the number of febrile illnesses present in Africa, such as malaria or typhoid fever that could potentially exhibit similar symptoms, particularly for non-specific manifestations of Lassa fever. In cases with abdominal pain, in countries where Lassa is common, Lassa fever is often misdiagnosed as appendicitis and intussusception which delays treatment with the antiviral ribavirin. In West Africa, where Lassa is most common, it is difficult to diagnose due to the absence of proper equipment to perform testing.The FDA has yet to approve a widely validated laboratory test for Lassa, but there are tests that have been able to provide definitive proof of the presence of the LASV virus. These tests include cell cultures, PCR, ELISA antigen assays, plaque neutralization assays, and immunofluorescence essays. However, immunofluorescence essays provide less definitive proof of Lassa infection. An ELISA test for antigen and Immunoglobulin M antibodies give 88% sensitivity and 90% specificity for the presence of the infection. Other laboratory findings in Lassa fever include lymphocytopenia (low white blood cell count), thrombocytopenia (low platelets), and elevated aspartate transaminase  levels in the blood. Lassa fever virus can also be found in cerebrospinal fluid.

Prevention
Control of the Mastomys rodent population is impractical, so measures focus on keeping rodents out of homes and food supplies, encouraging effective personal hygiene, storing grain and other foodstuffs in rodent-proof containers, and disposing of garbage far from the home to help sustain clean households. Gloves, masks, laboratory coats, and goggles are advised while in contact with an infected person, to avoid contact with blood and body fluids. These issues in many countries are monitored by a department of public health. In less developed countries, these types of organizations may not have the necessary means to effectively control outbreaks.

Vaccine
There is no vaccine for humans as of 2019. Researchers at the United States Army Medical Research Institute of Infectious Diseases facility had a promising vaccine candidate in 2002. They have developed a replication-competent vaccine against Lassa virus based on recombinant vesicular stomatitis virus vectors expressing the Lassa virus glycoprotein. After a single intramuscular injection, test primates have survived lethal challenge, while showing no clinical symptoms.

Treatment
Treatment is directed at addressing dehydration and improving symptoms. All persons suspected of Lassa fever infection should be admitted to isolation facilities and their body fluids and excreta properly disposed of.

Medications
The antiviral medication ribavirin has been recommended, but evidence to support its use is weak. Some evidence has found that it may worsen outcomes in certain cases. Fluid replacement, blood transfusions, and medication for low blood pressure may be required. Intravenous interferon therapy has also been used.

Pregnancy
When Lassa fever infects pregnant women late in their third trimester, inducing delivery is necessary for the mother to have a good chance of survival. This is because the virus has an affinity for the placenta and other highly vascular tissues. The fetus has only a one in ten chance of survival no matter what course of action is taken; hence, the focus is always on saving the life of the mother. Following delivery, women should receive the same treatment as other people with Lassa fever.

Prognosis
About 15–20% of hospitalized people with Lassa fever will die from the illness. The overall case fatality rate is estimated to be 1%, but during epidemics, mortality can climb as high as 50%. The mortality rate is greater than 80% when it occurs in pregnant women during their third trimester; fetal death also occurs in nearly all those cases. Abortion decreases the risk of death to the mother. Some survivors experience lasting effects of the disease, and can include partial or complete deafness.Because of treatment with ribavirin, fatality rates have declined.

Epidemiology
There are about 300,000 to 500,000 cases which result in 5,000 deaths a year. One estimate places  the number as high as 3 million cases per year.Estimates of Lassa fever are complicated by the lack of easy-available diagnosis, limited public health surveillance infrastructure, and high clustering of incidence near high intensity sampling.The infection affects females 1.2 times more than males. The age group predominantly infected is 21–30 years.

Geography
Lassa high risk areas are near the western and eastern extremes of West Africa. As of 2018, the Lassa belt includes Guinea, Nigeria, Sierra Leone and Liberia. As of 2003, 10-16% of people in Sierra Leone and Liberia admitted to hospital had the virus. The case fatality rate for those who are hospitalized for the disease is about 15-20%. Research showed a twofold increase risk of infection for those living in close proximity to someone with infection symptoms within the last year.
The high risk areas cannot be well defined by any known biogeographical or environmental breaks except for the multimammate rat, particularly Guinea (Kindia, Faranah and Nzérékoré regions), Liberia (mostly in Lofa, Bong, and Nimba counties), Nigeria (in about 10 of 36 states) and Sierra Leone (typically from Kenema and Kailahun districts).  It is less common in the Central African Republic, Mali, Senegal and other nearby countries, and less common yet in Ghana and the Democratic Republic of the Congo. Benin had its first confirmed cases in 2014, and Togo had its first confirmed cases in 2016.As of 2013, the spread of Lassa outside of West Africa had been very limited. Twenty to thirty cases had been described in Europe, as being caused by importation through infected individuals. These cases found outside of West Africa were found to have a high fatality risk because of the delay of diagnosis and treatment due to being unaware of the risk associated with the symptoms. Imported cases have not manifested in larger epidemics outside of Africa due to a lack of human to human transmission in hospital settings. An exception had occurred in 2003 when a healthcare worker became infected before the person showed clear symptoms.

Nigeria
2018 outbreak
An outbreak of Lassa fever occurred in Nigeria during 2018 and spread to 18 of the countrys states; it was the largest outbreak of Lassa recorded. On 25 February 2018, there were 1081 suspected cases and 90 reported deaths; 317 of the cases and 72 deaths were confirmed as Lassa which increased to a total of 431 reported cases in 2018.

2019 outbreak
The total cases in Nigeria in 2019 was 810 with 167 deaths, the largest case fatality rate(23.3%) until then.

2020 outbreak
The epidemic started from the second week of the January. By the tenth week the total number of cases has risen to 855 and deaths to 144, the case fatality rate of 16.8%.2021 Outbreak
On the 8th of December 2021, the Nigeria Centre for Disease Control (NCDC) was notified of the death of two persons from Lassa fever.2022 Outbreak
The epidemic took a new form, from 3 to 30 January 2022, 211 laboratory confirmed Lassa fever cases including 40 deaths (case fatality ratio: 19%) have been cumulatively reported in 14 of the 36 Nigerian states and the Federal Capital Territory across the country. In total from January until March, 132 deaths have been reported with a case fatality rate (CFR) of 19.1% which is lower than the CFR for the same period in 2021 (21.0%).

Liberia
Lassa fever is endemic in Liberia. From 1 January 2017 through 23 January 2018, 91 suspected cases were reported from six counties: Bong, Grand Bassa, Grand Kru, Lofa, Margibi, and Nimba. Thirty-three of these cases were laboratory confirmed, including 15 deaths (case fatality rate for confirmed cases = 45.4%).In February 2020, a total of 24 confirmed cases with nine associated deaths has been reported from nine health districts in six counties. Grand Bossa and Bong counties account for 20 of the confirmed cases.

History
The disease was identified in Nigeria in 1969. It is named after the town of Lassa, where it was discovered.A prominent expert in the disease, Aniru Conteh, died from the disease.

Research
The Lassa virus is one of several viruses identified by WHO as a likely cause of a future epidemic. They therefore list it for urgent research and development to develop new diagnostic tests, vaccines, and medicines.In 2007, SIGA Technologies, studied a medication in guinea pig with Lassa fever. Work on a vaccine is continuing, with multiple approaches showing positive results in animal trials.

References
Further reading

Echioya, Deborah U.; Hass, Meike; Olshlager, Stephan; Becker-Ziaja, Beate; Chukwu, Christian O. Onyebuchi; Coker, Jide; Nasidi, Abdulsalam; Ogugua, Osi-Ogdu; Gunther, Stephan; Omilabu, Sunday A. (2010). "Lassa Fever, Nigeria, 2005-2008". Emerging Infectious Diseases. 6. 16 (6): 1040–41 </s>