ORAL CAVITY

In biological anatomy, commonly referred to as the mouth, under formal names such as the oral
cavity, buccal cavity, or in Latin cavum oris, is the opening through which many animals take in
food and issue vocal sounds. It is also the cavity lying at the upper end of the alimentary canal,
bounded on the outside by the lips and inside by the pharynx and containing in higher
vertebrates the tongue and teeth. This cavity is also known as the buccal cavity, from the Latin
bucca ("cheek").
Some animal phyla, including vertebrates, have a complete digestive system, with a mouth at one
end and an anus at the other. Which end forms first in ontogeny is a criterion used to classify
animals intoprotostome and deuterostome.
In the first multicellular animals there was probably no mouth or gut and food particles were
engulfed by the cells on the exterior surface by a process known as endocytosis. The particles
became enclosed in vacuoles into which enzymes were secreted and digestion took
place intracellularly. The digestive products were absorbed into the cytoplasm and diffused into
other cells. This form of digestion is used nowadays by simple organisms such
as Amoeba andParamecium and also by sponges which, despite their large size, have no mouth
or gut and capture their food by endocytosis.
The vast majority of other multicellular organisms have a mouth and a gut, the lining of which is
continuous with the epithelial cells on the surface of the body. A few animals which live
parasitically originally had guts but have secondarily lost these structures. The original gut of
multicellular organisms probably consisted of a simple sac with a single opening, the mouth.
Many modern invertebrates have such a system, food being ingested through the mouth, partially
broken down by enzymes secreted in the gut, and the resulting particles engulfed by the other
cells in the gut lining. Indigestible waste is ejected through the mouth.
In animals at least as complex as an earthworm, the embryo forms a dent on one side,
the blastopore, which deepens to become the archenteron, the first phase in the formation of
the gut. In deuterostomes, the blastopore becomes the anus while the gut eventually tunnels
through to make another opening, which forms the mouth. In the protostomes, it used to be
thought that the blastopore formed the mouth (proto– meaning "first") while the anus formed
later as an opening made by the other end of the gut. More recent research, however, shows that
in protostomes the edges of the slit-like blastopore close up in the middle, leaving openings at
both ends that become the mouth and anus
 HALITOSIS

Halitosis, colloquially called bad breath, or fetor oris, is a symptom in which a noticeably
unpleasant odor is present on the exhaled breath. Concern about halitosis is estimated to be the
third most frequent reason for people to seekdental care, following tooth decay and gum
disease; and about 20% of the general population are reported to suffer from it to some degree.
Not all who think they have halitosis have a genuine problem. Of those who feel they have
halitosis, significant percentages (5–72%) have been reported to have no genuine halitosis when
professionally examined. Of those who have genuine halitosis, often the odor is caused
by bacteria present below the gumline and on the back of the tongue. The remaining 10% is
accounted for by many conditions, including disorders in the nasal cavity, sinuses, throat,
lungs, esophagus, stomach or elsewhere. Very rarely, halitosis can be one of many symptoms of
a serious underlying medical condition such as liver failure; but, in the vast majority of cases, the
cause is minor and can often be reduced by adjustments to oral hygiene, including brushing or
gently scraping the back of the tongue and improving the health of the gums by using dental
floss. Occasionally, however, especially if the origin of the odor is not in the mouth, halitosis can
be more difficult to diagnose and to manage successfully. Bad breath is a social taboo; and, as a
result, perceived or genuine halitosis can sometimes trigger social anxiety.
Two main classification schemes exist for halitosis, although none is universally accepted.
The Miyazaki et al. classification was originally described in 1999 in a Japanese scientific
publication, and has since been adapted to reflect North American society, especially with
regards halitophobia, The classification assumes three primary divisions of the halitosis
symptom, namely genuine halitosis, pseudohalitosis and halitophobia. This classification has
been suggested to be most widely used, but it has been criticized because it is overly simplistic
and is largely of use only to dentists rather than other specialties.

 Genuine halitosis
 A. Physiologic halitosis
 B. Pathologic halitosis
 (i) Oral
 (ii) Extra-oral
 Pseudohalitosis
 Halitophobia
The Tangerman and Winkel classification was suggested in Europe in 2002. This classification
focuses only on those cases where there is genuine halitosis, and has therefore been criticized for
being less clinically useful for dentistry when compared to the Miyazaki et al. classification.
 Intra-oral halitosis
 Extra-oral halitosis
 A. Blood borne halitosis
 (i) Systemic diseases
 (ii) Metabolic diseases
 (iii) Food
 (iv) Medication
 B. Non-blood borne halitosis
 (i) Upper respiratory tract
 (ii) Lower respiratory tract
The same authors also suggested that halitosis can be divided according to the character of the
odor into 3 groups:

 "Sulfurous or fecal" caused by volatile sulfur compounds (VSC), most notably methyl
mercaptan, hydrogen sulfide and dimethyl sulfide.
 "Fruity" caused by acetone, present in diabetes.
 "Urine-like or ammoniacal" caused by ammonia, dimethyl
amine and trimethylamine (TMA), present in trimethyl aminuria and uremia.
Based on the strengths and weaknesses of previous attempts at classification of halitosis, an
etiologic classification has now been proposed.

 Type 0 (physiologic)
 Type 1 (oral)
 Type 2 (airway)
 Type 3 (gastroesophageal)
 Type 4 (blood-borne)
 Type 5 (subjective)
Any halitosis symptom is potentially the sum of these types in any combination, superimposed
on the physiologic odor present in all healthy individuals.[8]

Differential diagnosis
Mouth
In about 90% of genuine halitosis cases, the origin of the odor is in the mouth itself. This is
known as intra-oral halitosis, oral malodor or oral halitosis.
There is an extensive list of possible causes of halitosis in the mouth alone, however by far the
most prevalent causes reported are halitogenic biofilm on the posterior dorsal tongue and
within gingival crevices and periodontal pockets (i.e. bacteria living on the back of the tongue
and below the gumline, and in the pockets created by gum disease between teeth and the gums).
Both of these main causes share a common theme of proteolytic putrefaction of sulfur containing
amino acids in dietary and salivary protein by mostly anaerobic, Gram negative bacterial species.
There are over 600 types of bacteria found in the average mouth. Some of these can produce high
levels of foul odors when incubated in the laboratory. The odors are produced mainly due to the
breakdown of proteins into individual amino acids, followed by the further breakdown of certain
amino acids to produce detectable foul gases. For example, the breakdown of cysteine and
methionine produce hydrogen sulfide and methyl mercaptan, respectively. Volatile sulfur
compounds have been shown to be statistically associated with oral malodor levels, and usually
decrease following successful treatment. Other parts of the mouth may also contribute to the
overall odor, but are not as common as the back of the tongue. These locations are, in order of
descending prevalence: inter-dental and sub-gingival niches, faulty dental work, food-impaction
areas in between the teeth, abscesses, and unclean dentures. Oral based lesions caused by viral
infections like Herpes Simplex and HPV may also contribute to bad breath.
The intensity of bad breath may differ during the day, due to eating certain foods (such
as garlic, onions, meat, fish, and cheese), smoking, and alcohol consumption. Since the mouth is
exposed to less oxygen and is inactive during the night, the odor is usually worse upon
awakening ("morning breath"). Bad breath may be transient, often disappearing following eating,
drinking, tooth brushing, flossing, or rinsing with specialized mouthwash. Bad breath may also
be persistent (chronic bad breath), which affects some 25% of the population in varying degrees.
Tongue
Normal appearance of the tongue, showing a degree of visible white coating and normal irregular
surface on the posterior dorsum.
The most common location for mouth-related halitosis is the tongue. Tongue bacteria produce
malodorous compounds and fatty acids, and account for 80 to 90% of all cases of mouth-related
bad breath. Large quantities of naturally-occurring bacteria are often found on the
posterior dorsum of the tongue, where they are relatively undisturbed by normal activity. This
part of the tongue is relatively dry and poorly cleansed, and the convoluted microbial structure of
the tongue dorsum provides an ideal habitat for anaerobic bacteria, which flourish under a
continually-forming tongue coating of food debris, dead epithelial cells, postnasal drip and
overlying bacteria, living and dead. When left on the tongue, the anaerobic respiration of such
bacteria can yield either the putrescent smell of indole, skatole, polyamines, or the "rotten egg"
smell of volatile sulfur compounds (VSCs) such as hydrogen sulfide, methyl mercaptan, Allyl
methyl sulfide, and dimethyl sulfide. The presence of halitosis-producing bacteria on the back of
the tongue is not to be confused with tongue coating. Bacteria are invisible to the naked eye, and
degrees of white tongue coating are present in most people with and without halitosis. A visible
white tongue coating does not always equal the back of the tongue as an origin of halitosis,
however a "white tongue" is thought to be a sign of halitosis. Inoral medicine generally, a white
tongue is considered a sign of several medical conditions. Patients with periodontal disease were
shown to have sixfold prevalence of tongue coating compared with normal subjects. Halitosis
patients were also shown to have significantly higher bacterial loads in this region compared to
individuals without halitosis.
The normal anatomy of the dorsal tongue surface consists of a posterior third and an anterior two
thirds. The posterior third constitutes the lingual tonsil, with cryptolymphatic units roughening
the surface of this area. Between the anterior and posterior portions of the dorsal tongue is the V
shaped line of vallate papillae. Anteriorly, the surface is even more irregular, with filiform,
fungiform and foliate papillae. This irregular surface is a perfect habitat for bacteria and it can
also trap debris. The roughly 25 cm2 area carries the heaviest bacterial loads in the oral cavity.
The posterior dorsum of the tongue is the site of greatest generation of VSC and hence usually
the greatest contributor to oral malodor. Hence, this irregular surface usually forms a coating
which can be easily removed. This coating consists of desquamated epilethia (shed skin cells
from the tongue), food debris, bacteria and their extracellular matrix. Essentially, a layer of
living and non living components referred to as a biofilm. Two conditions that may further
predispose to halitogenic biofilm on the dorsal tongue are lingua plicata (fissured or scrotal
tongue), a common condition where there are many grooves or fissures on the tongue, and lingua
villosa (hairy tongue) where the normal hair-like projections of the specializeds oral mucosa on
the dorsal tongue are longer than usual, and may even be discolored.
Gums
Gingival crevices are the small grooves between teeth and gums, and they are present in health,
although they may become inflamed when gingivitis is present. The difference between a
gingival crevice and periodontal pocket is that former is <3mm in depth and the latter is >3mm.
Periodontal pockets usually accompany periodontal disease (gum disease). There is some
controversy over the role of periodontal diseases in causing bad breath. However, advanced
periodontal disease is a common cause of severe halitosis. Waste products from the anaerobic
bacteria growing below the gumline (subgingival) have a foul smell and have been clinically
demonstrated to produce a very intense bad breath. Removal of the subgingival calculus (i.e.
tartar or hard plaque) and friable tissue has been shown to improve mouth odor considerably.
This is accomplished by subgingival scaling and root planing and irrigation with an antibiotic
mouth rinse. The bacteria that cause gingivitis and periodontal disease (periodontopathogens) are
invariably gram negative and capable of producing VSC.Methyl mercaptan is known to be the
greatest contributing VSC in halitosis that is caused by periodontal disease and gingivitis. The
level of VSC on breath has been shown to positively correlate with the depth of periodontal
pocketing, the number of pockets, and whether the pockets bleed when examined with a dental
probe. Indeed, VSC may themselves have been shown to contribute to the inflammation and
tissue damage that is characteristic of periodontal disease. However, not all patients with
periodontal disease have halitosis, and not all patients with halitosis have periodontal disease.
Although patients with periodontal disease are more likely to suffer from halitosis than the
general population, the halitosis symptom was shown to be more strongly associated with degree
of tongue coating than with the severity of periodontal disease. Another possible symptom of
periodontal disease is a bad taste, which does not necessarily accompany a malodor that is
detectable by others.
Other potential causes in the mouth
There have been myriad other reported causes of oral malodor, however these are all much less
common than the two above causes.

 Deep carious lesions (dental decay) which cause localized food impaction and stagnation
 Recent dental extraction sockets – fill with blood clot, and provide an ideal habitat for
bacterial proliferation
 Interdental food packing – (food getting pushed down between teeth) - this can be caused by
missing teeth, tilted, spaced or crowded teeth, or poorly contoured approximal dental fillings.
Food debris becomes trapped, undergoes slow bacterial putrefaction and release of
malodorous volatiles. Food packing can also cause a localized periodontal reaction,
characterized by dental pain that is relieved by cleaning the area of food packing with
interdental brush or floss.
 Acrylic dentures (plastic false teeth) inadequate denture hygiene practises such as failing to
clean and remove the prosthesis each night, may cause a malodour from the plastic itself or
from the mouth as microbiota responds to the altered environment. The plastic is actually
porous, and the fitting surface is usually irregular, sculpted to fit the edentulous oral
anatomy. These factors predispose to bacterial and yeast retention, which is accompanied by
a typical smell.
 Oral infections
 Oral ulceration
 Fasting
 Stress/anxiety
 Menstrual cycle – at mid cycle and during menstruation, increased breath VSC were reported
in women.
 Smoking – Smoking is linked with periodontal disease, which is the second most common
cause of oral malodor. Smoking also has many other negative effects on the mouth, from
increased rates of dental decay to premalignant lesions and even oral cancer.
 Alcohol
 Volatile foodstuffs e.g. onion, garlic, durian, cabbage, cauliflower and radish. Volatile
foodstuffs may leave malodorous residues in the mouth, which are the subject to bacterial
putrefaction and VSC release. However, volatile foodstuffs may also cause halitoisis via the
blood borne halitosis mechanism.
 Medication – often medications can cause xerostomia (dry mouth) which results in increased
microbial growth in the mouth.
Nose and sinuses
In this occurrence, the air exiting the nostrils has a pungent odor that differs from the oral odor.
Nasal odor may be due tosinus infections or foreign bodies.
Halitosis is often stated to be a symptom of chronic rhinosinusitis, however gold standard breath
analysis techniques have not been applied. Theoretically, there are several possible mechanisms
of both objective and subjective halitosis that may be involved.
Tonsils
There is disagreement as to the proportion of halitosis cases which are caused by conditions of
the tonsils. ]Some claim that the tonsils are the most significant cause of halitosis after the
mouth. According to one report, approximately 3% of halitosis cases were related to the
tonsils. Conditions of the tonsils which may be associated with halitosis include chronic
caseous tonsillitis (cheese-like material can be exuded from the tonsillar crypt
orifi), tonsillolithiasis (tonsil stones), and less commonly peritonsillar
abscess, actinomycosis, fungating malignancies, chondroid choristoma and inflammatory
myofibroblastic tumor.
Esophagus
The lower esophageal sphincter, which is the valve between the stomach and the esophagus, may
not close properly due to a Hiatal Hernia or GERD, allowing acid to enter the esophagus and
gases to escape to the mouth. A Zenker's diverticulum may also result in halitosis due to aging
food retained in the esophagus.
Stomach
The stomach is considered by most researchers as a very uncommon source of bad breath (except
in belching). Theesophagus is a closed and collapsed tube, and continuous flow (as opposed to a
simple burp) of gas or putrid substances from the stomach indicates a health problem such
as reflux serious enough to be bringing up stomach contents or afistula between the stomach and
the esophagus which will demonstrate more serious manifestations than just foul odor.
In the case of allyl methyl sulfide (the byproduct of garlic's digestion), odor does not come from
the stomach, since it does not get metabolized there.
Systemic diseases
There are a few systemic (non-oral) medical conditions that may cause foul breath odor, but
these are extremely infrequent in the general population. Such conditions are:

1. Fetor hepaticus: an example of a rare type of bad breath caused by chronic liver failure.
2. Lower respiratory tract infections (bronchial and lung infections).
3. Renal infections and renal failure.
 4. Carcinoma.
5. Trimethylaminuria ("fish odor syndrome," or "unclean vaginal scent syndrome").
6. Diabetes mellitus.
7. Metabolic conditions, e.g. resulting in elevated blood dimethyl sulfide.[7]
Individuals afflicted by the above conditions often show additional, more diagnostically
conclusive symptoms than bad breath alone.
Uncommon origins
According to research done by Theodoor Hendrik van de Velde in the 1920s, orgasm lead to bad
breath in females for about an hour after climax.
Halitophobia (delusional halitosis)
One quarter of the patients seeking professional advice on bad breath suffer from a highly
exaggerated concern of having bad breath, known as halitophobia, delusional halitosis, or as a
manifestation of Olfactory reference syndrome. These patients are sure that they have bad breath,
although many have not asked anyone for an objective opinion. Halitophobia may severely affect
the lives of some 0.5–1.0% of the adult population.

DENTAL CARIES
Dental caries, also known as tooth decay, cavities, or caries, is a breakdown of teeth due to activities
of 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.
 Destruction of a tooth by dental caries. This type of decay is also known as root decay.
The cause of caries is bacterial breakdown of the hard tissues of the teeth
(enamel, dentin and cementum). This occurs due to acid made from food debris or sugar on the
tooth surface. Simple sugars in food are these bacteria's 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, Sjogren's syndrome and some medications. Medications that decrease
saliva production include antihistamines and antidepressants. Caries is also associated with
poverty, poor cleaning of the mouth, and receding gums resulting in exposure of the roots of the
teeth.
Prevention includes: regular cleaning of the teeth, a diet low in sugar, and small amounts
of fluoride. Brushing the teeth twice per day and flossingbetween the teeth once a day is
recommended by many. Fluoride may be from water, salt or toothpaste among other
sources. Treating a mother's dental caries may decrease the risk in her children by decreasing the
numbers of certain bacteria. 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 2.43 billion people (36% of the population) have dental caries in their
permanent teeth. 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".
1. 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 "microcavity". 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 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,
infection can spread from the tooth to the surrounding soft tissues. Complications such
as cavernous sinus thrombosis and Ludwig angina can be life-threatening.

(A) A small spot of decay visible on the surface of a tooth. (B) The radiograph reveals an
extensive region of demineralization within the dentin (arrows). (C) A hole is discovered
on the side of the tooth at the beginning of decay removal. (D) All decay removed; ready
for a filling.
2. Cause
Four things are required for caries formation: a tooth surface (enamel or dentin), caries-
causing bacteria, fermentable carbohydrates (such as sucrose), and time. 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, andglucose.
Caries occur more often in people from the lower end of the socioeconomic scale than
people from the upper end of the socioeconomic scale.

Diagrammatic representation of acidogenic theory of causation of dental caries. Four

factors, namely, a suitable carbohydrate substrate (1), micro-organisms in dental
plaque (2), a susceptible tooth surface (3) and time(4); must be present together for dental
caries to occur (5). Saliva (6) and fluoride (7) are modifying factors
2.1 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,
no biofilm removal (a lack of toothbrushing) .If left untreated, the disease can lead to
pain, tooth loss andinfection.
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 andLactobacillus species among them. These organisms can produce high levels
of lactic acid following fermentation of dietary sugars, and are resistant to the adverse
 effects of low pH, properties essential for cariogenic bacteria. 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., andStreptococcus mutans. Bacteria collect around the teeth and gums in a sticky,
creamy-coloured mass called plaque, which serves as a biofilm. Some sites collect plaque
more commonly than others, for example sites with a low rate of salivary flow (molar
fissures). Grooves on the occlusal surfaces of molar and premolar teeth provide
microscopic retention sites for plaque bacteria, as do the interproximal sites. Plaque may
also collect above or below the gingiva, where it is referred to as supra- or sub-gingival
plaque, respectively.
These bacterial strains, most notably S. mutans, can be inherited by a child from a
caretaker's kiss or through feedingpremasticated.

o 2.1Bacteria
o 2.2Dietary sugars
o 2.3Exposure
o 2.4Teeth
o 2.5Other factors
 3Pathophysiology
o 3.1Enamel
o 3.2Dentin
o 3.3Cementum
 4Diagnosis
o 4.1Classification
o 4.2Early childhood caries
o 4.3Rate of progression
o 4.4Affected hard tissue
 5Prevention
o 5.1Oral hygiene
o 5.2Dietary modification
o 5.3Other measures
 6Treatment
 7Epidemiology
 8History
o 8.1Etymology and usage
 9Society and culture
 10Other animals
 11References
 12External links

Cause[edit]
Diagrammatic representation of acidogenic theory of causation of dental caries. Four factors,
namely, a suitable carbohydrate substrate (1), micro-organisms in dental plaque (2), a susceptible
tooth surface (3) and time(4); must be present together for dental caries to occur (5).
Saliva (6) and fluoride (7) are modifying factors
Bacteria[edit]

A gram stain image of Streptococcus mutans.

Dietary sugars[edit]
Bacteria in a person's mouth convert glucose, fructose, and most commonly sucrose (table sugar)
into acids such as lactic acid through a glycolytic process called fermentation.[21] 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.[27] If demineralization continues over time, enough mineral content may be lost
so that the soft organicmaterial left behind disintegrates, forming a cavity or hole. The impact
such sugars have on the progress of dental caries is called cariogenicity. Sucrose, although a
bound glucose and fructose unit, is in fact more cariogenic than a mixture of equal parts of
glucose and fructose. This is due to the bacteria utilising the energy in the saccharide bond
between the glucose and fructose subunits. S.mutans adheres to the biofilm on the tooth by
converting sucrose into an extremely adhesive substance called dextran polysaccharide by the
enzyme dextransucranase.[28]
Exposure[edit]
"Stephan curve", showing sudden decrease in plaque pH following glucose rinse, which returns
to normal after 30-60 min. Net demineralization of dental hard tissues occurs below the critical
pH (5.5), shown in yellow.
The frequency with which teeth are exposed to cariogenic (acidic) environments affects the
likelihood of caries development.[29] 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 salivaand 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.[30] Since teeth are vulnerable
during these acidic periods, the development of dental caries relies heavily on the frequency of
acid exposure.
The carious process can begin within days of a tooth's erupting into the mouth if the diet is
sufficiently rich in suitable carbohydrates. Evidence suggests that the introduction of fluoride
treatments has slowed the process.[31] Proximal caries take an average of four years to pass
through enamel in permanent teeth. Because thecementum enveloping the root surface is not
nearly as durable as the enamel encasing the crown, root caries tends to progress much more
rapidly than decay on other surfaces. The progression and loss of mineralization on the root
surface is 2.5 times faster than caries in enamel. In very severe cases where oral hygiene is very
poor and where the diet is very rich in fermentable carbohydrates, caries may cause cavities
within months of tooth eruption. This can occur, for example, when children continuously drink
sugary drinks from baby bottles (see later discussion).
Teeth[edit]
There are certain diseases and disorders affecting teeth that may leave an individual at a greater
risk for cavities.
Molar incisor hypomineralization, which is increasing in prevalence.[32] It is caused by systemic
factors such as high levels of dioxins or polychlorinated biphenyl (PCB) in the mother’s
milk, premature birth and oxygen deprivation at birth, and certain disorders during the child’s
first 3 years such as such as mumps, diphtheria, scarlet
fever, measles,hypoparathyroidism, malnutrition, malabsorption, hypovitaminosis D,
chronic respiratory diseases, or undiagnosed and untreated coeliac disease, which usually
presents with mild or absent gastrointestinal symptoms.[33][32][34][35][36][37]
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.[38] In both cases, teeth may be left more vulnerable to decay because the enamel is not
able to protect the tooth.[39]
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.[40] These minerals,
especially hydroxyapatite, will become soluble when exposed to acidic environments. Enamel
begins to demineralize at a pH of 5.5.[41] Dentin and cementum are more susceptible to caries
thanenamel because they have lower mineral content.[42] 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;[43][44] 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[edit]
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 mouthand thus to
widespread tooth decay. Examples include Sjögren's syndrome, diabetes mellitus, diabetes
insipidus, andsarcoidosis.[45] 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 ("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.[45] Radiation therapy of the head and neck
may also damage the cellsin salivary glands, somewhat increasing the likelihood of caries
formation.[46][47]
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.[48]
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.[49] Tobacco use is a
significant risk factor for periodontal disease, which can cause the gingiva to recede.[50] 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.[51] 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.[52] Exposure of
children to secondhand tobacco smoke is associated with tooth decay.[53]
Intrauterine and neonatal lead exposure promote tooth decay.[54][55][56][57][58][59][60] Besides lead,
all atoms with electrical charge and ionic radius similar to bivalent calcium,[61] such as cadmium,
mimic the calcium ion and therefore exposure to them may promote tooth decay.[62]
Poverty is also a significant social determinant for oral health.[63] Dental caries have been linked
with lower socio-economic status and can be considered a disease of poverty.[64]
Forms are available for risk assessment for caries when treating dental cases; this system using
the evidence-based Caries Management by Risk Assessment (CAMBRA).[65] 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.[66]

Pathophysiology[edit]

The progression of pit and fissure caries resembles two triangles with their bases meeting along
the junction of enamel and dentin.
Teeth are bathed in saliva and have a coating of bacteria on them (biofilm) that continually
forms. The minerals in the hard tissues of the teeth (enamel, dentin andcementum) are constantly
undergoing processes of demineralization andremineralisation. Dental caries results when the
demineralization rate is faster than the remineralisation 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.[67]
Enamel[edit]
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.[68]
As the enamel loses minerals, and dental caries progresses, the enamel develop several distinct
zones, visible under a light microscope. From the deepest layer of the enamel to the enamel
surface, the identified areas are the: translucent zone, dark zones, body of the lesion, and surface
zone.[69] The translucent zone is the first visible sign of caries and coincides with a one to two
percent loss of minerals.[70] 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.[71] 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[edit]
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.[72]
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.[68] The advancing
front represents a zone of demineralised 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 collage matrix is not severely damaged, giving it
potential for repair. The outer more superficial zone is highly infected with proteolytic
degradation of the collagen matrix and as a result the dentin is irreversibly demineralised.
The faster spread of caries through dentin creates this triangular appearance in smooth surface
caries.
Sclerotic dentin[edit]
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.[73] 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.[74] 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.[75] 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 andphosphorus 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.[76]Since sclerotic
dentin prevents the passage of such fluids, pain that would otherwise serve as a warning of the
invading bacteria may not develop at first. Consequently, dental caries may progress for a long
 period of time without any sensitivity of the tooth, allowing for greater loss of tooth
structure.[citation needed]
Calculus

Calculus (from Latin calculus, literally "small pebble used for counting")[1] is
the mathematical study of change, in the same way that geometry is the study of shape
and algebra is the study of operations and their application to solving equations. It has two major
branches, differential calculus (concerning rates of change and slopes of curves),[2] and integral
calculus (concerning accumulation of quantities and the areas under and between curves);[3] these
two branches are related to each other by the fundamental theorem of calculus. Both branches
make use of the fundamental notions of convergenceof infinite sequences and infinite series to a
well-defined limit. Generally, modern calculus is considered to have been developed in the 17th
century byIsaac Newton and Gottfried Leibniz. Today, calculus has widespread uses
inscience, engineering and economics[4] and can solve many problems thatelementary
algebra alone cannot.
Calculus is a part of modern mathematics education. A course in calculus is a gateway to other,
more advanced courses in mathematics devoted to the study of functions and limits, broadly
called mathematical analysis. Calculus has historically been called "the calculus
of infinitesimals", or "infinitesimal calculus". The word "calculus" comes from Latin (calculus)
and refers to a small stone used for counting. Calculus (plural calculi) is also used for naming
some methods of calculation or theories of computation, such as propositional calculus, calculus
of variations, lambda calculus, and process calculus.

Contents
[hide]

 1History
o 1.1Ancient
o 1.2Medieval
o 1.3Modern
o 1.4Foundations
o 1.5Significance
 2Principles
o 2.1Limits and infinitesimals
o 2.2Differential calculus
o 2.3Leibniz notation
o 2.4Integral calculus
o 2.5Fundamental theorem
 3Applications
 4Varieties
o 4.1Non-standard calculus
 o 4.2Smooth infinitesimal analysis
o 4.3Constructive analysis
 5See also
o 5.1Lists
o 5.2Other related topics
 6References
o 6.1Notes
o 6.2Books
 7Other resources
o 7.1Further reading
o 7.2Online books
 8External links

History[edit]
Main article: History of calculus
Modern calculus was developed in 17th-century Europe by Isaac Newton and Gottfried Wilhelm
Leibniz, but elements of it have appeared in ancient India, Greece, China, medieval Europe, and
the Middle East.
Ancient[edit]
The ancient period introduced some of the ideas that led to integral calculus, but does not seem
to have developed these ideas in a rigorous and systematic way. Calculations of volume and area,
one goal of integral calculus, can be found in theEgyptian Moscow papyrus (c. 1820 BC), but the
formulas are simple instructions, with no indication as to method, and some of them lack major
components.[5] From the age of Greek mathematics, Eudoxus (c. 408–355 BC) used the method
of exhaustion, which foreshadows the concept of the limit, to calculate areas and volumes,
while Archimedes (c. 287–212 BC)developed this idea further, inventing heuristics which
resemble the methods of integral calculus.[6] The method of exhaustion was later reinvented
in China by Liu Hui in the 3rd century AD in order to find the area of a circle.[7] In the 5th
century AD, Zu Chongzhi established a method[vague] that would later be called Cavalieri's
principle to find the volume of asphere.[8][how?]
Medieval[edit]
Indian mathematicians gave a semi-rigorous method of differentiation of some trigonometric
functions. In the Middle East,Alhazen derived a formula for the sum of fourth powers. He used
the results to carry out what would now be called anintegration, where the formulae for the sums
of integral squares and fourth powers allowed him to calculate the volume of aparaboloid.[9] In
the 14th century, Indian mathematician Madhava of Sangamagrama and the Kerala school of
astronomy and mathematics stated components of calculus such as the Taylor series and infinite
series approximations.[10] However, they were not able to "combine many differing ideas under
the two unifying themes of the derivative and the integral, show the connection between the two,
and turn calculus into the great problem-solving tool we have today".[9]
Modern[edit]
"The calculus was the first achievement of modern mathematics and it
is difficult to overestimate its importance. I think it defines more
unequivocally than anything else the inception of modern mathematics,
and the system of mathematical analysis, which is its logical
development, still constitutes the greatest technical advance in exact
thinking." —John von Neumann[11]

In Europe, the foundational work was a treatise due toBonaventura Cavalieri, who argued that
volumes and areas should be computed as the sums of the volumes and areas of infinitesimally
thin cross-sections. The ideas were similar to Archimedes' in The Method, but this treatise is
believed to have been lost in the 13th century, and was only rediscovered in the early 20th
century, and so would have been unknown to Cavalieri. Cavalieri's work was not well respected
since his methods could lead to erroneous results, and the infinitesimal quantities he introduced
were disreputable at first.
The formal study of calculus brought together Cavalieri's infinitesimals with the calculus of
finite differences developed in Europe at around the same time. Pierre de Fermat, claiming that
he borrowed from Diophantus, introduced the concept ofadequality, which represented equality
up to an infinitesimal error term.[12] The combination was achieved by John Wallis,Isaac Barrow,
and James Gregory, the latter two proving the second fundamental theorem of calculus around
1670.

Isaac Newton developed the use of calculus in his laws of motion andgravitation.
The product rule and chain rule, the notion of higher derivatives, Taylor series, andanalytical
functions were introduced by Isaac Newton in an idiosyncratic notation which he used to solve
problems of mathematical physics.[13] In his works, Newton rephrased his ideas to suit the
mathematical idiom of the time, replacing calculations with infinitesimals by equivalent
geometrical arguments which were considered beyond reproach. He used the methods of
calculus to solve the problem of planetary motion, the shape of the surface of a rotating fluid, the
oblateness of the earth, the motion of a weight sliding on a cycloid, and many other problems
discussed in his Principia Mathematica (1687). In other work, he developed series expansions
for functions, including fractional and irrational powers, and it was clear that he understood the
principles of the Taylor series. He did not publish all these discoveries, and at this time
infinitesimal methods were still considered disreputable.

Gottfried Wilhelm Leibniz was the first to publish his results on the development of calculus.

These ideas were arranged into a true calculus of infinitesimals by Gottfried Wilhelm Leibniz,
who was originally accused of plagiarism by Newton.[14]He is now regarded as an independent
inventor of and contributor to calculus. His contribution was to provide a clear set of rules for
working with infinitesimal quantities, allowing the computation of second and higher
derivatives, and providing the product rule and chain rule, in their differential and integral forms.
Unlike Newton, Leibniz paid a lot of attention to the formalism, often spending days determining
appropriate symbols for concepts.
Leibniz and Newton are usually both credited with the invention of calculus. Newton was the
first to apply calculus to general physics and Leibniz developed much of the notation used in
calculus today. The basic insights that both Newton and Leibniz provided were the laws of
differentiation and integration, second and higher derivatives, and the notion of an approximating
polynomial series. By Newton's time, the fundamental theorem of calculus was known.
When Newton and Leibniz first published their results, there was great controversy over which
mathematician (and therefore which country) deserved credit. Newton derived his results first
(later to be published in his Method of Fluxions), but Leibniz published his Nova Methodus pro
Maximis et Minimis first. Newton claimed Leibniz stole ideas from his unpublished notes, which
Newton had shared with a few members of the Royal Society. This controversy divided English-
speaking mathematicians from continental European mathematicians for many years, to the
detriment of English mathematics. A careful examination of the papers of Leibniz and Newton
shows that they arrived at their results independently, with Leibniz starting first with integration
and Newton with differentiation. Today, both Newton and Leibniz are given credit for
developing calculus independently. It is Leibniz, however, who gave the new discipline its name.
Newton called his calculus "the science of fluxions".
Since the time of Leibniz and Newton, many mathematicians have contributed to the continuing
development of calculus. One of the first and most complete works on both infinitesimal
and integral calculus was written in 1748 by Maria Gaetana Agnesi.[15][16]

Maria Gaetana Agnesi

Foundations[edit]
In calculus, foundations refers to the rigorous development of the subject from axioms and
definitions. In early calculus the use of infinitesimal quantities was thought unrigorous, and was
fiercely criticized by a number of authors, most notably Michel Rolle and Bishop Berkeley.
Berkeley famously described infinitesimals as the ghosts of departed quantities in his book The
Analyst in 1734. Working out a rigorous foundation for calculus occupied mathematicians for
much of the century following Newton and Leibniz, and is still to some extent an active area of
research today.
Several mathematicians, including Maclaurin, tried to prove the soundness of using
infinitesimals, but it would not be until 150 years later when, due to the work
of Cauchy andWeierstrass, a way was finally found to avoid mere "notions" of infinitely small
quantities.[17] The foundations of differential and integral calculus had been laid. In
Cauchy's Cours d'Analyse, we find a broad range of foundational approaches, including a
definition of continuity in terms of infinitesimals, and a (somewhat imprecise) prototype of an (ε,
δ)-definition of limit in the definition of differentiation. In his work Weierstrass formalized the
concept of limit and eliminated infinitesimals. Following the work of Weierstrass, it eventually
became common to base calculus on limits instead of infinitesimal quantities, though the subject
is still occasionally called "infinitesimal calculus". Bernhard Riemann used these ideas to give a
precise definition of the integral. It was also during this period that the ideas of calculus were
generalized to Euclidean space and the complex plane.
In modern mathematics, the foundations of calculus are included in the field of real analysis,
which contains full definitions and proofs of the theorems of calculus. The reach of calculus has
also been greatly extended. Henri Lebesgue inventedmeasure theory and used it to define
integrals of all but the most pathological functions. Laurent Schwartz introduceddistributions,
which can be used to take the derivative of any function whatsoever.
Limits are not the only rigorous approach to the foundation of calculus. Another way is to
use Abraham Robinson's non-standard analysis. Robinson's approach, developed in the 1960s,
uses technical machinery from mathematical logic to augment the real number system
with infinitesimal and infinite numbers, as in the original Newton-Leibniz conception. The
resulting numbers are called hyperreal numbers, and they can be used to give a Leibniz-like
development of the usual rules of calculus.
Significance[edit]
While many of the ideas of calculus had been developed earlier in Greece, China, India, Iraq,
Persia, and Japan, the use of calculus began in Europe, during the 17th century, when Isaac
Newton and Gottfried Wilhelm Leibniz built on the work of earlier mathematicians to introduce
its basic principles. The development of calculus was built on earlier concepts of instantaneous
motion and area underneath curves.
Applications of differential calculus include computations involving velocity and acceleration,
the slope of a curve, andoptimization. Applications of integral calculus include computations
involving area, volume, arc length, center of mass, work, and pressure. More advanced
applications include power series and Fourier series.
Calculus is also used to gain a more precise understanding of the nature of space, time, and
motion. For centuries, mathematicians and philosophers wrestled with paradoxes
involving division by zero or sums of infinitely many numbers. These questions arise in the
study of motion and area. The ancient Greek philosopher Zeno of Elea gave several famous
examples of such paradoxes. Calculus provides tools, especially the limit and the infinite series,
which resolve the paradoxes.
 Abscess
his article is about the medical condition. For the death metal band, see Abscess (band).

Abscess

Five-day-old abscess. The black dot is a

clogged hair follicle.

Classification and external resources

Specialty General surgery, infectious disease

ICD-10 L02

ICD-9-CM 682.9, 324.1

MedlinePlus 001353

MeSH D000038

[edit on Wikidata]
 An abscess (Latin: abscessus) is a collection of pus that has built up within the tissue of the
body.[1] Signs and symptoms of abscesses include redness, pain, warmth, and swelling.[1] The
swelling may feel fluid filled when pressed.[1]The area of redness often extends beyond the
swelling.[2] Carbuncles andboils are types of abscess that often involve hair follicles with
carbuncles being larger.[3]
They are usually caused by a bacterial infection.[4] Often many different types of bacteria are
involved in a single infection.[2] In the United States and many other areas of the world the most
common bacteria present is methicillin-resistant Staphylococcus aureus.[1] Rarely, parasites can
cause abscesses and this is more common in the developing world.[5] Diagnosis of a skin abscess
is usually made based on what it looks like and is confirmed by cutting it
open.[1] Ultrasound imaging may be useful in cases in which the diagnosis is not clear.[1] In
abscesses around the anus, computer tomography (CT) may be important to look for deeper
infection.[5]
Standard treatment for most skin or soft tissue abscesses is cutting it open and drainage.[6] There
does not appear to be any benefit from also usingantibiotics for this type of abscess in most
people who are otherwise healthy.[1][7] A small amount of evidence supports not packing the
cavity that remains with gauze after drainage.[1] Closing this cavity right after draining it rather
than leaving it open may speed healing without increasing the risk of the abscess
returning.[8] Sucking out the pus with a needle is often not sufficient.[1]
Skin abscesses are common and have become more common in recent years.[1] Risk factors
include intravenous drug usewith rates reported as high as 65% in this population.[9] In 2005 in
the United States 3.2 million people went to the emergency department for an abscess.[10] In
Australia around 13,000 people were hospitalized in 2008 with the condition.[11]

Contents
[hide]

 1Signs and symptoms

 2Causes
o 2.1Perianal abscess
o 2.2Incisional abscess
 3Pathophysiology
 4Diagnosis
o 4.1Classification
o 4.2IV drug use
o 4.3Differential
 5Treatment
 o 5.1Incision and drainage
o 5.2Antibiotics
o 5.3Packing
o 5.4Loop Drainage
o 5.5Primary closure
 6Prognosis
 7Epidemiology
 8Society and culture
o 8.1Etymology
o 8.2Other types
 9References
 10External links

Signs and symptoms[edit]

An abscess

Abscesses may occur in any kind of solid tissue but most frequently on skin surface (where they
may be superficial pustules (boils) or deep skin abscesses), in the lungs, brain, teeth, kidneys and
tonsils. Major complications are spreading of the abscess material to adjacent or remote tissues
and extensive regional tissue death (gangrene).
The main symptoms and signs of a skin abscess are redness, heat, swelling, pain and loss of
function. There may also be high temperature (fever) and chills.[12]
An internal abscess is more difficult to identify, but signs include pain in the affected area, a high
temperature, and generally feeling unwell. Internal abscesses rarely heal themselves, so prompt
medical attention is indicated if such an abscess is suspected. An abscess could potentially be
fatal (although this is rare) if it compresses vital structures such as the trachea in the context of a
deep neck abscess.[citation needed]
If superficial, abscesses may be fluctuant when palpated. This is a wave-like motion that is
caused by movement of the pus inside the abscess.[13]

Causes[edit]
Risk factors for abscess formation include intravenous drug use.[14] Another possible risk factor
is a prior history of disc herniation or other spinal abnormality,[15] though this has not been
proven.
Abscesses are caused by bacterial infection, parasites, or foreign substances. Bacterial infection
is the most common cause.[4] Often many different types of bacteria are involved in a single
infection.[2] In the United States and many other areas of the world the most common bacteria
present is methicillin-resistant Staphylococcus aureus.[1] Among spinal subdural abscesses,
methicillin-sensitive Staphylococcus aureus is the most common organism involved.[15]
Rarely parasites can cause abscesses and this is more common in the developing
world.[5] Specific parasites known to do this include: dracunculiasis and myiasis.[5]
Perianal abscess[edit]
See also: Anorectal abscess
Surgery of the anal fistula to drain an abscess treats the fistula and reduces likelihood of its
recurrence and the need for repeated surgery.[16] There is no evidence that fecal incontinence is a
consequence of this surgery for abscess drainage.[16]
Perianal abscesses can be seen in patients with for example inflammatory bowel disease (such
as Crohn's disease) ordiabetes. Often the abscess will start as an internal wound caused by
ulceration, hard stool or penetrative objects with insufficient lubrication. This wound typically
becomes infected as a result of the normal presence of feces in the rectal area, and then develops
into an abscess. This often presents itself as a lump of tissue near the anus which grows larger
and more painful with time. Like other abscesses, perianal abscesses may require prompt
medical treatment, such as an incision and debridement or lancing.
Incisional abscess[edit]
An incisional abscess is one that develops as a complication secondary to a surgical incision. It
presents as redness and warmth at the margins of the incision with purulent drainage from
it.[17] If the diagnosis is uncertain, the wound should be aspirated with a needle, with aspiration
of pus confirming the diagnosis and availing for Gram stain and bacterial culture.[17]

Pathophysiology[edit]
A diagram of an abscess

An abscess is a defensive reaction of the tissue to prevent the spread of infectious materials to
other parts of the body.
The organisms or foreign materials kill the local cells, resulting in the release ofcytokines. The
cytokines trigger an inflammatory response, which draws large numbers of white blood cells to
the area and increases the regional blood flow.
The final structure of the abscess is an abscess wall, or capsule, that is formed by the adjacent
healthy cells in an attempt to keep the pus from infecting neighboring structures. However, such
encapsulation tends to prevent immune cells from attacking bacteria in the pus, or from reaching
the causative organism or foreign object.

Diagnosis[edit]

Ultrasound image of breast abscess, appearing as a mushroom-shaped dark (hypoechoic) area

An abscess is a localized collection of pus (purulent inflammatory tissue) caused by suppuration

buried in a tissue, an organ, or a confined space, lined by pyogenic membrane.[18]
Classification[edit]
Abscesses may be classified as either skin abscesses or internal abscesses. Skin abscesses are
common; internal abscesses tend to be harder to diagnose, and more serious.[12] Skin abscesses
are also called cutaneous or subcutaneous abscesses.[19]
IV drug use[edit]
For those with a history of intravenous drug use, an X-ray is recommended before treatment to
verify that no needle fragments are present.[14] In this population if there is also a fever
present infectious endocarditis should be considered.[14]
Differential[edit]
Abscesses should be differentiated from empyemas, which are accumulations of pus in a
preexisting rather than a newly formed anatomical cavity.
Other conditions that can cause similar symptoms include: cellulitis, a sebaceous
cyst and necrotising fasciitis.[5] Cellulitis typically also has an erythematous reaction, but does
not confer any purulent drainage.[17]

Treatment[edit]
The standard treatment for an uncomplicated skin or soft tissue abscess is opening and
draining.[6] There does not appear to be any benefit from also using antibiotics in most cases.[1] A
small amount of evidence did not find benefit from packing the abscess with gauze.[1]
Incision and drainage[edit]
See also: Incision and drainage

Abscess five days after incision and drainage

Abscess following curettage

The abscess should be inspected to identify if foreign objects are a cause, which may require
their removal. If foreign objects are not the cause, incising and draining the abscess is standard
treatment.[6][20]
In critical areas where surgery presents a high risk, it may be delayed or used as a last resort. The
drainage of a lung abscess may be performed by positioning the patient in a way that enables the
contents to be discharged via the respiratory tract. Warm compresses and elevation of the limb
may be beneficial for a skin abscess.
Antibiotics[edit]
Most people who have an uncomplicated skin abscess should not use antibiotics.[6]Antibiotics in
addition to standard incision and drainage is recommended in persons with severe abscesses,
many sites of infection, rapid disease progression, the presence of cellulitis, symptoms indicating
bacterial illness throughout the body, or a health condition causing immunosuppression.[1] People
who are very young or very old may also need antibiotics.[1] If the abscess does not heal only
with incision and drainage, or if the abscess is in a place that is difficult to drain such as the face,
hands, or genitals, then antibiotics may be indicated.[1]
In those cases of abscess which do require antibiotic treatment, Staphylococcus aureus bacteria is
a common cause and an anti-staphylococcus antibiotic such asflucloxacillin or dicloxacillin is
used. The Infectious Diseases Society of Americaadvises that the draining of an abscess is not
enough to address community-acquired methicillin-resistant Staphylococcus aureus (MRSA),
and in those cases, traditional antibiotics may be ineffective.[1] Alternative antibiotics effective
against community-acquired MRSA often includeclindamycin, doxycycline, minocycline,
and trimethoprim-sulfamethoxazole.[1] The American College of Emergency Physicians advises
that typical cases of abscess from MRSA get no benefit from having antibiotic treatment in
addition to the standard treatment.[6] If the condition is thought to be cellulitis rather than
abscess, consideration should be given to possibility of strep species as cause that are still
sensitive to traditional anti-staphylococcus agents such as dicloxacillin or cephalexin in patients
able to tolerate penicillin. Antibiotic therapy alone without surgical drainage of the abscess is
seldom effective due to antibiotics often being unable to get into the abscess and their
ineffectiveness at low pH levels.
Culturing the wound is not needed if standard follow-up care can be provided after the incision
and drainage.[6] Performing a wound culture is unnecessary because it rarely gives information
which can be used to guide treatment.[6]
Packing[edit]
In North America, after drainage, an abscess cavity is often packed, perhaps with cloth, in an
attempt to protect the healing wound. However, evidence from emergency medicine literature
reports that packing wounds after draining causes pain to the person and does not decrease the
rate of recurrence, bring more rapid healing, or lead to fewer physician visits.[21]
Loop Drainage[edit]
More recently, several North American hospitals have opted for less-invasive loop drainage over
standard drainage and wound packing. In one study of 143 pediatric outcomes, a failure rate of
1.4% was reported in the loop group versus 10.5% in the packing group (P<.030),[22] while a
separate study reported a 5.5% failure rate among loop patients.[23]
Primary closure[edit]
Closing an abscess immediately after draining it appears to speed healing without increasing the
risk of recurrence.[8] This may not apply to anorectal abscesses. While they heal faster, there may
be a higher rate of recurrence than those left open.[24]

Prognosis[edit]
Even without treatment they rarely result in death as they will naturally break through the skin.[5]

Epidemiology[edit]
Skin abscesses are common and have become more common in recent years.[1] Risk factors
include intravenous drug usewith rates reported as high as 65% in this population.[9] In 2005 in
the United States 3.2 million people went to the emergency department for an abscess.[10] In
Australia around 13,000 people were hospitalized in 2008 for the disease.[11]

Society and culture[edit]

The Latin medical aphorism "ubi pus, ibi evacua" expresses "where there is pus, there evacuate
it" and is classical advice in the culture of Western medicine.
Needle exchange programmes often administer or provide referrals for abscess treatment
to injection drug users as part of a harm reduction public health strategy.[25][26]
Etymology[edit]
An abscess is so called because there is an abscessus (a going away or departure) of portions of
the animal tissue from each other to make room for the suppurated matter lodged between
them.[27]
The word carbuncle is believed to have originated from the Latin: carbunculus, originally a
small coal; diminutive of carbon-,carbo: charcoal or ember, but also a carbuncle stone, "precious
stones of a red or fiery colour", usually garnet

Cyst
From Wikipedia, the free encyclopedia

This article is about cysts in the body. For the ICAO airport code CYST, see St. Theresa Point
Airport. For hard-shelled resting stages of some small organisms, see Microbial cyst.

Cyst

Micrograph of a mediastinal bronchogenic

cyst.H&E stain.

Classification and external resources

Specialty Pathology, general surgery

MedlinePlus 007675

MeSH D003560

[edit on Wikidata]
A cyst is a closed sac, having a distinct membrane and division compared to the nearby tissue.
Hence, it is a cluster of cells that have grouped together to form a sac (not unlike the manner in
which water molecules group together, forming a bubble); however, the distinguishing aspect of
a cyst is that the cells forming the "shell" of such a sac are distinctly abnormal (in both
appearance and behaviour) when compared to all surrounding cells for that given location. It
may contain air, fluids, or semi-solid material. A collection of pus is called anabscess, not a cyst.
Once formed, a cyst may sometimes resolve on its own. When a cyst fails to resolve it may need
to be removed by surgery but this will depend on what type of cyst it is and where in the body it
has formed.
Some cysts are neoplastic and are thus called cystic tumors; many types are not neoplastic. Some
are dysplastic or metaplastic. Pseudocysts are similar to cysts (having a sac filled with fluid) but
lack an epithelial lining.
Gingivitis
From Wikipedia, the free encyclopedia

Gingivitis

A case of gingivitis

Classification and external resources

Specialty Dentistry

ICD-10 K05.0-K05.1

ICD-9-CM 523.0-523.1

DiseasesDB 34517

MedlinePlus 001056
 eMedicine article/763801

MeSH D005891

[edit on Wikidata]

Gingivitis ("inflammation of the gum tissue") is a non-destructive periodontal disease.[1] The

most common form of gingivitis, and the most common form ofperiodontal disease overall, is in
response to bacterial biofilms (also calledplaque) adherent to tooth surfaces, termed plaque-
induced gingivitis. Gingivitis is reversible with good oral hygiene. However, in the absence of
treatment, or if not controlled, gingivitis can progress to periodontitis, where the inflammation
results in tissue destruction and alveolar bone resorption, which can ultimately lead to tooth
loss.[2]
While some cases of gingivitis never progress to periodontitis,[3] data indicate that periodontitis
is always preceded by gingivitis.[4]

Contents
[hide]

 1Signs and symptoms

 2Risk factors
 3Cause
 4Diagnosis
o 4.1Classification
 5Prevention
 6Treatment
 7Complications
 8See also
 9References
 10External links

Signs and symptoms[edit]

Gingivitis
The symptoms of gingivitis are somewhat non-specific and manifest in the gum tissue as
the classic signs of inflammation:

 Swollen gums
 Bright red or purple gums
 Gums that are tender or painful to the touch
 Bleeding gums or bleeding after brushing and/or flossing
 Bad breath (halitosis)
Additionally, the stippling that normally exists on the gum tissue of some individuals will often
disappear and the gums may appear shiny when the gum tissue becomes swollen and stretched
over the inflamed underlying connective tissue. The accumulation may also emit an unpleasant
odor. When the gingiva are swollen, the epithelial lining of the gingival crevice
becomes ulcerated and the gums will bleed more easily with even gentle brushing, and especially
when flossing.

Risk factors[edit]
Risk factors associated with gingivitis are:

 low dental care utilization

 poor oral hygiene levels
 smoking
 psychosocial stress and genetic factors
 pre-existing conditions

Cause[edit]
Because plaque-induced gingivitis is by far the most common form of gingival diseases, the
following sections will deal primarily with this condition.

The etiology, or cause, of plaque-induced gingivitis is bacterial plaque, which acts to initiate the
body's host response. This, in turn, can lead to destruction of the gingival tissues, which may
progress to destruction of the periodontal attachment apparatus.[5] The plaque accumulates in the
small gaps between teeth, in the gingival grooves and in areas known asplaque traps: locations
that serve to accumulate and maintain plaque. Examples of plaque traps include bulky and
overhanging restorative margins, claps of removable partial dentures and calculus (tartar) that
forms on teeth. Although these accumulations may be tiny, the bacteria in them produce
chemicals, such as degrative enzymes, and toxins, such aslipopolysaccharide (LPS, otherwise
known as endotoxin) or lipoteichoic acid (LTA), that promote an inflammatory response in the
gum tissue. This inflammation can cause an enlargement of the gingiva and subsequent
formation. Early plaque in health consists of a relatively simple bacterial community dominated
by Gram-positive cocci and rods. As plaque matures, and gingivitis develops, the communities
become increasingly complex with higher proportions of Gram-negative rods, fusiforms,
filaments, spirilla and spirochetes. Later experimental gingivitis studies, using culture, provided
more information regarding the specific bacterial species present in plaque. Taxa associated with
gingivitis included Fusobacterium nucleatum subsp. polymorphum, Lachnospiraceae [G-2] sp.
HOT100, Lautropia sp. HOTA94, and Prevotella oulorum, whilst Rothia dentocariosa was
associated with periodontal health.[6] Further study of these taxa is warranted and may lead to
new therapeutic approaches to prevent periodontal disease.

Diagnosis[edit]
Gingivitis is a category of periodontal disease where there is no loss of bone but there is presence
of inflammation and bleeding.
Each tooth is divided into four gingival units (mesial, distal, buccal, and lingual) and given a
score from 0-3 based on the gingival index. The four scores are then averaged to give each tooth
a single score.
The diagnosis of the periodontal disease gingivitis is done by a dentist. The diagnosis is based on
clinical assessment data acquired during a comprehensive periodontal exam. Either a registered
dental hygienist or a dentist may perform the comprehensive periodontal exam but the data
interpretation and diagnosis is done by the dentist. The comprehensive periodontal exam consists
of a visual exam, a series of radiographs, probing of the gingiva, determining the extent of
current or past damage to the periodontium and a comprehensive review of the medical and
dental histories.
Current research shows that activity levels of the following enzymes in saliva samples are
associated with periodontal destruction: asparatate aminotransferase (AST), alanine
aminotransferase (ALT), gamma glutamyl transferase (GGT), alkaline phosphatase (ALP), and
acid phosphatase (ACP). Therefore, these enzyme biomarkers may be used to aid in the
diagnosis and treatment of gingivitis and periodontitis.
A dental hygienist or dentist will check for the symptoms of gingivitis, and may also examine the
amount of plaque in the oral cavity. A dental hygienist or dentist will also look for signs
of periodontitis using X-rays or periodontal probing as well as other methods.
If gingivitis is not responsive to treatment, referral to a periodontist (a specialist in diseases of
the gingiva and bone around teeth and dental implants) for further treatment may be necessary.
Classification[edit]
As defined by the 1999 World Workshop in Clinical Periodontics, there are two primary
categories of gingival diseases, each with numerous subgroups:[7]

1. Dental plaque-induced gingival diseases.

1. Gingivitis associated with plaque only
2. Gingival diseases modified by systemic factors
3. Gingival diseases modified by medications
4. Gingival diseases modified by malnutrition
2. Non-plaque-induced gingival lesions
1. Gingival diseases of specific bacterial origin
2. Gingival diseases of viral origin
3. Gingival diseases of fungal origin
4. Gingival diseases of genetic origin
5. Gingival manifestations of systemic conditions
6. Traumatic lesions
 7. Foreign body reactions
8. Not otherwise specified

Prevention[edit]
Gingivitis can be prevented through regular oral hygiene that includes
daily brushing and flossing.[8] Hydrogen peroxide,saline, alcohol or chlorhexidine mouth
washes may also be employed. In a 2004 clinical study, the beneficial effect of hydrogen
peroxide on gingivitis has been highlighted.[9]
Rigorous plaque control programs along with periodontal scaling and curettage also have proved
to be helpful, although according to the American Dental Association, periodontal
scaling and root planing are considered as a treatment for periodontal disease, not as a preventive
treatment for periodontal disease.[10] In a 1997 review of effectiveness data, the U.S. Food and
Drug Administration (FDA) found clear evidence showing that toothpaste
containing triclosan was effective in preventing gingivitis.[11]

Treatment[edit]

Gingivitis before (top) and after (bottom) a thorough mechanical debridement of the teeth.

Analgesic and antiseptic gum paint with applicator buds used in treatment of gingivitis
The focus of treatment is to remove plaque. Therapy is aimed at the reduction of oral bacteria,
and may take the form of regular periodic visits to a dental professional together with adequate
oral hygiene home care. Thus, several of the methods used in the prevention of gingivitis can
also be used for the treatment of manifest gingivitis, such as scaling, root
planing, curettage, mouth washescontaining chlorhexidine or hydrogen peroxide, and flossing.
Interdental brushes also help remove any causative agents.
Powered toothbrushes work better than manual toothbrushes in reducing the disease.[12]
The active ingredients approved by the American Dental Association that "reduce plaque and
demonstrate effective reduction of gingival inflammation over a period of time" are triclosan,
chlorhexidine digluconate, and a combination of thymol, menthol, eucalyptol and methyl
salicylate. These ingredients are found in toothpaste and mouthwash. Hydrogen peroxide was
long considered a suitable over-the-counter agent to treat gingivitis. There has been evidence to
show the positive effect on controlling gingivitis in short-term use. A study indicates the
fluoridated hydrogen peroxide-based mouth rinse can remove teeth stain and reduce gingivitis.
Mouthwashes with essential oils are also useful.[13]
The bacteria that causes gingivitis can be controlled by using an oral irrigator daily with a
mouthwash containing an antibiotic. Either amoxicillin, cephalexin, orminocycline in 16 ounces
of a non-alcoholic fluoride mouthwash is an effective mixture.[14]
Overall, intensive oral hygiene care has been shown to improve gingival health in individuals
with well-controlled type 2 diabetes. Periodontal destruction is also slowed down due to the
extensive oral care. Intensive oral hygiene care (oral health education plus supra-gingival
scaling) without any periodontal therapy improves gingival health, and may prevent progression
of gingivitis in well-controlled diabetes.
Periodontitis
From Wikipedia, the free encyclopedia

"Pyorrhea" redirects here. For the Polish band, see Pyorrhoea. For urine containing pus,
see Pyuria.

Periodontitis

This radiograph shows significant bone loss between

the two roots of a tooth (black region). The spongy
bone has receded due to infection under tooth,
reducing the bony support for the tooth.
 Classification and external resources

Pronunciation Periodontitis/ˌpɛrioʊdɒnˈtaɪtɪs/,
pyorrhea /ˌpaɪəˈriə/

Specialty Dentistry

ICD-10 K05.4

DiseasesDB 29362

MedlinePlus 001059

MeSH D010518

[edit on Wikidata]

Periodontitis, also known as pyorrhea, is a set of inflammatory diseasesaffecting

the periodontium, i.e., the tissues that surround and support theteeth. Periodontitis involves
progressive loss of the alveolar bone around the teeth, and if left untreated, can lead to the
loosening and subsequent loss of teeth. Periodontitis is caused by microorganisms that adhere to
and grow on the tooth's surfaces, along with an over-aggressive immune response against these
microorganisms. A diagnosis of periodontitis is established by inspecting the soft gum
tissues around the teeth with a probe (i.e., a clinical examination) and by evaluating the
patient's X-ray films (i.e., a radiographic examination), to determine the amount of bone loss
around the teeth.[1] Specialists in the treatment of periodontitis are periodontists; their field is
known as "periodontology" or "periodontics".

Contents
[hide]

 1Classification
o 1.1Extent
o 1.2Severity
 2Signs and symptoms
 3Associated medical conditions
 4Causes
 5Mechanism
 6Prevention
 7Management
 o 7.1Initial therapy
o 7.2Reevaluation
o 7.3Surgery
o 7.4Maintenance
o 7.5Alternative treatments
 8Prognosis
 9Epidemiology
 10Society and culture
o 10.1Etymology
o 10.2Economics
 11Other animals
 12See also
 13Footnotes
 14External links

Classification[edit]
The 1999 classification system for periodontal diseases and conditions listed seven major
categories of periodontal diseases,[2] of which 2-6 are termed destructive periodontal disease,
because the damage is essentially irreversible. The seven categories are as follows:

1. Gingivitis
2. Chronic periodontitis
3. Aggressive periodontitis
4. Periodontitis as a manifestation of systemic disease
5. Necrotizing ulcerative gingivitis/periodontitis
6. Abscesses of the periodontium
7. Combined periodontic-endodontic lesions
Moreover, terminology expressing both the extent and severity of periodontal diseases are
appended to the terms above to denote the specific diagnosis of a particular patient or group of
patients.
Extent[edit]
The "extent" of disease refers to the proportion of the dentition affected by the disease in terms
of percentage of sites. Sites are defined as the positions at which probing measurements are taken
around each tooth and, generally, six probing sites around each tooth are recorded, as follows:

1. mesiobuccal
2. midbuccal
3. distobuccal
4. mesiolingual
5. midlingual
6. distolingual
If up to 30% of sites in the mouth are affected, the manifestation is classified as "localized"; for
more than 30%, the term "generalized" is used.
Severity[edit]
The "severity" of disease refers to the amount of periodontal ligament fibers that have been lost,
termed "clinical attachment loss". According to the American Academy of Periodontology, the
classification of severity is as follows:[3]

 Mild: 1–2 mm (0.039–0.079 in) of attachment loss

 Moderate: 3–4 mm (0.12–0.16 in) of attachment loss
 Severe: ≥ 5 mm (0.20 in) of attachment loss

Signs and symptoms[edit]

1: Total loss of attachment (clinical attachment loss, CAL) is the sum of 2: Gingival recession,
and 3: Probing depth
In the early stages, periodontitis has very few symptoms, and in many individuals the disease has
progressed significantly before they seek treatment.
Symptoms may include:

 Redness or bleeding of gums while brushing teeth, using dental floss or biting into hard food
(e.g., apples) (though this may occur even in gingivitis, where there is no attachment loss)
 Gum swelling that recurs
 Spitting out blood after brushing teeth
 Halitosis, or bad breath, and a persistent metallic taste in the mouth
 Gingival recession, resulting in apparent lengthening of teeth. (This may also be caused by
heavy-handed brushing or with a stiff tooth brush.)
 Deep pockets between the teeth and the gums (pockets are sites where the attachment has
been gradually destroyed by collagen-destroying enzymes, known as collagenases)
 Loose teeth, in the later stages (though this may occur for other reasons, as well)
Patients should realize gingival inflammation and bone destruction are largely painless. Hence,
people may wrongly assume painless bleeding after teeth cleaning is insignificant, although this
may be a symptom of progressing periodontitis in that patient.
Associated medical conditions[edit]
Periodontitis has been linked to increased inflammation in the body, such as indicated by raised
levels of C-reactive proteinand interleukin-6.[4][5][6][7] It is linked through this to increased risk
of stroke,[8][9] myocardial infarction,[10] andatherosclerosis.[11][12][13][14][15][16][17] It also linked in
those over 60 years of age to impairments in delayed memory and calculation
abilities.[18][19] Individuals with impaired fasting glucose and diabetes mellitus have higher
degrees of periodontal inflammation, and often have difficulties with balancing
their blood glucose level owing to the constant systemic inflammatory state, caused by the
periodontal inflammation.[20][21] Although no causal association was proven, a recent study
showed correlation between chronic periodontitis and erectile dysfunction.[22]

Causes[edit]
Periodontitis is an inflammation of the periodontium, i.e., the tissues that support the teeth. The
periodontium consists of four tissues:

 gingiva, or gum tissue,

 cementum, or outer layer of the roots of teeth,
 alveolar bone, or the bony sockets into which the teeth are anchored, and
 periodontal ligaments (PDLs), which are the connective tissue fibers that run between the
cementum and the alveolar bone.

This X-ray film displays two lone-standing mandibular teeth, the lower left first premolar and
canine, exhibiting severe bone loss of 30–50%. Widening of the periodontal
ligament surrounding the premolar is due to secondary occlusal trauma.
The primary etiology (cause) of gingivitis is poor or ineffective oral hygiene, which leads to the
accumulation of a mycotic[23][24][25][26] and bacterial matrix at the gum line, called dental plaque.
Other contributors are poor nutrition and underlying medical issues such
as diabetes.[27] Diabetics must be meticulous with their homecare to control periodontal
disease.[28] New finger prick tests have been approved by the Food and Drug Administration in
the US, and are being used in dental offices to identify and screen patients for possible
contributory causes of gum disease, such as diabetes.
In some people, gingivitis progresses to periodontitis –- with the destruction of thegingival
fibers, the gum tissues separate from the tooth and deepened sulcus, called a periodontal pocket.
Subgingival micro-organisms (those that exist under the gum line) colonize the periodontal
pockets and cause further inflammation in the gum tissues and progressive bone loss. Examples
of secondary etiology are those things that, by definition, cause microbic plaque accumulation,
such as restoration overhangs and root proximity.

The excess restorative material that exceeds the natural contours of restored teeth, such as these,
are termed "overhangs", and serve to trap microbic plaque, potentially leading to localized
periodontitis.
Smoking is another factor that increases the occurrence of periodontitis, directly or
indirectly,[29][30][31] and may interfere with or adversely affect its treatment.[32][33][34]
Ehlers–Danlos syndrome is a periodontitis risk factor and so is the Papillon-Lefèvre
syndrome also known as palmoplantar keratoderma.
If left undisturbed, microbial plaque calcifies to form calculus, which is commonly called tartar.
Calculus above and below the gum line must be removed completely by the dental hygienist or
dentist to treat gingivitis and periodontitis. Although the primary cause of both gingivitis and
periodontitis is the microbial plaque that adheres to the tooth surfaces, there are many other
modifying factors. A very strong risk factor is one's genetic susceptibility. Several conditions and
diseases, including Down syndrome, diabetes, and other diseases that affect one's resistance to
infection, also increase susceptibility to periodontitis.
Another factor that makes periodontitis a difficult disease to study is that human host response
can also affect the alveolar bone resorption. Host response to the bacterial-mycotic insult is
mainly determined by genetics; however, immune development may play some role in
susceptibility.
According to some researchers periodontitis may be associated with higher
stress.[35] Periodontitis occurs more often in people from the lower end of the socioeconomic
scale than people from the upper end of the socioeconomic scale.[36]
Mechanism[edit]

Biofilm image of chronic periodontitis patient with phase contrast microscope at low power 100x
magnification on a salivary mount. About 20 black oval objects testifies of the presence of
amoebae and their movement forming channels upon displacement. 1000x magnification would
confirm diagnostic.
Another line of thinking was introduced in the early 1900s. This one proposes, following a
microscopic examination of the biofilm, the existence of a definitive correlation between the
presence of the amoeba Entamoeba gingivalis and active periodontal disease then called
pyorrhea.[37] This notion has been highlighted half a century later and corroborated by
demonstrating that gingival health biofilm consists mostly of non-motile bacteria, gingivitis
presenting mostly motile bacteria in the form of bacilli, spirillae and vibrios, accompanied by a
significant number of PMNleukocytes and finally, that periodontitis proceeds from a similar
bacterial condition but added the absolute presence of protozoan Entamoeba gingivalis, less
frequentTrichomonas tenax and more that significant numbers of granulocytes.[38] This theory
applied in the 1980s by a Canadian dentist seem to confirm periodontal healing according to him
by reestablishing, through hygiene, pharmaceutics and phase contrast microscope monitoring, a
commensal biofilm constituted of simple bacteria of various cocoid shapes, motionless filaments
and absence ofleukocytes.[39][40][41][42] This microscopic correlation has recently been mostly
confirmed by PCR molecular biology analysis relating the presence of thisprotozoan in cases of
active periodontal disease and its absence during gingival health, even in local areas of the
mouth.[43] This antiparasitic control technique was proposed as an effective therapy to overcome
periodontitis.[44] This medical protocol is mainly based on the phagocytosis process
of PMN leukocyte nucleus by the amoeba and a resulting enucleated cell spilling its proteolytic
enzymes content on the surrounding tissues as being proposed in the amebic liver abscess
figuring Entamoeba histolytica pathogen in amoebic dysentery. This particular therapy has the
advantage to eliminate concomitant pathogenic bacteria in the same time as the protozoa, being
considered at minimum by the dental practitioner and the patient an easy to visualize
microscopic target. This phagocytosis process newly called exonucleophagy would account for
the local deterioration of the immune system in the deep periodontal pocket and also be present
in peri-implantitis infections. Systematic presence of protozoan and the recessed ghost cells
exempt of nucleus would then impaired PMN to realise their defense activity Neutrophil
extracellular traps. The first data on such an antiparasitic therapy seem effective to heal
periodontal sulcus.[45]

Prevention[edit]
Daily oral hygiene measures to prevent periodontal disease include:

 Brushing properly on a regular basis (at least twice daily), with the patient attempting to
direct the toothbrush bristles underneath the gum-line, helps disrupt the bacterial-mycotic
growth and formation of subgingival plaque.
 Flossing daily and using interdental brushes (if the space between teeth is large enough), as
well as cleaning behind the last tooth, the third molar, in each quarter
 Using an antiseptic mouthwash: Chlorhexidine gluconate-based mouthwash in combination
with careful oral hygiene may cure gingivitis, although they cannot reverse any attachment
loss due to periodontitis.
 Using periodontal trays to maintain dentist-prescribed medications at the source of the
disease: The use of trays allows the medication to stay in place long enough to penetrate the
biofilms where the micro-organism are found.
 Regular dental check-ups and professional teeth cleaning as required: Dental check-ups serve
to monitor the person's oral hygiene methods and levels of attachment around teeth, identify
any early signs of periodontitis, and monitor response to treatment.
 Microscopic evaluation of biofilm may serve as a guide to regain commensal health flora.[46]
Typically, dental hygienists (or dentists) use special instruments to clean (debride) teeth below
the gumline and disrupt any plaque growing below the gumline. This is a standard treatment to
prevent any further progress of established periodontitis. Studies show that after such a
professional cleaning (periodontal debridement), microbial plaque tends to grow back to
precleaning levels after about three to four months. Nonetheless, the continued stabilization of a
patient's periodontal state depends largely, if not primarily, on the patient's oral hygiene at home,
as well as on the go. Without daily oral hygiene, periodontal disease will not be overcome,
especially if the patient has a history of extensive periodontal disease.
Periodontal disease and tooth loss are associated with an increased risk, in male patients,
of cancer.[47]
Contributing causes may be high alcohol consumption or a diet low in antioxidants.[48]

Management[edit]

This section from a panoramic X-ray film depicts the teeth of the lower left quadrant, exhibiting
generalized severe bone loss of 30–80%. The red linedepicts the existing bone level, whereas
the yellow line depicts where the gingiva was located originally (1–2 mm above the bone), prior
to the patient developing periodontal disease. Thepink arrow, on the right, points to afurcation
involvement, or the loss of enough bone to reveal the location at which the individual roots of a
molar begin to branch from the single root trunk; this is a sign of advanced periodontal disease.
The blue arrow, in the middle, shows up to 80% bone loss on tooth #21, and clinically, this
tooth exhibited gross mobility. Finally, the peach oval, to the left, highlights the aggressive
nature with which periodontal disease generally affects mandibular incisors. Because their roots
are generally situated very close to each other, with minimalinterproximal bone, and because of
their location in the mouth, where plaque and calculus accumulation is greatest because of the
pooling ofsaliva,[citation needed] mandibular anteriors suffer excessively. The split in the red
line depicts varying densities of bone that contribute to a vague region of definitive bone height.
The cornerstone of successful periodontal treatment starts with establishing excellent oral
hygiene. This includes twice-daily brushing with daily flossing. Also, the use of an interdental
brush is helpful if space between the teeth allows. For smaller spaces, products such as narrow
picks with soft rubber bristles provide excellent manual cleaning. Persons with dexterity
problems, such as arthritis, may find oral hygiene to be difficult and may require more frequent
professional care and/or the use of a powered tooth brush. Persons with periodontitis must realize
it is a chronic inflammatory disease and a lifelong regimen of excellent hygiene and professional
maintenance care with a dentist/hygienist or periodontist is required to maintain affected teeth.
Initial therapy[edit]
Removal of microbial plaque and calculus is necessary to establish periodontal health. The first
step in the treatment of periodontitis involves nonsurgical cleaning below the gumline with a
procedure called scaling and debridement. In the past, root planing was used (removal of
cemental layer as well as calculus). This procedure involves use of specialized curettes to
mechanically remove plaque and calculus from below the gumline, and may require multiple
visits and local anesthesia to adequately complete. In addition to initial scaling and root planing,
it may also be necessary to adjust the occlusion (bite) to prevent excessive force on teeth that
have reduced bone support. Also, it may be necessary to complete any other dental needs, such
as replacement of rough, plaque-retentive restorations, closure of open contacts between teeth,
and any other requirements diagnosed at the initial evaluation.
Reevaluation[edit]
Multiple clinical studies have shown nonsurgical scaling and root planing are usually successful
if the periodontal pockets are shallower than 4–5 mm (0.16–0.20 in).[49][50][51] The dentist or
hygienist must perform a re-evaluation four to six weeks after the initial scaling and root planing,
to determine if the patient's oral hygiene has improved and inflammation has regressed. Probing
should be avoided then, and an analysis by gingival index should determine the presence or
absence of inflammation. The monthly reevaluation of periodontal therapy should involve
periodontal charting as a better indication of the success of treatment, and to see if other courses
of treatment can be identified. Pocket depths of greater than 5–6 mm (0.20–0.24 in) which
remain after initial therapy, with bleeding upon probing, indicate continued active disease and
will very likely lead to further bone loss over time. This is especially true in molar tooth sites
where furcations (areas between the roots) have been exposed.
Surgery[edit]
If nonsurgical therapy is found to have been unsuccessful in managing signs of disease activity,
periodontal surgery may be needed to stop progressive bone loss and regenerate lost bone where
possible. Many surgical approaches are used in treatment of advanced periodontitis, including
open flap debridement and osseous surgery, as well as guided tissue regeneration and bone
grafting. The goal of periodontal surgery is access for definitive calculus removal and surgical
management of bony irregularities which have resulted from the disease process to reduce
pockets as much as possible. Long-term studies have shown, in moderate to advanced
periodontitis, surgically treated cases often have less further breakdown over time and, when
coupled with a regular post-treatment maintenance regimen, are successful in nearly halting
tooth loss in nearly 85% of patients.[52][53]
Maintenance[edit]
Once successful periodontal treatment has been completed, with or without surgery, an ongoing
regimen of "periodontal maintenance" is required. This involves regular checkups and detailed
cleanings every three months to prevent repopulation of periodontitis-causing microorganism,
and to closely monitor affected teeth so early treatment can be rendered if disease recurs.
Usually, periodontal disease exists due to poor plaque control, therefore if the brushing
techniques are not modified, a periodontal recurrence is probable.
Alternative treatments[edit]
Periodontitis has an inescapable relationship with subgingival calculus (tartar). The first step in
any procedure is to eliminatecalculus under the gum line, as it houses destructive anaerobic
microorganisms that consume bone, gum and cementum (connective tissue) for food.
Most alternative “at-home” gum disease treatments involve injecting antimicrobial solutions,
such as hydrogen peroxide, into periodontal pockets via slender applicators or oral irrigators.
This process disrupts anaerobic micro-organism colonies and is effective at reducing infections
and inflammation when used daily. A number of other products, functionally equivalent to
hydrogen peroxide, are commercially available, but at substantially higher cost. However, such
treatments do not address calculus formations, and so are short-lived, as anaerobic microbial
colonies quickly regenerate in and around calculus.
Doxycycline may be given alongside the primary therapy of scaling (see § initial
therapy).[54] Doxycycline has been shown to improve indicators of disease progression (namely
probing depth and attachment level).[54] Its mechanism of action involves inhibition of matrix
metalloproteinases (such as collagenase), which degrade the teeth's supporting tissues
(periodontium) under inflammatory conditions.[54] To avoid killing beneficial oral microbes, only
small doses of doxycycline (20mg) are used.[54]

Prognosis[edit]
Dentists and dental hygienists measure periodontal disease using a device called a periodontal
probe. This thin "measuring stick" is gently placed into the space between the gums and the
teeth, and slipped below the gumline. If the probe can slip more than 3 mm (0.12 in) below the
gumline, the patient is said to have a gingival pocket if no migration of the epithelial attachment
has occurred or a periodontal pock if apical migration has occurred. This is somewhat of a
misnomer, as any depth is in essence a pocket, which in turn is defined by its depth, i.e., a 2-mm
pocket or a 6-mm pocket. However, pockets are generally accepted as self-cleansable (at home,
by the patient, with a toothbrush) if they are 3 mm or less in depth. This is important because if a
pocket is deeper than 3 mm around the tooth, at-home care will not be sufficient to cleanse the
pocket, and professional care should be sought. When the pocket depths reach 6 to 7 mm (0.24 to
0.28 in) in depth, the hand instruments and cavitrons used by the dental professionals may not
reach deeply enough into the pocket to clean out the microbial plaque that cause gingival
inflammation. In such a situation, the bone or the gums around that tooth should be surgically
altered or it will always have inflammation which will likely result in more bone loss around that
tooth. An additional way to stop the inflammation would be for the patient to receive subgingival
antibiotics (such as minocycline) or undergo some form of gingival surgery to access the depths
of the pockets and perhaps even change the pocket depths so they become 3 mm or less in depth
and can once again be properly cleaned by the patient at home with his or her toothbrush.
If patients have 7-mm or deeper pockets around their teeth, then they would likely risk eventual
tooth loss over the years. If this periodontal condition is not identified and the patients remain
unaware of the progressive nature of the disease, then years later, they may be surprised that
some teeth will gradually become loose and may need to be extracted, sometimes due to a severe
infection or even pain.
According to the Sri Lankan tea labourer study, in the absence of any oral hygiene activity,
approximately 10% will suffer from severe periodontal disease with rapid loss of attachment
(>2 mm/year). About 80% will suffer from moderate loss (1–2 mm/year) and the remaining 10%
will not suffer any loss.[55][56]

Epidemiology[edit]

Disability-adjusted life year for peridontal disease per 100,000 inhabitants in 2004.[57]

no data 6-6.5

<3.5 6.5-7

3.5-4 7-7.5

4-4.5 7.5-8

4.5-5 8-8.5

5-5.5 >8.5

5.5-6

Periodontitis is very common, and is widely regarded as the second most common dental disease
worldwide, after dental decay, and in the United States has aprevalence of 30–50% of the
population, but only about 10% have severe forms.
Chronic periodontitis affects about 750 million people or about 10.8% of the population as of
2010.[58]
Like other conditions intimately related to access to hygiene and basic medical monitoring and
care, periodontitis tends to be more common in economically disadvantaged populations or
regions. Its occurrence decreases with higher standard of living. In Israeli population, individuals
of Yemenite, North-African, South Asian, or Mediterranean origin have higher prevalence of
periodontal disease than individuals from European descent.[59] Periodontitis is frequently
reported to be socially patterned, i.e. people from the lower end of the socioeconomic scale
suffer more often from it than people from the upper end of the socioeconomic scale.[60