Topographical classification cavities decay and cavities shutter

Map document:

I. Introduction
II. Nomenclature
1. Nomenclature cavities
2. Nomenclature walls
1. Definition of the axis of the tooth
3. Classification of edges
4. Nomenclature angles

III. Classification cavities of caries
1. Classification BLACK (1907)
1. Class I
2. Class II
3. Class III
4. Class IV
5. Class V

IV. Classification cavities shutter
1. Classification Johnson
1. Single cavity
2. Compound cavity
2. Classification of Jean-Claude HESS
1. Class A
2. Class B
3. Class C
4. D
5. Class E
6. Class F
V. Conclusion
VI. Bibliography

I Introduction

The study of different parts of the cavities and the classification of these cavities requires a precise nomenclature it is essential to know.
According to the dictionary "Larousse", the term nomenclature denotes the set of technical terms in a discipline standings.
• Tooth decay is the defect that causes, is mainly on the crown,
Nomenclature and classification were established by different authors to describe the identification and understanding of different parts of the tooth decay and cavities filling cavities.

Nomenclature II

II.A. Nomenclature cavities

Called "simple cavity" cavities that affects only one side of the tooth, called "cavity complex or compound" a cavity for two or more sides of the tooth.
• A cavity is designated by the name of the relevant face or faces
By equating the cavities of a cube in the case of a molar or premolar.
We speak of cavity:
a: occlusal
b: mesial
c: distal
d: vestibular
e: lingual


II.B. Nomenclature walls


The words used to name the faces of the teeth are also used to designate the cavity walls (the walls of the cavity are called faces that are both near and parallel).
• Definition of the axis of the tooth


This is an imaginary line that enters the longitudinal center of the ring and drops vertically at this level.
• If this is the incisor or canine, the axis coincides with the extended pulp (root canal).

Figure 3-1: Classification of walls: single cavity

In a single cavity situated on a labial surface of the tooth, will have a substantially parallel to said face and to the axis of the tooth, will be spoken of "axial wall"

Figure 3-2: Axial wall

• In the case of a proximal cavity, there will be four walls

 Figure 3-3: proximal cavity

• In the case of a cervical cavity, there will be five walls:
a: Occlusal
b: Distal
c: mesial
d: wall gingival or cervical
e: axial wall parallel to the axis of the tooth

• In the presence of two cavities, the name of the walls is followed by the name of the cavity
Example: You speak of vestibular walls of the cavity proximal distal.

Figure 3-4: Cavity composed occlusal cavity proximal

Note! Sub-pulpal wall When removing the pulp, the pulpal wall disappears, the new are perhaps floored pulp is called "sub-pulpal wall". • If the cavity developed on a vertical faces, the walls axial is called "wall of the pulp chamber."

II.C. Classification of edges

Any cavity is delimited by the edges of enamel, the edge of the cavity is defined as the line connecting the walls of the cavity to the surfaces of the tooth or between two walls it
• These edges are called bounding walls, it has an edge:
a: Vestibular
b: Lingual
c: Cervical
d: mesial
e: Distal

II.D. Nomenclature angles

• 2 walls meet at an angle Diede, this angle is called the 2 walls that have given birth.
• three walls which meet at an angle Triede
Example: vestibulo-cervico-angle axial

The external angle (= cavo-surface) is the angle formed by the outer surface of the tooth with the walls of the cavity at a given point.

III. Classification cavities of caries

• Classification BLACK (1907)

This classification is the seat of caries cavities, cavities cavities cavities as a result of natural progression of the carious lesion
These cavities have been classified into five classes according BLACK seat of caries.

III.Aa Class I BLACK

It includes all the cavities of caries sitting at anatomical depressions of all teeth
• The occlusal grooves molars and premolars
• The vestibular dimples lower molars
• The upper molars palatal dimples

Figure 3-5: Molars and premolars

• The cingulum of anterior teeth

Figure 3-6: Cingulum anterior teeth

III.Ab Class II BLACK

It concerns caries cavities located on the proximal surfaces of molars and premolars.

Figure 3-7: Face of a premolar proximal

III.Ac Class III BLACK

Were caries cavities located on the proximal surfaces of incisors and canines without destruction reached the corner incisor.


Figure 3-8: Face proximal incisor

III.Ad Class IV black

Were caries cavities located on the proximal surfaces of incisors and canines with destruction reached the corner incisor.


Figure 3-9: Face of a maxillary vestibular

III.Ae Class V BLACK

It concerns the cavities of caries at the gingival third (= neck) of all teeth as vestibular side of lingual side.


Figure 3-10: Face of a maxillary vestibular

IV Classification cavities shutter

IV.A. Classification Johnson

The simplest classification filling cavities, he unscrewed the cavities in two types:

Single cavity IV.Aa

Interested cavity one side of the tooth.

Cavity composed IV.Ab


Interested cavity 2 or more surfaces of the tooth.

IV.B. Classification of Jean-Claude HESS

It is important not to confuse cavity decay (pathological lesion that is observed and that locates) and cavity filling (preparation that is created), it is the transformation of the previous thinking.

• To avoid confusion between decay and restoration, Jean-Claude HESS proposed a classification in complementary to black.
Hess called these cavities by subdividing the classification of black depending on the importance of each cavity and the extent of carious destruction.
It includes six classes as many classes as faces, each class characterized by a Shift from "A" to "F".

IV.Ba Class A


Restoration interested one side of the crown

IV.Bb Class B


Restoration of interest 2 sides
Example: proximo-occlusal


IV.Bc Class C


Restoration of interest 3 faces

IV.Bd Class D


Restoration interested 4 sides

IV.Be Class E


Interest 5 faces (leading to a crown coating)

IV.Bf Class F


For the restoration of interest 6 faces, if the crown completely disappeared, there remains only the root (tooth tenon)
The union of the Roman numeral classification of Black and uppercase Jean-Claude Hess clarifies, there will be as follows:
• Class IA, Class IIA, Class IB ...
Greek letters are used to specify the walls
: Α: occlusal
: Β: Vestibular
: Γ: lingual
: Δ: Distal
: Ε: mesial

Example

Cavities
• Class IAα: single cavity
• Class II.A.δ: single cavity proximodistal


Caries
Black Class Preparation and Restoration Class Hess
Simple class I
o Furrows
o Dimples cavity
o Occlusal
o Vestibular
o A Lingual
Cavity composed
o Union between cavity and fissure cavity pit
o occlusal caries weakening too another wall to be treated as a cavity composed B
Cavities
o occlusal buccal
o occlusal-lingual
o occlusal-proximal
Class II Single cavity without proximal adjacent tooth A
Compound cavity cavity cavity bifaces proximo-occlusal B
Cavity trifaces mesio-occlusal cavity distal C
Recovery complex cavity of the crown, 4/5 and complete D, E
Class III Single cavity without proximal adjacent tooth A
Composed cavity cavity bifaces
Buccal cavity opening proximo-vestibular B
Cavity bifaces
Opening
proximo-lingual lingual cavity
Complex cavity Crown and ¾ full
Taking tooth D, E, F
Class IV consists Cavity Cavity Cavity bifaces angle B
Complex cavity Crown and ¾ full
Tooth pin D, E, F
Class V cavity simple cavity composed of: cervical cavity A, B, C

V Conclusion


Classifications described allow to remove all confusion in the mind of the practitioner same classification and restoration curries facilitate language of different clinicion.

VI Bibliography


Operative Dentistry: Tomme 2, conservative dentistry
Teaching of dentistry concervatrice: Jean-Claude HESS, Tomme 6 and 7 tomme

Dental caries

Dental caries, also known as tooth decay or a cavity, is an infection, bacterial in origin, that causes demineralization and destruction of the hard tissues (enamel, dentin and cementum), usually by production of acid by bacterial fermentation of the food debris accumulated on the tooth surface.
 If demineralization exceeds saliva and other remineralization factors such as from calcium and fluoridated toothpastes, these hard tissues progressively break down, producing dental caries (cavities, holes in the teeth). The bacteria most responsible for dental cavities are the mutans streptococci, most prominently Streptococcus mutans and Streptococcus sobrinus, and lactobacilli. If left untreated, the disease can lead to pain, tooth loss and infection.
Today, caries remain one of the most common diseases throughout the world. Cariology is the study of dental caries.

he presentation of caries is highly variable. However the risk factors and stages of development are similar. Initially it may appear as a small chalky area (smooth surface caries), which may eventually develop into a large cavitation. Sometimes caries may be directly visible. However other methods of detection such as X-rays are used for less visible areas of teeth and to judge the extent of destruction. Lasers for detecting caries allow detection without radiation and are now used for detection of interproximal decay (between the teeth). Disclosing solutions are also used during tooth restoration to minimize the chance of recurrence.
Tooth decay disease is caused by specific types of bacteria that produce acid in the presence of fermentable carbohydrates such as sucrose, fructose, and glucose. The mineral content of teeth is sensitive to increases in acidity from the production of lactic acid. To be specific, a tooth (which is primarily mineral in content) is in a constant state of back-and-forth demineralization and remineralization between the tooth and surrounding saliva. For people with little saliva, especially due to radiation therapies that may destroy the salivary glands, there also exists remineralization gel. These patients are particularly susceptible to dental caries. When the pH at the surface of the tooth drops below 5.5, demineralization proceeds faster than remineralization (meaning that there is a net loss of mineral structure on the tooth's surface). Most foods are in this acidic range and without remineralization, this results in the ensuing decay. Depending on the extent of tooth destruction, various treatments can be used to restore teeth to proper form, function, and aesthetics, but there is no known method to regenerate large amounts of tooth structure. Instead, dental health organizations advocate preventive and prophylactic measures, such as regular oral hygiene and dietary modifications, to avoid dental caries.


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 an incipient carious lesion or "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 brown and shiny suggests dental caries was once present but the demineralization process has stopped, leaving a stain. A brown spot that is dull in appearance is probably a sign of active caries.
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 a toothache. The pain may worsen with exposure to heat, cold, or sweet foods and drinks. 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's angina can be life-threatening

Causes
There are four main criteria required for caries formation: a tooth surface (enamel or dentin); caries-causing bacteria; fermentable carbohydrates (such as sucrose); and time. The caries process does not have an inevitable outcome, and different individuals will be susceptible to different degrees depending on the shape of their teeth, oral hygiene habits, and the buffering capacity of their saliva. Dental caries can occur on any surface of a tooth that is exposed to the oral cavity, but not the structures that are retained within the bone. All caries occur from acid demineralization that exceeds saliva and fluoride remineralization, and almost all acid demineralization occurs where food (containing carbohydrate like sugar) is left on teeth. Because most trapped food is left between teeth, over 80% of cavities occur inside pits and fissures on chewing surfaces where brushing, fluoride, and saliva cannot reach to remineralize the tooth as they do on easy-to-reach surfaces that develop few cavities.

Teeth

There are certain diseases and disorders affecting teeth that may leave an individual at a greater risk for caries. Amelogenesis imperfecta, which occurs between 1 in 718 and 1 in 14,000 individuals, is a disease in which the enamel does not fully form or forms in insufficient amounts and can fall off a tooth.In both cases, teeth may be left more vulnerable to decay because the enamel is not able to protect the tooth.
In most people, disorders or diseases affecting teeth are not the primary cause of dental caries. Ninety-six percent of tooth enamel is composed of minerals. These minerals, especially hydroxyapatite, will become soluble when exposed to acidic environments. Enamel begins to demineralize at a pH of 5.5. Dentin and cementum are more susceptible to caries than enamel because they have lower mineral content. Thus, when root surfaces of teeth are exposed from gingival recession or periodontal disease, caries can develop more readily. Even in a healthy oral environment, however, the tooth is susceptible to dental caries.
The evidence for linking malocclusion and/or crowding to the dental caries is weak; however,the anatomy of teeth may affect the likelihood of caries formation. Where the deep grooves of teeth are more numerous and exaggerated, pit and fissure caries are more likely to develop. Also, caries are more likely to develop when food is trapped between teeth.

Pathophysiology

The progression of pit and fissure caries resembles two triangles with their bases meeting along the junction of enamel and dentin.

Enamel

Enamel is a highly mineralized acellular tissue, and caries act upon it through a chemical process brought on by the acidic environment produced by bacteria. As the bacteria consume the sugar and use it for their own energy, they produce lactic acid. The effects of this process include the demineralization of crystals in the enamel, caused by acids, over time until the bacteria physically penetrate the dentin. Enamel rods, which are the basic unit of the enamel structure, run perpendicularly from the surface of the tooth to the dentin. Since demineralization of enamel by caries, in general, follows the direction of the enamel rods, the different triangular patterns between pit and fissure and smooth-surface caries develop in the enamel because the orientation of enamel rods are different in the two areas of the tooth.
As the enamel loses minerals, and dental caries progresses, the enamel 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. The translucent zone is the first visible sign of caries and coincides with a one to two percent loss of minerals. A slight remineralization of enamel occurs in the dark zone, which serves as an example of how the development of dental caries is an active process with alternating changes. The area of greatest demineralization and destruction is in the body of the lesion itself. The surface zone remains relatively mineralized and is present until the loss of tooth structure results in a cavitation.

Dentin

Unlike enamel, the dentin reacts to the progression of dental caries. After tooth formation, the ameloblasts, which produce enamel, are destroyed once enamel formation is complete and thus cannot later regenerate enamel after its destruction. On the other hand, dentin is produced continuously throughout life by odontoblasts, which reside at the border between the pulp and dentin. Since odontoblasts are present, a stimulus, such as caries, can trigger a biologic response. These defense mechanisms include the formation of sclerotic and tertiary dentin.
In dentin from the deepest layer to the enamel, the distinct areas affected by caries are the advancing front, the zone of bacterial penetration, and the zone of destruction.
The advancing front represents a zone of demineralised dentine due to acid and has no bacteria present. The zones of bacterial penetration and destruction are the locations of invading bacteria and ultimately the decomposition of dentin. The zone of destruction has a more mixed bacterial population where proteolytic enzymes have destroyed the organic matrix. The innermost dentine caries has been reversibly attacked because the collage matrix is not severely damaged, giving it potential for repair. The outer more superficial zone is highly infected with proteolytic degradation of the collagen matrix and as a result the dentine is irreversibly demineralised.

The faster spread of caries through dentin creates this triangular appearance in smooth surface caries.

Sclerotic dentin

The structure of dentin is an arrangement of microscopic channels, called dentinal tubules, which radiate outward from the pulp chamber to the exterior cementum or enamel border. The diameter of the dentinal tubules is largest near the pulp (about 2.5 μm) and smallest (about 900 nm) at the junction of dentin and enamel. The carious process continues through the dentinal tubules, which are responsible for the triangular patterns resulting from the progression of caries deep into the tooth. The tubules also allow caries to progress faster.
In response, the fluid inside the tubules bring immunoglobulins from the immune system to fight the bacterial infection. At the same time, there is an increase of mineralization of the surrounding tubules This results in a constriction of the tubules, which is an attempt to slow the bacterial progression. In addition, as the acid from the bacteria demineralizes the hydroxyapatite crystals, calcium and phosphorus are released, allowing for the precipitation of more crystals which fall deeper into the dentinal tubule. These crystals form a barrier and slow the advancement of caries. After these protective responses, the dentin is considered sclerotic.
Fluids within dentinal tubules are believed to be the mechanism by which pain receptors are triggered within the pulp of the tooth. Since sclerotic dentin prevents the passage of such fluids, pain that would otherwise serve as a warning of the invading bacteria may not develop at first. Consequently, dental caries may progress for a long period of time without any sensitivity of the tooth, allowing for greater loss of tooth structure.

Tertiary dentin

In response to dental caries, there may be production of more dentin toward the direction of the pulp. This new dentin is referred to as tertiary dentin. Tertiary dentin is produced to protect the pulp for as long as possible from the advancing bacteria. As more tertiary dentin is produced, the size of the pulp decreases. This type of dentin has been subdivided according to the presence or absence of the original odontoblasts.
If the odontoblasts survive long enough to react to the dental caries, then the dentin produced is called "reactionary" dentin. If the odontoblasts are killed, the dentin produced is called "reparative" dentin.
In the case of reparative dentin, other cells are needed to assume the role of the destroyed odontoblasts. Growth factors, especially TGF-β, are thought to initiate the production of reparative dentin by fibroblasts and mesenchymal cells of the pulp. Reparative dentin is produced at an average of 1.5 μm/day, but can be increased to 3.5 μm/day. The resulting dentin contains irregularly shaped dentinal tubules that may not line up with existing dentinal tubules. This diminishes the ability for dental caries to progress within the dentinal tubules.

what is dystonia ?

Dystonia is a neurological movement disorder, in which sustained muscle contractions cause twisting and repetitive movements or abnormal postures.[1] The disorder may be hereditary or caused by other factors such as birth-related or other physical trauma, infection, poisoning (e.g., lead poisoning) or reaction to pharmaceutical drugs, particularly neuroleptics.[1] Treatment is difficult and has been limited to minimizing the symptoms of the disorder, since there is no cure available.

Classification
Types of dystonia
    Generalized
    Focal
    Segmental
    Sexual
    Intermediate
    Psychogenic
    Acute Dystonic Reaction
Generalized dystonias
    Normal birth history and milestones
    Autosomal dominant
    Childhood onset
    Starts in lower limbs and spreads upwards
    Also known as "idiopathic torsion dystonia" (old terminology "dystonia musculorum deformans")
Focal dystonias

neurocirculatory dystonia

neurocirculatory dystonia (Cardiopsychoneurosis )

Cardiopsychoneurosis (NDC) - a set of disorders of the cardiovascular system of a functional nature, which develops as a result of violations of the neuroendocrine regulation. Cardiopsychoneurosis polietiologichesky genesis is accompanied by a variety of, mainly cardiovascular diseases, symptoms, caused or aggravated under the influence of stress effects, different benign course and a satisfactory outcome.

Cardiopsychoneurosis (neurocirculatory dystonia)
    Classification of neuro dystonia
    The causes of neuro dystonia
    Neuro symptoms of dystonia
    Diagnosis of neuro dystonia
    Neuro treatment of dystonia
    The prognosis of neuro dystonia
    Prevention neuro dystonia

Cardiopsychoneurosis in literature is sometimes described by the term "cardiac neurosis", "neuro-circulatory asthenia," "excitable heart." Taken to distinguish between two types of functional disorders of the cardiovascular system: vegetative-vascular and neuro-circulatory dystonia. Vegetative-vascular dystonia together various manifestations of autonomic dysfunction that come with organic lesions of the nervous, endocrine and other systems. Cardiopsychoneurosis an independent nosological form with its etiology, pathogenesis, symptoms and prognosis and has a number of features of autonomic dysfunction. Distinctive features of neuro dystonia is the prevalence of clinical manifestations of cardiovascular symptoms, primary-functional nature of the disturbances of autonomic regulation and lack of communication with organic pathology, including neurosis.

With neuro dystonia often face neurologists , cardiologists , general practitioners. Among patients and therapeutic cardiology NDC occurs in 30-50% of individuals. Neurocirculatory dysfunction may develop at different ages, but is more common in young people, mainly women, suffering from it 2-3 times more often than men. The disease rarely occurs in people younger than 15 and older than 40-45 years.

Classification of neuro dystonia

On the etiological forms of essential release (constitutional-hereditary), psychogenic (neurotic), infectious-toxic, dishormonal mixed cardiopsychoneurosis and NDC physical stress.

Depending on the leading clinical syndrome classification V.P.Nikitina (1962) and N.N.Savitskogo (1964) distinguishes four types of neuro dystonia: cardiac (with a primary disorder of cardiac activity), hypotensive (with the decrease of blood pressure), hypertensive ( with primary elevated blood pressure), mixed (combined disturbance of blood pressure and cardiac activity).

On the severity of symptoms distinguish mild, moderate and severe neuro dystonia, the variant of flow - the phase of exacerbation and remission.

The causes of neuro dystonia

By the development of neuro disorders can cause a variety of factors, but these do not include organic lesions of the endocrine and nervous systems.

In adolescence and early period cardiopsychoneurosis usually due to imperfections in the neuroendocrine mechanism of regulation of autonomic processes. NDC development in prepubertal and pubertal periods contribute to enhanced mental and physical activities, social environment.

Individuals of any age can develop cardiopsychoneurosis against acute and chronic infections , lack of sleep, fatigue, trauma, exposure to physical and chemical factors (sun exposure, hot weather, vibration), improper diet, physical activity (or inactivity overload), intoxication, including alcohol and tobacco. In the development of neuro dystonia serve as periods of hormonal changes the body (puberty, abortion , pregnancy, menopause , ovarian dysfunction ).

A number of patients have a hereditary-constitutional predisposition to the development of neuro dystonia.

The impact of these factors causes dysfunction neurohumoral control of the cardiovascular system, where as the leading pathogenetic mechanisms protruding lesions of the hypothalamic-pituitary structures responsible for the coordination of these processes. Violation of neurohumoral control disorder manifested systems functions, ensuring the processes of homeostasis in the body: cholinergic sympathetic-adrenal, kallikreinkininovoy, gistaminserotoninovoy etc.

This in turn triggers the mechanisms leading to disruption and multiple changes of the carbohydrate, water and electrolyte metabolism, acid-base balance, neurotransmitter and hormonal systems.

In the myocardial tissue is activation of biologically active substances (histamine, serotonin, kinins, etc.), causing the development of metabolic disorders and malnutrition. On the part of the circulatory system are marked variations in vascular tone, peripheral vascular spasm, slowing of microcirculation, leading to the development of tissue hypoxia.

Once formed, the pathogenetic mechanisms become autonomous and cardiopsychoneurosis - a separate disease. Any stimuli (weather changes, stress, etc.) cause pathological reaction, for expression of a type neuro dystonia.

Neuro symptoms of dystonia

Common to all types of neuro dystonia is a manifestation of neurosis-a condition characterized by fatigue, weakness, insomnia, irritability, memory loss, mood and willpower, the deterioration of concentration, joined functional circulatory disorder is predominant.

During cardiac type neuro dystonia manifested false angina, palpitations, disruptions of the heart, sometimes shortness of breath during physical activity, significant changes in blood pressure is not observed. Can be determined objectively tachycardia , respiratory arrhythmia , paroxysmal tachycardia, supraventricular arrhythmias, inadequate cardiac output load change, the ECG - changing voltage of the T wave (high or reduced).

Cardiopsychoneurosis hypertensive type is characterized by the phenomena of chronic vascular insufficiency: a decrease in systolic blood pressure less than 100 mm Hg. Art., chilliness feet and hands, prone to orthostatic collapse and fainting. And for patients with hypertensive type NDC typical complaints of fatigue, muscle weakness, headaches . Such patients usually have asthenic physique, pale skin, cold and wet hands.

For hypertensive type neuro dystonia characterized by transient increase in blood pressure to 130-140/85-90 mm Hg. Art., which half the time is not accompanied by changes in subjective well-being of patients and detected on physical examination. Less frequent complaints of palpitations, headache, fatigue. Hypertensive type NDC in performance coincides with the boundary of arterial hypertension .

Mild neuro dystonia is characterized by moderately severe symptoms that occur only in connection with psycho-overload. Disabled patients maintained, there may be a slight decrease in physical endurance, drug therapy is not indicated.

At moderate neuro dystonia are multi symptoms, decreased physical performance by more than 50%. Reduction or temporary disability requires use of drug therapy.

In severe forms of dystonia neuro long lasting and multiple clinical symptoms, sudden decrease or loss of earning capacity, requiring hospital treatment of patients.

Diagnosis of neuro dystonia

Malospetsifichnost neuro symptoms of dystonia is difficult to diagnose and requires careful verification of the diagnosis.

Supporting diagnostic criteria based on neuro dystonia patient's complaints may serve as symptoms traced for 1-2 months: false angina, palpitations, feeling short of breath, precordial pulsation in the field or in the vessels of the neck, weakness, fatigue, neurotic symptoms (irritability, anxiety , insomnia ), dizziness , cold and wet limbs. For neuro dystonia characterized multiplicity of complaints that have a clear link with stress or periods of hormonal changes, illness with periods of remissions and exacerbations, but no tendency to progression.

By the criteria of significant physical presence NDCs are erratic heart rhythm with a tendency to tachycardia, which appears spontaneously or inadequate situation, labile blood pressure, presence of respiratory arrhythmia (tachypnea, dyspnea), hyperalgesia in the heart.

On ECG in patients may register tachycardia, arrhythmia, pacemaker migration (21.3%), arrhythmias (8.8%), paroxysmal tachycardia and atrial fibrillation (3%), negative T waves in two or more leads (39.4 %).

Informative methods for diagnosis of dystonia are neuro-diagnostic ECG test with a load .

• Physiological test with hyperventilation implies a for 30-40 minutes forced breaths followed by ECG recordings and comparing it with the original. Positive samples indicating NDC is increased heart rate by 50-100% and the appearance of the ECG negative T waves or increase their amplitude.
• Tilt test provides ECG in the supine position, and then after 10 to 15 minutes of standing. Positive results of the sample are the same changes as in the sample with hyperventilation found at the NDC in 52% of patients.
• Drug test (with β-blockers, potassium) are aimed at distinguishing neuro dystonia and organic heart disease. ECG-registration is carried out after 40-60 minutes after taking 60-80 mg of β-blockers (obzidan, inderal, Inderal), or 6 g of potassium chloride. In organic kardiopatologiyah ( myocarditis , coronary artery disease , myocardial hypertrophy) recorded positive T waves, the NDC - negative T waves.

During cycle ergometry determined typical neuro dystonia reduced exercise capacity, that is, patients with neuro dystonia can do less weight than a healthy person of the same age and sex.
Laboratory data indicate an increase in the activity of sympathetic-adrenal system: in response to the load in the blood is inadequate increase in noradrenaline, adrenaline, metabolites, lactic acid.

Neuro treatment of dystonia

In the treatment of neuro dystonia extremely important place occupied by non-drug activities to increase the adaptive capacity of the organism to changing conditions. When NDC shown holding tempering procedures, sports (athletics, swimming), rational psihiterapiya, normalization of work and leisure.

Positive impact on the training of the system of regulation of autonomic function has balneotherapy , physiotherapy ( therapeutic showers and baths, electric sleep , reflexology , electrophoresis with bromine, magnesium, Novocain), physical therapy , spa treatment.

Sleep disturbances, irritability, sedation can assign medicines: motherwort, valerian valokordin, tranquilizers (nozepama etc.).

For the treatment of neuro dystonia of hypertensive cardiac and type shown receiving β-blockers (atenolol, Inderal, trazikora), eliminates tachycardia, hypertension, false angina, as well as products that will improve the metabolism of the heart muscle (riboksina, preparations of potassium, B vitamins).

When neuro dystonia of hypertensive type with the presence of fatigue and postural disorders prescribed tincture of ginseng (lemongrass, Aralia), caffeine.

The prognosis of neuro dystonia

During any type of neuro dystonia does not cause the development of cardiomegaly, heart failure or life-threatening arrhythmias and conduction. In adolescence, with early treatment or cure itself comes complete recovery. With age, the prognosis for complete recovery of neuro dystonia decreases. Reduction or temporary disability may occur during exacerbations.

Hypertensive patients with type neuro dystonia are at risk for hypertension , with any type of NDC in relation to lipid metabolism can not exclude the risk of atherosclerosis and coronary artery disease.

Prevention neuro dystonia

Prevention issues neuro dystonia go beyond purely medical measures. Prevention includes proper physical, mental and adolescent health education, increase their self-esteem and social adjustment. The role of health promotion, exercise, avoid smoking and drinking alcohol.

Medical prevention neuro dystonia include combating focal infections, stress factors, hormonal regulation in women in menopause.

Pulpitis

Pulpitis is inflammation of dental pulp tissue. Usually it is associated with toothache.


Symptoms
Increased sensitivity to stimuli, specifically hot and cold, is a common symptom of pulpitis. A prolonged throbbing pain may be associated with the disease. However, pulpitis can also occur without any pain.

Causes
Pulpitis may be caused by a dental caries that penetrate through the enamel and dentin to reach the pulp, or it may be a result of trauma, such as thermal insult from repeated dental procedures.
Inflammation is commonly associated with a bacterial infection but can also be due to other insults such as repetitive trauma or in rare cases periodontitis. In the case of penetrating decay, the pulp chamber is no longer sealed off from the environment of the oral cavity.

When the pulp becomes inflamed, pressure begins to build up in the pulp cavity, exerting pressure on the nerve of the tooth and the surrounding tissues. Pressure from inflammation can cause mild to extreme pain, depending upon the severity of the inflammation and the body's response. Unlike other parts of the body where pressure can dissipate through the surrounding soft tissues, the pulp cavity is very different. It is surrounded by dentin, a hard tissue that does not allow for pressure dissipation, so increased blood flow, a hallmark of inflammation, will cause pain.

Pulpitis can often create so much pressure on the tooth nerve that the individual will have trouble locating the source of the pain, confusing it with neighboring teeth, called referred pain. The pulp cavity inherently provides the body with an immune system response challenge, which makes it very difficult for a bacterial infection to be eliminated.
If the teeth are denervated, this can lead to irreversible pulpitis, depending on the area, rate of infection, and length of injury. This is why people who have lost their dental innervation have a reduced healing ability and increased rate of tooth injury. Thus, as people age, their gradual loss of innervation leads to pulpitis.[6]
Responses
Immune/Inflammatory Response
In the pulp, just as in other areas of the body, inflammation can be present. Inflammation of the pulp does not take place only when the bacteria in the decay have reached the pulp. Bacterial products may reach the pulp much earlier and begin the inflammatory response. The inflammation may be acute or chronic because just like other tissues in the body, the pulp will react to irritants with innate and/or adaptive immune responses.

Innate immunity in the pulp is not specific but uses receptors to recognize molecular patterns common to microbes to initiate bacterial killing (phagocytosis). The components of the innate response of the dentin/pulp complex to caries include at least the following six: (1) outward flow of dentinal fluid; (2) odontoblasts; (3) neuropeptides and neurogenic inflammation; (4) innate immune cells, including immature dendritic cells (DCs), natural killer (NK) cells, and T cells, as well as (5) their cytokines and (6) chemokines. Although the first two items are not classic components of innate immunity, they are uniquely involved in the initial inflammatory response to caries.[7]
Odontoblasts, (the cells that form dentin) have cellular processes that extend into dentinal tubules and are the first to encounter the caries bacterial antigens. They express low levels of interleukin 8 (IL-8) and genes related to chemokines and chemokine receptors. The odontoblasts have been shown to attract immature dendritic cells.[7]
Dendritic cells (DCs) are a heterogeneous leukocyte (white blood cell) population. DCs in healthy peripheral tissues (steady state) are in an immature state. The cells are capable of sensing microbes as well as antigen capture and processing capabilities. A rapid accumulation of pulpal DCs has been observed beneath cavity preparations, and an increased number of DCs accumulated under caries. Immature DCs are therefore considered to be part of the innate phase of pulpal immune response.[7]
Persistent infection leads to the activation of adaptive immunity. A transition to an adaptive immune response will take place in the dental pulp as the caries and bacteria approach the pulp. Antigens are recognized individually and lines of lymphocytes are developed to produce specific antibodies which attach to the recognized cells and initiate their destruction. Phagocytes remove the remains. B cells and T cells are the major lymphocytes involved.[9]
A variety of cytokines have been observed in the pulp. Patients with symptomatic and asymptomatic irreversible pulpitis have been shown to have an almost 23-fold increase in the cytokine IL-8 in the pulp. Cytokines in the pulp interact with each other. The ultimate effect on pulpal inflammation and healing is dependent upon the integrated actions of these inflammatory mediators.[10]
In addition to the lymphocytes, macrophages also provide defense against certain intracellular pathogens. Activated macrophages can function as class II antigen-presenting cells, similar to pulpal dendritic and B cells. In addition, activated macrophages secrete many inflammatory mediators.[11]
Macrophages in the pulp become activated after receiving two signals. The first is a priming stimulus and the second is an activating signal. The priming stimulus is secreted by activated T-helper cells. The activating stimulus may include bacterial lipopolysaccharides, muramyl dipeptide, and other chemical mediators.[11]
Macrophages are professional phagocytes in innate immune responses. Activated macrophages are effective killers that eliminate pathogens in both innate and adaptive immune responses, and are also important in tissue homeostasis, through the clearance of senescent cells, and in remodeling and repair of tissue after inflammation. The number of macrophages increases with the progression of caries and is always higher than that of DCs at all stages of the caries invasion.[10]
Neurological Responses
According to the Brännström's hydrodynamic theory, activated nociceptors from fluid movement and other irritants through the patent dentine tubules result in pulp pain. Unmyelinated, slow conducting C-fibers aid in feeling a slowset, burning pain.[12] According to neuronal studies, 70-80% of pulpal axons are unmyelinated.[13] Highly myelinated Aδ-fibers, which allow for fast conduction, are responsible for the sharp, shooting paining.[12]
Thus, the stimulus intensities are based on various fibers. Fast-conducting Aβ and Aδ-fibers provide the lowest stimulus intensities (typically referred to as prepain sensations), and those sensations eventually receive higher stimulation levels. The dull aches are associated with C-fibers and slow Aδ-fibers. As inflammation intensifies, the A-fibers are increasingly activated. C-fiber innervation and Aδ-fibers are polymodal receptors that are sensitive to capsaicin and inflammatory mediators.[6]
The pain mechanisms associated with pulpitis are similar to those of the rest of the body (i.e. receptors, intracellular signaling, transmitters, etc.). The inflammatory mediators act on specific receptors relating to nociceptive neurons, leading to the production of ssecond messengers and activation of phospholipases and protein kinases. The second messengers regulate receptors ion channels that deal with sensitization. The ion channels open based on pain stimuli propagating action potentials in sensory neurons.[14]
In order for excitability and conduction to occur, voltage-gated sodium channels must be activated. Changes in sodium channel (NaCH) expression occur after inflammatory lesions, which may generate different pain states seen when neuronal fibers are activated. Studies have been done on major NaCh isoforms to examine expression patterns. Nav1.6 nodal accumulations do not vary in size or immunofluorescence staining activity in typical or atypical nodal sites; however, the proportion of typical nodal sites decreases and increase in atypical nodes in painful tooth samples compared to normal tooth samples. Nav1.7 has an increased expression in typical and atypical nodal sites in painful samples. As a result, an increased co-expression of multiple isoforms at demyelinating nodal sites in painful dental pulp. This isoforms of sodium channels may be a main factor in pain sensations due to their production of axonal excitability properties.[15]
Neuropeptides are increasingly being researched for having a role in molecular mechanisms involved with pain, including ion channels and inflammation. Substance P (SP) is a neuropeptide produced by capsaicin neuron cell bodies (localized in trigeminal ganglia and dorsal root) and plays a major role in dental pain and inflammation. Other peptides include cGRP, galanin, somatostatin, and neurokinin A-B. The biological effects of SP are expressed by the binding of specific G protein-coupled NK receptors. Interaction with SP receptors induces vasodilation and allows for plasma extravasation and mastocyte degranulation. SP is highly expressed in dental pulp and dentin. When pain, thermal, and/or chemical stimulation is present, SP production and release increases. Current studies focus on whether controlling Substance P expression may control tooth pain.[14]
In addition, dental caries are more likely to develop pulpitis due to less time for the dental pulp to react and protect itself by occluding the dentinal tubules.[12] Based on the tooth injury, sensory nerve fibers react to pulpitis by growing terminal branches into the adjacent surviving pulp, which also changes the cytochemical phenotype. This neural growth typically lasts few a few days and function and form is retained.[6] Thus, pain is poorly localized, and the level of pain stemming from pulpitis varies based on severity, quality, duration, onset, trigger.
As caries turn into dentin, the number of permeable dentinal tubules correlates with the degree of pain. Intrapulp pressure have an effect on the sensory nerves of varying diameters: blocking larger diameter Aδ-fibres and activating smaller C-fibers. Under hypxoic environments and pulp degeneration (symptom of pulpitis), C-fibers may still function.[12] Once reparative dentin forms, odontoblasts associated with the dentin change, and the pulpal fibroblasts lose p75 expression, which is a neurotrophin receptor.[6]
Cells involved in Immune Response
Cell Type     Function
Mast Cells     Rapid release of granules rich in histamine and heparin, along with various hormonal mediators and chemokines
Macrophages     Phagocytic leukocytes that engulf and destroy bacteria
Neutrophils     Contain a variety of toxic substances that kill or inhibit growth of bacteria and fungi
Dendritic Cells     Antigen presentation
Basophils     Release histamine, which is important in allergic reactions and defense against parasites.
Eosinophils     Secrete a range of highly toxic proteins and free radicals that are highly effective in killing bacteria and parasites
Natural Killer Cells     Destroy compromised host cells, such as tumor cells or virus-infected cells
Pulp Sensibility tests
Electric pulp testing (EPT) has been available for over a century and used by dentists worldwide. It is used to determine the health of the pulp and pulp-related pain. It does not provide information on vascular supply to the pulp. EPT produces electrical stimuli that cause an ionic change across the neural membrane, inducing an action potential in myelinated nerves. The threshold of pain level will be determined by increasing the voltage. The requirements of an EPT are appropriate application method, careful interpretation of the results, and an appropriate stimuli. The tests must be done with tooth isolation and conduction media. EPT is not recommended for patients with orthodontic bands or crowned teeth. Key factors in testing are the enamel and dentine thickness and the number of nerve fibers underlying the pulp. Pulp nerve fibers respond to lower current intensities and a small number of pulpal afferents, creating neural responses when electrical stimulation is applied. EPTs may be unreliable and lead to false-positive and false-negative results. False-positive responses in teeth may be attributed to pulpal necrosis. Also, since pulpal and periodontal nerve thresholds may overlap, the periodontal nerves may give a false indication in tooth sensibility.[16][17]
Possible explanations for false-positives include:
    Response caused by conduction of the current because of periodontal or gingival issues
    Breakdown products associated with pulp necrosis may be able to conduct electrical current next to infected and hypersensitive pulp tissue
    Inflamed pulp tissue may still be present
    Metallic restorations or orthodontic gear are still present
Studies have indicated that there is little correlation between histopathological status of the pulp and clinical information. A negative EPT response showed localized necrosis in 25.7% of cases and 72% of cases. Thus, 97.7% of cases with a negative response to EPT indicated that a root canal treatment should be carried out.[17]
Treatment
Once the pulp has become inflamed, the tooth can be diagnostically divided into two categories.
    Reversible pulpitis
    Irreversible pulpitis
Reversible pulpitis
This is the condition where the pulp is inflamed and is actively responding to an irritant. This may include a carious lesion that has not reached the pulp.
Symptoms include transient pain or sensitivity resulting from many stimuli, notably hot, cold, sweet,[18] water and touch. The pulp is still considered to be vital. This means that once the irritant is eliminated, usually by removal of decay and the placement of a restoration, that the pulp will return to its normal, healthy state.[5]
Irreversible pulpitis
This is the condition where the pulp is irreversibly damaged. The pulp can not recover from the insult and damage. For example, decay that has reached the pulp of the tooth introduces bacteria into the pulp. The pulp is still alive, but the introduction of bacteria into the pulp will not allow the pulp to heal and it will ultimately result in necrosis, or death, of the pulp tissue.[5]
Symptoms associated with irreversible pulpitis may include dull aching, pain from hot or cold (though cold may actually provide relief) lingering pain after removal of a stimulus, spontaneous pain, or referred pain.

Clinical signs may include reduced response to electronic pulp testing and painful response to thermal stimuli. Today electronic pulp testers are rarely used for diagnosis of the reversibility of pulpitis due to their unreliable nature. Instead they should only be used to test the vitality of teeth.

The pulp of a tooth with irreversible pulpitis may not be left alone to heal. That is at least the general viewpoint of the dental profession, and not every dentist would agree that a dead tooth must be treated. No statistics are known but it is possible to have a trouble-free tooth after irreversible pulpitis, albeit a dead tooth. The tooth may be endodontically treated whereby the pulp is removed and replaced by gutta percha. An alternative is extraction of the tooth. This may be required if there is insufficient coronal tissue remaining for restoration once the root canal therapy has been completed.