Stomatolog y



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2. Basics of Restorative Stomatology



Restorative stomatology deals with causes of the dental caries origin, diseases of the pulp and the apical periodontium. Treatment of the dental caries and complications associated with it belong to the basic practices of the inpatient stomatological care.

2.1 Dental Caries and Associated Issues


The dental caries is the most widespread disease in the population, it affects 80-90% of the population. The most remarkable feature of prehistorical findings of jaws is the teeth abrasion. The dental caries may already be found on teeth dating back to paleolith and mesolith. Until the end of the 17th century, the dental decay occurrence was rather small and its frequency continued to grow until the 18th century. The dental caries incidence is directly related to the food composition and means of preparation.

The origin of caries has not been satisfactorily explained yet. During certain periods the opinions on the dental caries origin reflected contemporary level of knowledge and they possess rather historical value these days. A group of exogenous - localistic - theories deem the cause for caries in external effects. The endogenous - vital - theories explain the origin of caries by the influence of endogenous factors.



Factors influencing appearance of the dental caries.

Occurrence of the dental caries depends on numerous endogenous and exogenous factors:



The saliva. The saliva is a product of both large and small salivary glands. Most of saliva is produced by the glandula submandibularis (40%) and glandula parotis (26%). Composition of the saliva is variable. More than 99% of it is made of water. The saliva contains 0.7% of solid substances, of those 0.5% are organic compounds and 0.2% inorganic compounds. Calcium is present in form phosphates and to the lesser extent as carbonate. The saliva further contains potassium, magnesium, chlorides, sulfate and some other elements, e.g. iodine. The amount of iodine in saliva is 20 to 100 times higher than in plasma which reflects the thyroid gland function. Carbon dioxide is an important part of the saliva as well, it acts as a buffer to maintain the saliva’s pH. Organic compounds of the saliva are represented by mucoids, albumins, globulins and peptides. Urea, uric acid, creatin and ammonia are present in low concentrations in saliva. Among the most important enzymes are amylase, esterase, lipase and peroxidase. Lysozyme is an important component as well. The saliva contains small amounts of erythrocytes, leukocytes from the gingival grooves and lymphocytes from the tonsils. However, phagocytotic ability of leukocytes from saliva is low.

Microorganisms of the oral cavity. A mixed microbial flora, both aerobic and anaerobic inhabits the oral cavity. Streptococcus mutans which forms 28 to 96% of the total microbial flora present in the dental microbial plaque, has the closest relationship with the occurrence of a dental caries. This relation is supported by its ability to produce acids and both intracellular and extracellular polysaccharides. Intracellular polysaccharides may be also produced by various strains of staphylococci, diplococci and rods. That is why the microbial flora in general is responsible for the dental caries origin, not just a single strain of microorganism.

Microbial plaque. This coating is one of the most important factors playing a role in the dental caries occurrence having also a relation to the origin and course of parodontopathies. The first stage of its development is the secondary cuticle which is made of salivary glycoproteins and covers teeth, fillings, crowns and dentures. At the early stages the cuticle contains cocci and short rods. The microbial plaque itself is made of the secondary cuticle, microorganisms and an intermicrobial substance. Some bacteria can produce glucanes and fructanes and promote the plaque growth even when no food is being consumed. Besides streptococci, a developed microbial plaque contains also actinomycetes (40-60%). The amount of plaque varies - most of it is present in the morning and after food ingestion. The plaque’s formation is linked to places that are habitually non-clean (i.e. places where the process of self-cleaning is restrained) - grooves of premolars and molars, cervical parts of crowns. According to its location, the plaque can be divided into fissural, supragingival, and subgingival. At the surface of the microbial plaque, there is materia alba that is made of the peeled off epithelium, leukocytes and food residues.

The dental calculus is formed by mineralization of the microbial plaque. It can be found in mouth especially around the large salivary glands ducts.



Food intake, nutrition, hereditary factors. The occurrence of caries is influenced by the presence of low-molecular saccharides from food, time intervals of a food ingestion and its composition. Concentration of sugar in saliva has a great influence, as well as the period of its activity. Food that is long-persistent and sticks to the teeth (honey, chocolate) has a negative effect. The origin of caries is not directly caused by genetic factors, although a predisposition to it is hereditary. Genetic factors are rather manifested by the teeth arrangement at some orthodontic anomalies. These abnormalities create a condition for easier deposition of the microbial plaque, thus causing caries and parodontopathies.
Dental caries and its clinical manifestations.

Dental caries is linked to the hard dental tissues. It starts with the enamel surface’s decalcification during which the hydroxyapatite crystals loose its orientation, change their shape and the interprismatic spaces are enlarged. When more rods become affected, a macroscopically detectable defect of the enamel can be observed. After the decay crosses the enamel-dentine boundary, it spreads more rapidly through dentine towards the pulp. The carious focus consists of large cavities on the surface which are filled with numerous microorganisms producing acids and proteolytic enzymes. As the caries process widens, it affects the enamel, dentine, and the cement. The primary caries occurs on those teeth surfaces that have not been treated yet, the secondary caries starts at the close vicinity of fillings. The occurrence of the secondary caries depends on the physical and chemical properties of the filling materials, faults during its preparation, and during a tooth preparation and filling. Profession - related caries are caused by the sugar or flour dust at workers in bakeries and mills. These caries occur mainly as circular forms around the tooth cervix. Ignoring safety rules when working with acids or hydroxides leads to damage of the frontal teeth labial surfaces. According to the extent of damage to teeth, caries can be divided into surface caries (extending to the enamel), medium caries (extends into dentine) and caries close to the pulp (at the close proximity of the pulp chamber).


Clinical manifestations of the dental caries.

The enamel caries is manifested as a white spot where the enamel looses its gloss. It may be brown colored by deposition of a pigment. It is not painful. A large carious defect, extending to a various depth into dentine, is usually painful when a tooth is irritated directly (mechanical, chemical, thermal effects). Pain is relieved, however, immediately after the causing effect stops. The affected tooth has clinical signs of rough surfaces or sharp-edged cavities which may accumulate food residues.

The caries close to the pulp is a result of further progression of the carious process. Dental pulp defends itself by producing the tertiary and transparent dentine. The tertiary dentine is synthesized as a response of odontoblasts to an irritation and it contains more of the basal substance and less dentine tubules. The transparent dentine is made of mineralized processes of odontoblasts. The pulp does not usually display any signs of inflammation and a patient may not have heavy problems. Pain caused on cold, salty, sweet and sour irritation is often reported, however, this pain is relieved after the causing effect stops.

Caries close to the pulp are treated by the method of indirect pulp capping . This treatment is based on supporting the pulp’s resistance by calcium hydroxide (Calxyd brand) that is applied to the pulpal wall of a prepared cavity after soft dentine has been removed. Calxyd has antimicrobial and anti-inflammatory effects and stimulates the pulp’s resistance mechanisms. The Ca2+ and OH- ions penetrate the pulp. OH- ions cause coagulation of protein components of the pulp and neutralize acidic inflammation products. Ca2+ ions stimulate phagocytosis, decrease permeability of capillaries and upon reaction with CO2 form calcium carbonate in the tissue. A layer of Calxyd is covered by the zinc oxide -an eugenol based cement that has good insulation properties, a weak antimicrobial action and stimulates production of the tertiary dentine. This kind of treatment provides for successful results in up to 90% cases. Failures are usually accounted to a false diagnosis, caused by leaving a rather thick layer of softened dentine, or low resistance abilities of the pulp. In cases when the pulp chamber is exposed either by an injury or by careless preparation of a cavity, the direct pulp capping method is indicated. Here, the most appropriate material is calcium hydroxide (Calxyd) as well. This material is applied directly on the exposed pulp providing a perforation is not too large. By these means, a layer of a coagulation necrosis is formed, and the layer of a connective tissue barrier forms underneath it. Non-differentiated mesenchymal cells produce new odontoblasts that differentiate further. A dentine bridge is gradually formed above the perforation which takes 4 to 6 weeks. The success rate of this method is 80%-90%. Failures may be caused by too large a perforation, by infecting the dental pulp, or decrease of the pulp’s immunity.



Materials used for the dental caries treatment.

The underlying principle of the dental caries treatment is a careful removal of carious, softened parts of dentine and providing for sufficient retention and resistance of a filling. Filling materials used in restorative stomatology practice can be divided into two classes: temporary and permanent. To isolate the pulp from thermal and chemical irritation, zinc oxide - phosphate, carboxyl or zinc oxide - eugenol cements are used as bases. Zinc oxide - phosphate cement is used also for root canals filling before a surgery (apicectomy) and for cementing during prosthetic works. Zinc oxide - phosphate cement is often used as a temporary filling material , e.g. as a cavity closure after the pulp necrotizing compounds or disinfecting dressings have been applied.



Permanent fillings are either plastic (that solidify after filling into a prepared cavity) or cast (made in a laboratory according to a previously taken impression). The major requirements for filling materials are their volume, mechanical and chemical stability, they have to be non-irritating, and should provide for an esthetic appearance in the frontal sections of the dentition. Amalgam is the most widely used plastic filling for the lateral sections of the dentition. It is prepared as a mixture of a metal powder (containing various weight parts of silver, zinc and copper) with mercury. Pleasantly looking composite filling materials are used at the frontal sections of the dental arch (Evicrol brand). These materials meet the requirement of a perfect seal of a prepared cavity, they adhere well directly onto hard dental tissues and they are color stable. Cast fillings are usually made of precious dental metals (gold). Due to its disturbing appearance they are used mainly at the lateral sections of the dentition.

2.1.1 Diseases of the Pulp


Many effects, such as infectious, chemical, physical and combined contribute to origin of the dental pulp diseases. In most cases, a mixed bacterial flora enters the pulp from a carious focus through the dentine tubules. Less frequently, an infection enters the pulp retrogradely via foramen apicale (in case of deep periodontal pockets) or by the blood stream. Silica-phosphate fillings that lack bases and to the lesser extent also composite fillings may cause chemical irritation. The pulp inflammation may occur after an acute trauma or by a chronic traumatic irritation, as well.

Regressive changes of the pulp.

As a reaction of the pulp to either external or internal irritation, the true pulp stones arise from odontoblasts. Their structure is similar to the tertiary dentine. Mock pulp stones are formed by mineralizing deposits surrounding an organic core. Pulp stones may be located freely inside the pulp’s interstitium or adhere to the walls of the pulp’s chamber or a root canal. The proof of pulp stone presence is done by an X-ray examination. Clinically, pulp stones may be a cause of neuralgic pains.




The pulp hyperemia.

This change is characterized by a short and well localized pain in response to physical or chemical stimuli which diminishes after a causing effect stops. The treatment in this case is an indirect pulp capping.




Acute pulp inflammation (pulpitis acuta).

The inflammation may affect a part of the pulp (pulpitis acuta partialis) or the whole pulp (pulpitis acuta totalis). It may have a serous (pulpitis acuta serosa) or purulent (pulpitis acuta purulenta) forms. The pain at serous pulpitis is caused by an external irritation at the beginning, later it may be spontaneous. Pain is described by a patient as blunt, radiating and pulsating. At a total pulpitis, the pain is often hard to localize (possesses a neuralgic character). Treatment for a serous pulpitis: pulpotomy or extirpation of the pulp by the vital or mortal methods. The purulent form of pulpitis accompanied by formation of small abscesses inside the pulp chamber has clinical signs similar to those at serous total pulpitis. A significant anamnestic feature is a pain relief by cooling. Treatment for the purulent form: pulpotomy or extirpation of the pulp by the vital method.



Chronic pulp inflammation (pulpitis chronica) takes forms of a closed inflammation of the pulp chamber (pulpitis chronica clausa, granulomatosa, interna) or an open inflammation (pulpitis chronica aperta hypertophica, ulcerosa). Closed pulpitis often has a course without significant clinical manifestations. A diagnosis is based on an objective finding completed by an X-ray examination (e.g. a resorption of the pulp chamber or a root canal - an internal granuloma). Pulpitis chronica aperta is characterized by growing of the pulp through a cavity, its ulceration on the surface, and sometimes by an outgrowth of the granulomatous tissue through a cavity to the oral cavity and formation of the pulpous polyp. Clinical signs are mild, bleeding occurs often as a result of the pulpal tissue injury.

The treatment of the pulp altered by an inflammation is performed by its partial removal (pulpotomy) or total removal (extirpation). The pulp removal may be done under a local or block anesthesia (the vital method) or after a devitalization of the pulp by treatment of various substances (the mortal method). As devitalizers, arsenic trioxide, cobalt paste (arsenic metal), or paraformaldehyde are often utilized. Arsenic trioxide (Arsodent) is a protoplasmic poison that affects blood vessels, cells of the pulp and nerve endings. Its application results in necrosis of the pulp that can be removed painlessly. Arsodent is applied as close to the pulp as possible or directly on an exposed pulp, and a cavity is then sealed hermetically by a temporary filling. Its effect on molars lasts for 48 hours, after that it is necessary to remove the necrotic pulp, to fill the root canal by a root filling material and to make a permanent filling. Arsenic metal has the same effects as Arsodent, although its action is prolonged and is usually applied for a period of 3 to 5 days. The paraformaldehyde paste releases formaldehyde. Anesthetics that are contained in the paste relieve the pain. Since the paste is not very stable, its activity decreases with time. The mortal method is indicated for all kinds of pulp inflammation except the purulent, ulcerous and polypous forms. The use of Arsodent is contraindicated at teeth with incomplete root development. At this method, a patient has to be informed that a pain won’t disappear immediately and that a devitalizer has to be removed from a dental cavity on time. For these reasons the vital method of treatment is preferred. Requirements for a good result of the vital method are proper diagnosis of the disease, good anatomical conditions of the root canal and sufficient amount of time for the treatment. The greatest advantage of this method is completion of the whole treatment during one visit.

The consequence of inflammatory and degenerative changes of the pulp is pulp necrosis that may affect just a part or the whole pulp. If there is an infection at a necrotic pulp, the pulp gangrene occurs. A patient with gangrene feels pain during a heat test.



2.1.2 Periodontitis


Periodontitis is characterized by spreading an infection into the periodontium. They are caused mostly by the root canal infection that proceeds into periodontium through foramen apicale or through ramifications in the apical area. Among other causes there may be traumas (both chronic and acute), chemical effects (devitalization or disinfecting agents).

Periodontitis acuta is characterized by dilatation of vessels near the root apex and an edematous infiltration of periapical tissues. According to the extent of inflammatory changes, an acute periodontitis has the following stages:

  • at the periodontal phase, the inflammation is located at the apex area

  • for the enosseal phase, the serous exudation and formation of a cellular infiltrate with a pus colliquation are characteristic

  • at the subperiosteal phase, the inflammatory process spreads under the periosteum of an alveolar ridge

  • after the periosteum necrosis the pus containing exudate leaks under a mucosa; the submucosal phase is accompanied by formation of an abscess that sometimes empties spontaneously by an intra-oral fistula.

An acute periodontitis often originates by exacerbation of a chronic periodontitis due to decrease of an organism’s immunity or after a treatment of an infected root canal. After examination of the oral cavity, a doctor formulates a diagnosis and makes it more specific after an X-ray examination. A physician can identify an aching tooth and the apical area sensitivity upon percussion. It is also possible to find a submucous tissue infiltration, eventually redness, swelling and fluctuation at a vestibule surrounding the affected tooth. At more developed cases, enlargement of regional lymph nodes occurs and the patient’s general condition is altered, often accompanied by a fever. Pain is severe during the early phases of the inflammation. After the submucosal infiltrate or a fistula are formed, an obvious pain relief comes. The aim of the acute periodontitis treatment is to ensure that an exudate may flow away from the periapical area. This may be achieved by a tooth trepanation (at periodontal and enosseal phases) and by making a passage through the root canal. A patient feels a distinct relief after this treatment. At the subperiosteal and submucosal phases, the tooth trepanation has to be complemented by an intra-oral incision. Antibiotics should be prescribed if a patient’s general state is altered and an elevated body temperature occurs. After acute problems are relieved, further treatment is applied as in the case of diagnosis of periodontitis chronica.

Periodontitis chronica. The underlying cause of the disease is formation of a granulomatous tissue at the tooth apex area. The course of the disease is either in the form of a non-limited, diffuse process (periodontitis chronica diffusa) or it tends to be localized (periodontitis chronica circumscripta). A focus is then encapsulated by a fibrous membrane, with small abscess cavities or a single continuous abscess cavity inside. Mallaséz’s epithelial cells, remnants of the Hertwig’s sheath occurring during the tooth development, can often be found. These cells grow as a result of an inflammatory irritation and form clusters of epithelial cells - an epithelial granuloma.

At periodontitis chronica granulomatosa progresiva, the granulomatous tissue spreads into surrounding structures and mucosal, even cutaneous fistulas arise. If the process affects the upper jaw near the antrum, an antral fistula may be formed. Chronic periodontitis usually runs with no clinical difficulties and it is diagnosed by an X-ray examination. An X-ray image shows large or small, diffuse or sharp-edged radiolucency around the tooth apex. A mucosal fistula can be sometimes found next to an affected tooth. A chronic inflammation may also exacerbate acutely, causing obvious difficulties. The treatment for a necrotic, gangrenous pulp and for chronic periodontitis is by conservative or surgico-protective means.



Conservative therapy relies on a mechanical widening of the root canal, treatment of a microbial infection and filling the root canal with a filler that prevents re-infection and allows for healing of periapical tissues.

At the surgico-conservative therapy, the root canal is filled with the zinc oxide - phosphate cement, after a previous root canal treatment. The surgery - tooth apex resection (apicectomy, amputation) - the basis of which is an removal of a treated tooth apex, excochleation of the granulomatous tissue followed by a toilet of the bone wound.



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