DANYLO HALYTSKYI LVIV NATIONAL MEDICAL UNIVERSITY PEDIATRIC DEPARTMENT

Methodical Guides on Pediatric Dentistry for the 4th -year students of dental faculty

LVIV - 2012 Practical class № 1 The periapical of the temporary and permanent teeth. Etiology, pathogenesis, clinic. The influence of the chronic periapical inflammation of the primary teeth on the permanent teeth development. Diagnostics, differential diagnostic, radiographic diagnostics

Teaching objective: to learn with students the peculiarities of structure of the periodontium in children, its change in the process of root formation and resorption of primary teeth; classification of the periapical inflammation, diagnostics, differential diagnostics of acute and chronic periapical inflammation in primary and permanent teeth.

Pre-study test questions 1. Peculiarities of the structure of the periodontium in children. 2. Function of the periodontium. 3. Anatomical and physiological changes in the periodontium during the root formation and resorption of primary and permanent teeth in children. 4. Types of physiologic root resorption in primary teeth. 5. Types of pathologic root resorption in primary teeth. 6. Classification of the periapical inflammation.

Contents of the class Definition: periapical inflammation ( apical periodontitis) is usually due to spread of following death of the . It characteristically causes tenderness of the tooth in its socket. Local ( periapical ) inflammation must be distinguished from chronic ( marginal ) periodontitis, in which infection and destruction of the supporting tissues spread from chronic infection of the gingival margin. Infection is far the most common cause. The usual sequence of events is caries, , death of the pulp and periodontitis.

Etiology. The nature and behavior of that form at the apex of the tooth are a reflection of the conditions that lead to the destruction of the pulp of the associated tooth. Causes of apical periodontitis: - infection - trauma - chemical irritation - immune factor/ immunifaction.

I. Infection 1. Dental caries: Dental plaque → Dental caries →Pulpitis → Apical periodontitis 2. Periodontal pocket: the necrotic pulp probably becomes infected by bacteria from the gingival margins, leading to apical periodontitis. 3. Systemic infection ( rare).

II. Trauma 1. The pulp sometimes dies from a blow which damage the apical vessels. 2. during endodontic treatment, instruments may be pushed through the apex or side of the root, damaging the periodontal membrane and carryng infected debris from the pulp chamber into the wound. 3. A high filling or biting suddenly on a hard object, sometimes caused an acute but usually transient periodontitis. 4. Oclusal trauma and orthodontic lead to trauma.

III. Chemical irritation: 1. irritant antiseptics used to sterilize a root canal can escape through the apex and damage the surrounding tissue. 2. A root-canal filling may also extend beyond the apex with similar effect. 3. Devital materials.

Clinic of the apical periodontitis of the primary teeth

The most often the chronic granulated periapical periodontitis and the exacerbation of the chronic periapical periodontitis are observed in the primary teeth in children. The main features of the chronic granulated periapical periodontitis are following: - the expansion of the granulated tissues; - the osteoclastic bone resorption and signs of its renovation; - the cement and root resorption.

Clinic: - no pain - fistulae tract formation or scar - deep carious cavity with no reaction to thermal and electric stimuli; - discoloration of the tooth; - painless probing and drilling of the enamel-dentin junction - tooth is not tender to percussion; - regional chronic lymphoadenitis

Radiographically: - cortical plate destruction; - bone with radiolucency.

The main features of the exacerbation of the chronic periapical periodontitis are the following: - the body’s defenses weaken; - the serous inflammation lasts no more than 24 hours and continuous into the festering one; - constant or aching pain; - pain during chewing; - the temperature arises, paleness, “smouldering” - discoloration of the tooth or deep cavity; - tooth mobility; - extreme sensitivity to percussion; - no reaction to thermal and electric stimuli; - fistulation with suppuration; - reddened. Edematous swelling of mucosa, tenderness to palpation; - lymphatic nodules are enlarged and painful; - cortical plate destruction.

The main differences between acute periapical periodontitis and the exacerbation of the chronic periapical periodontitis are: - no evidence of bone lesions on the X-ray; - no evidence of fistulae, scar or .

Chronic periapical periodontitis can lead to the following complications: - expansion of the pathological process on the permanent tooth follicle which can cause its death; - infication of the permanent tooth follicle on the early stages of its mineralization can cause the local formation; - spreading of the inflammatory process on the follicle can cause its death, and as the result the sequestration of follicle can occur; - the long lasting chronic periapical inflammation can lead to the changes of the permanent tooth follicle location which clinically is observed as oral or vestibular tooth location after the tooth eruption or torsivertion; - destroying of the bone between primary tooth and permanent follicle due to expansion of the granulated tissue can cause the prematurely tooth eruption with low level of the enamel mineralization and risk of caries development; - premature primary tooth extraction caused by chronic periapical inflammation, especially during the period of the root formation and at the beginning of their stabilization can lead to the permanent tooth retention, delaying of its eruption and formation of the orthodontic anomalies; - expansion of the chronic inflammatory processes on the adjacent follicle in some causes follicular cyst formation.

Clinic of the apical periodontitis of the permanent teeth.

Acute periapical periodontitis

Serous form. The following signs are observed: - General condition is satisfied; - Aching pain; - Tooth elongation; - The tooth probing is painless; - There are no evidence of the transitional fold mucosa changes; - No changes on the X-ray picture.

Festering form. The following signs are observed: - General condition turn for the worse (temperature arises) - Permanent severe throbbing pain; - Half-opened mouth; - Tenderness to percussion; - Tooth mobility may be present in some cases; - Tenderness to palpation of the mucogingival fold; - No changes on the X-ray picture.

Chronic periapical periodontitis

Granulated form The clinic is similar to the clinic of the primary teeth.

Chronic periapical peridintitis with This form of chronic inflammation mainly is observed in mature teeth. The following signs are present: - the granulated tissue is surrounded by capsule; - asymptomatic course; - the cortical plate of alveolar processus is evaginated during palpation; - on the radiograph, CAP appears as a round or oval radiolucency that is usually sharply demarcated.

Chronic fibrous periodontitis. The following signs are present: - Tough fibrous connective tissue is observed on the apical part of the root; - Deformation of periodontal ligament space (expanded or constricted).

The clinical picture of the exacerbation of the chronic periapical periodontitis of the permanent teeth is similar to the clinic of the primary teeth.

Comprehension control 1. Peculiarities of clinical course of acute infectious periapical inflammation of primary teeth. 2. Clinical course of the acute toxic periapical inflammation of primary teeth. 3. Peculiarities of clinical course of acute traumatic periapical inflammation of primary teeth. 4. Ways of spreading of the exudate at acute periapical inflammation. 5. Peculiarities of clinical course of chronic periapical inflammation of primary teeth 6. Symptoms of chronic periapical inflammation at stage of exacerbation at period of root formation, stabilization and resorption. 7. Role of the roentgenologic method of examination in diagnostics and differential diagnostics of periapical inflammation. 8. Influence of the periapical inflammation on the permanent teeth buds. 9. Influence of the periapical inflammation on the general state of the child organism. 10.Peculiarities of clinical course of acute periapical inflammation of permanent teeth. 11.Peculiarities of clinical course of chronic periapical inflammation of permanent teeth. 12. Differential diagnostics of acute, chronic periapical inflammation and exacerbation of periapical inflammation 13.Roentgenologic method of examination of periapical inflammation of permanent teeth.

Practical class № 2

Treatment of periapical inflammation of the primary teeth in children. Indications of the choice of the treatment methods. Methods and materials for the root canals obturation of the primary teeth in children in the different stages of their development. Indications and contraindications for the conservative treatment of the primary teeth with periapical inflammation. Prognosis.

Teaching objective: to learn with students the principles of treatment of the periapical inflammation in primary teeth, indications to conservative and surgical treatment of the periapical inflammation of primary teeth, influence of the periapical inflammation on the development of permanent tooth follicle.

Pre-study test questions 1. Factors which influence on the treatment methods of periapical inflammation of primary teeth in children. 2. General plan of treatment of acute periapical inflammation in children. 3. Difficulties of the treatment of acute periapical inflammation in teeth with immature root. 4. Complication during treatment of periapical inflammation of primary teeth. 5. Changes in the organism in patient with periapical inflammation of primary teeth.

Contents of the class The methods of treatment of the primary teeth: - Conservative treatment with tooth preservation; - Surgical treatment (the tooth extraction).

Indications for the primary tooth extraction: - the tooth is responsible of the acute septic state; - the tooth is the source of the acute odontogenic processes ( permanent exacerbated periostitis, ); - the hosts defence system is weakened; - arresting of the root formation before ending of the root development; - damaging of the cortical lamina of the permanent tooth follicle by inflammatory process; - pathological or physiological root resorption more than for 1/3 of its length; - tooth mobility (II-III degree); - the crown of the tooth is destroyed and the physiological tooth changing occurs in 18 month; - root or tooth floor perforation; - inner resorption of the roots; - extensive pathological destroying of the bone; - the failure of the conservative treatment; - the patients with complicated anamnesis vitae; - retained primary tooth with radiographic evidence of the presence of permanent tooth.

The main goal of the conservative treatment of the primary teeth with periapical periodontitis is to eliminate the infection from the periodontum for the maintenance of the physiological root development and prevention of damaging of the permanent tooth. It can be achieved due to precise mechanical instrumentation, thorough irrigation and subsequent tight obturation of the root canal system. The choice of treatment methods depends on the etiology of the inflammatory process (infection, traumatic, toxic processes), root development stage (stage of the root growth, phase of the root stabilization, phase of the root resorption), size of the bone lesion and somatic health of the child.

Treatment of the primary tooth in phase of the root stabilization Conservative treatment of the primary teeth is pointed at elimination of infection in the periapical tissue, pain relief and prevention of proceeding and spreading of the inflammatory process into adjacent tissue and organs. The purulent effluent which is formed in the periodontum can go out from the periapical tissue by the different ways: - through the root canal system, - from the apex towards the periosteum (through the bone structure), - through the fistulae ( exacerbation of the chronic granulated periodontitis), - through the ligamental space, - through the tooth extraction. It is essential to provide outflow of the pus from the periapical tissue through the root canal at the first stage of the .

The first appointment treatment includes: - anesthesia; - opening of the pulp chamber and canal orifices; - initial instrumentation of the root canal system (shaping and cleaning) with considerable quantity of irrigation solution; - careful opening of the root apex without pushing of the debris behind the apex.

The doctor can leave the tooth opened for one day when the considerable quantity of the purulent effluent is present and there are no possibilities to achieve the dry canal at the first appointment. In these cases the clear recommendation should be refered to the patient: - frequent mouth soda bath; - maintenance of the drainage through the root canal (pulp chamber should be opened for all the time; just during feeding it should be closed by the cotton pallet).

The second appointment treatment includes: - final root canal instrumentation and irrigation with considerable quantity of the irrigation solution; - drying of the root canal by means of sterile paper points; - placement of temporary dressing into the root canal; - placement of temporary crown filling.

The completion of the root canal treatment with the root canal filling can be providing when: - there is no evidence of edema of the face or transitional fold; - the tooth is painless; - there is no tenderness to percussion; - there is no sensitivity to palpation of mucogingival fold nearby the tooth apex; - absence of the pus into the root canal; - the tooth is odour free.

Peculiarities of the endodontic treatment of the temporary teeth. - wide opening of the pulp chamber; - work-length determination 1-2 mm less than roentgenologically found out; - there is no necessity to form the tapered canal; - mechanical instrumentation should be gently provided as the structure of dentin of temporary root is low mineralized and the root walls are thin; - irrigation of the root canal space with un-irritative antiseptic solutions; - using of resorbable pastes with antimicrobial effects for permanent root canal obturation.

The endodontic treatment of the immature teeth The treatment of choice for necrotic teeth with wide opened apexes is apexification, which is induction of apical closure to produce more favourable conditions for conventional root canal filling. In the past, techniques for management of the open apex in non-vital teeth were confined to custom fitting the filling material, paste fills and apical surgery. A number of authors have described the use of custom fitted gutta-percha cones, but this is not advisable as the apical portion of the root is frequently wider that the coronal portion, making proper condensation of the gutta- percha impossible. Sufficient widening of the coronal segment to make its diameter greater than that of the apical portion would significantly weaken the root and increase the risk of fracture. The disadvantages of the surgical intervention include the difficulty of obtaining the necessary apical seal in the young pulpless tooth with its thin, fragile, irregular walls at the root apex. The wide foramen results in a large volume of filling material and a compromised seal. Apicoectomy further reduces the root length resulting in a very unfavourable crown root ratio. Some believe that instrumentation may in fact hamper root development and that preparation of these canals should be done cautiously, if at all. Although a variety of materials have been proposed for induction of apical barrier formation, calcium hydroxide has gained the widest acceptance. Calcium hydroxide had a unique potential to induce formation of heterotopic bone. The reaction of the periapical tissues to calcium hydroxide is similar to that of pulp tissue. Calcium hydroxide produces a multilayered necrosis with subjacent mineralization. It appears that the high pH of calcium hydroxide is an important factor in its ability to induce hard tissue formation. In recent times interest has centered on the use of mineral trioxide aggregate (MTA) for apexification. This material was first introduced in 1993 .This material has demonstrated good sealability and biocompatibility. MTA has a pH of 12.5 after setting which is similar to the pH of calcium hydroxide and it has been suggested that this may impart some antimicrobial properties. It has been used in both surgical and non-surgical applications including root end fillings, direct pulp caps, perforation repairs in roots or furcations and apexification.

Comprehension control 1. Indications to conservative treatment of periapical inflammation of primary teeth. 2. Indications to extraction of primary teeth with periapical inflammation. 3. Peculiarities of treatment of acute periapical inflammation of primary teeth. 4. Principles of treatment of exacerbation of periapical inflammation of primary teeth. 5. Peculiarities of instrumentation of root canals in primary teeth with periapical inflammation. 6. Peculiarities of treatment of chronic periapical inflammation in primary teeth at stage of root resorption. 7. Mistakes of choice of treatment methods of periapical inflammation in primary teeth. 8. Complications during the treatment of the periapical inflammation of primary teeth.

Practical class № 3

Treatment of periapical inflammation of the permanent teeth in children. Indications of the choice of the treatment methods. Apexification. The treatment methods and indications. Prognosis

Teaching objective: to familiarize students with different treatment methods of the periapical inflammation; to teach students to choose the treatment methods of periapical inflammation of teeth depending on the type of disease.

Pre-study test questions 1. Definition of the periodontium. 2. Classification of the periapical inflammation. 3. Peculiarities of the clinical course of the periapical inflammation of permanent teeth. 4. Treatment methods of periapical inflammation. 5. Topographic and morphological peculiarities of root canal system of permanent teeth.

Contents of the class The methods of treatment of periapical inflammation of the permanent teeth: - conservative; - surgical; - combinative (conservative-surgical).

Conservative method Indications: - acute and exacerbation of chronic apical periodontitis - chronic apical periodontitis Contraindications: - increasing of inflammation in spite of periosteotomy and opening of the root apex. - radicular cysts.

The main principle of treatment of acute apical periodontitis - to create a good exudate evacuation. Ways of exudates evacuation: 1. Through the root canal 2. Through the dentogingival junction 3. Through the incision 4. Through the alveole

Conservative method of treatment is conducted with absence of following sings : - the tooth is responsible of the acute septic state, chronic infection and intoxication of the organism; - fully destroyed crown, without possibility of its restoration; - perforation of the tooth bottom.

Treatment of Acute periapical inflammation. Technique stages: 1st visit 1. Anesthesia 2. Operative field isolation 3. Carious cavity preparation 4. Evacuation of necrotic tissues from the root canal 5. Opening of the root canal apex 6. Cleaning of the root canal with strong antiseptics 7. Hermetization of the root canal with cotton with antiseptic, temporary filling (in the 1-st stage of periapical inflammation) or leaving the tooth open (in the 2-nd stage of periapical inflammation)

2nd visit 1.Widening and cleaning of root canal 2.Hermetization of the root canal with cotton with antiseptic 3.Temporary filling

3rd visit 1.Removing of the temporary filling 2.Cleaning of root canals with antiseptics 3.Drying of root canals 4. Filling of root canals 5.Tooth restoration

Treatment of chronic periapical inflammation of the tooth at root stabilization stage

To achieve goods results root canal must be widely opened at full length allows the influence on the periapical focus and excludes the canal as the seat (breeding ground, nidus) of bacterial toxins. In the front teeth and often in premolars, where root canals are usually single and not obturated, treatment of chronic periapical inflammation will be less complicated. Indications to conservative treatment are periapical changes up to 0.5 cm in diameter. The treatment is conducted in 2-3 visits. 1 st visit : - necrectomy, formation of carious cavity, taking into consideration the necessity of good access to the canals with all endodontic instruments. Portions under the protection of antiseptic solutions must evacuate necrotic remnants of the pulp very carefully - tooth can be closed by temporary filling with strong antiseptic and instrumentation of the canal will be done in next visit. In the I-st visit instrumentation can also be done but sometimes it can provoke exacerbation.

2 nd visit: (in 2-3 days) -instrumentation of the canals, widening the canals. If the signs of exudates are finding on the paper point taken out from the canal, medication of the canal with enzymes, antiseptics has be continued. -when the canal is clean the dentist must check up the apical foramen (it must be open). Reamers or K-files can do the opening of apical foramen. Only in the case of opened apical foramen we can influence on the periapical focus of inflammation.

3 rd visit : Filling of the root is usually done in the 2 or 3 visit. Before filling the root, biologically active pastes (with Ca (OH)2, lysozym, metacyl and others) can be put in periapical focus to stimulate bone regeneration.

Comprehension control 1. Indications to surgical treatment of periapical inflammation. 2. Armamentarium for the mechanic treatment of root canals, its characteristic. 3. Engine instruments for the mechanic treatment of root canals, its characteristic. 4. Characteristic of the filling materials for the root obturation.

Practical class № 4 Mistakes and complications during the diagnostics and treatment of the periapical inflammation of the primary and permanent teeth in children. Their prevention and treatment. Summary lesson.

Teaching objective: to teach students to eliminate the mistakes during the diagnostics and treatment of periapical inflammation of primary and permanent teeth.

Pre-study test questions 1. Classification of periapical inflammation. 2. Diagnostic methods of periapical inflammation. 3. What diseases should be differentiated with periapical inflammation. 4. Characteristic of the filling materials for the root canal obturation in primary and permanent teeth.

Contents of the class

Endodontic mishaps:

- Access related - Treating the wrong tooth - Missed canals - Damage to existing restoration - Access cavity perforations - Crown fractures - Instrument related - Ledge formation - Cervical canal perforations - Midroot perforations - Apical perforations - Separated instruments and foreign objects - Canal blockage - Obturation related - Over- or underextended root canal fillings - Nerve paresthesia - Vertical root fractures - Miscellaneous - Post space perforations - Irrigant related mishaps - Tissue emphysema - Instrument aspiration and ingestion

Treatment of the Wrong Tooth Treatment of the wrong tooth can be so easily prevented. One should make sure through inquiry, testing, examining, and radiography that one has confirmed which tooth requires treatment and then mark it with a felt-tip pen.

Missed Canals Additional canals in the mesial roots of maxillary molars and the distal roots of mandibular molars are the most frequently missed. Second canals in lower incisors, and second canals and bifurcated canals in lower premolars, as well as third canals in upper premolars are also missed. One must be diligent and prepare adequate occlusal access! Always expect there will be an extra canal. Magnification with either telescopic lenses or a surgical microscope is indispensable. Damage to an Existing Restoration Porcelain crowns are the most susceptible to chipping and fracture. When one is present, use a water-cooled, smooth diamond point and not place a rubber dam clamp on the gingiva of any porcelain or porcelain-faced crown.

Access Cavity Perforations Often the first sign of an access cavity perforation is blood in the cavity or the patient complaining of a taste of NaOCl. This most frequently happens in the floor of molar preparations when one is searching for a third or fourth canal. The site of the perforation must be found, the floor of the preparation cleansed, the bleeding stopped, and mineral trioxide aggregate (MTA) applied to the perforation. Because it takes MTA more than 3 hours to set, it should be covered with a fast- setting cement. The other canal orifices should be protected by placing paper points or an instrument in the canals to prevent blockage. In the event MTA cannot be immediately applied, it is best to stop the bleeding, place calcium hydroxide over the “wound,” place a good temporary filling, and set an appointment with the patient, the sooner the better. The perforation area will be dry at the next appointment; then MTA can be applied and treatment continued.

Crown Fractures Remember, preparing an endodontic access cavity in a tooth, particularly a molar or premolar with a large restoration, materially weakens the crown. Infrequently the crown fractures, either during preparation or at a subsequent appointment. One of the frequent causes is failure to relieve the occlusion. If the fracture is chisel shaped and a cusp breaks off down to the periodontal ligament, the tooth can usually be salvaged. If the fracture extends through the pulp chamber and down into the root, however, the case is hopeless and the tooth should be extracted.

Instrumentation-related mishaps Overzealous cleaning and shaping have lead to many mishaps, zipping and perforations among them. Many of these iatral accidents begin with ledging during canal preparation.

Ledge Formation Many ledges are caused from inadequate access. The operator does not retain complete control over the direction of the tip of the instrument and it gouges into the wall of the canal starting a ledge. Newer instruments with noncutting tips have materially reduced this problem. The rounded tip does not cut into the wall but slips by it. Curved roots are another impediment in canal preparation. This is especially true near the apex of maxillary lateral incisors and the palatal root of maxillary first molars

Perforations Canal perforations may be categorized by their location. Access cavity perforations, such as perforations through the floor into the furcation, have already been discussed. Root perforations can be identified as cervical, midroot, or apical. These are usually caused by three errors: creating a ledge and persisting until a perforation develops, or wearing a hole in the lateral surface of the midroot by overinstrumentation (canal stripping), or using too long an instrument and perforating the apex. Cervical perforations usually occur when too large an instrument is used to widen canal access, frequently a Gates-Glidden or Peeso drill. The first indication is the appearance of blood in the cavity. Again, the bleeding is stopped and MTA is applied to the perforation. Cotton should be placed in the chamber and a good temporary placed to allow time for the MTA to set (> 3 hr). Preparation is continued at a subsequent appointment. Midroot perforations are usually caused by zipping, frequently in the distal wall of a curved mesial root of a mandibular molar. Again, blood in the canal indicates that a perforation has occurred. By using paper points in the canal, the location of the perforation can be determined . MTA is the material of choice to close the perforation; an appointment is made with the patient for continued treatment. Apical perforations are usually due to overeager instrumentation, just plain drilling out through the apical orifice. Again, this can usually be determined with paper points—they appear bloody at the tip. If a canal curves at or near the apex, using larger and larger instruments will cause zipping that hollows out this area and leads to perforation. Remember, a curved canal is gradually straightened through cleaning and shaping. A straight line is the shortest distance between two points; therefore, the cleaning and shaping actually shorten the working length! One has to compensate for this change by shortening the working length on the shaft of the instrument. Maybe the difference will only be 0.5 mm. Confirm the new length by radiographing an instrument in place. Apical perforation destroys the resistance form. This means that the tip of the primary gutta-percha point must be blunted and fit to place so that it does not extend beyond the orifice, even when compaction is exerted during obturation. A good method is to deposit a tiny pack of MTA at the apex, checking its placement radiographically. The patient returns at a later appointment, after the MTA has set and plugs the apical foramen. At the subsequent appointment, this new plug (resistance form) allows compaction of the gutta-percha. Later, MTA will encourage cementumformation at the apex

Comprehension control 1. Causes of complication during the treatment of periapical inflammation. 2. Methods of their elimination. 3. Dentist’s tactic when the periapical tissue is traumatically damaged. 4. Dentist’s tactic when the filling material extended beyond the apex. 5. Dentist’s tactic when the overdose of arsenious paste occurs. Practical class № 5 Periodontal diseases in children and young person. : etiology, pathogenesis, clinic, diagnostics, differential diagnosis. The choice of the remedies, the forms of their application and mechanism of action.

Teaching objective: to teach students the peculiarities of examination of child with the periodontium diseases. To learn the major principles of the diagnostics of gingivitis in children.

Pre-study test questions 1. Definition of the periodontium. 2. Anatomical and physiological peculiarities of structure of periodontium in children at different age. 3. Prevalence of the marginal periodontitis. 4. Role of local and general factors in periodontium diseases in children. 5. Diagnostic methods of periodontium diseases in children. 6. Assessment of the periodontium tissue in children. Periodontal indexes.

Contents of the class

"" is used as a generic term to describe all diseases of the periodontium. At the XVI plenary session All-Union Society of dentists (1983) the classification of the peiodontium diseases was approved which meets to requirements of pediatric dentistry. According to this classification periodontal disease are divided into 5 groups.

1.Gingivitis Forms: catarrhal, hypertrophic, ulcerative. The course of the disease: acute, chronic. The spreading of the pathological process: localized, generalized. Severity of process: mild, moderate, severe. 2. Periodontitis The course of the disease: chronic, exacerbation, abscesses, remission. The spreading of the pathological process: localized, generalized. Severity of process: mild, moderate, severe. 3. Periodontosis (periodontosis ) The course of the disease: chronic, remission. The spreading of the pathological process: generalized. Severity of process: mild, moderate, severe.

4. Progressing idiopathic diseases of the periodontium. 5. Tumor-like processes in the periodontal tissue.

Classification based on children’s ages ( Page and Schroeder, 1982 ) I. Pubertal periodontitis ( up 12 years ) A. Localized. B. Generalized. II. Juvenile periodontitis ( age – 13-17 years) III. Rapidly progressing periodontitis ( age – 17-35 years ) IV. Adult type periodontitis ( over 35 years ).

Gingivitis is an inflammatory process affecting the soft tissues surrounding the teeth. The inflammatory process does not extend into the alveolar bone, periodontal ligament, or .

Catarrhal ( simple ) gingivitis is characterized by the red colour, loss of surface stippling, puffiness and softening of the , easy bleeding upon probing or spontaneons bleeding and the pain during mastication and palpation. Chronic simple gingivitis . Discomfort in gingiva, gingival bleeding provoked by mechanical trauma (tooth-brushing, food impaction by biting solid foods such as apples) and bleeding upon probing is of great value for the early diagnosis of chronic gingivitis. Gingival bleeding varies in severity, duration and ease with which it is provoked. The severity of the bleeding and the case with which it is provoked depend on the intensity of inflsmmation. In chronic inflammation gums are bluish red. At the first stage of disease it is sometimes even difficult to distinguish clinically chronic simple gingivitis and normal gingiva. Originating as a light redness the colour changes through varying shades of red, reddish blue, and deep blue with increasing chronicity of the inflammatory process.

Hypertrophic (Hyperplastic) gingivitis. The clinical signs and symptoms include gingival overgrowth in the form of a diffuse swelling of the interdental papillae, or multiple, tiny nodules on the labial of the interdental papillae of anterior teeth, or as a marginal collar or festoon of tissue around the clinical crown of the tooth. Other symptoms include moderate to acute inflammation, soreness, tenderness, and moderate (4 to 7 mm) pocket depths. Hypertrophic (Hyperplastic) gingivitis can be classified as follows: forms: oedematic fibrous generalized localized 3 stages: light - gums cover 1/3 of the tooth crown moderate - gums cover not more than 1/2 of the tooth crown heavy - gums cover 2/3 of the tooth crown or more

Acute Necrotizing Ulcerative Gingivitis. Also called “Vincent’s infection” and “Trench Mouth”. Infection caused by bacteria like – Borrelia vincentii, Fusobacterium nucleatum, Prevotella intermedia and species of Treponema and Selenomona. Necrotizing ulcerative gingivitis most often occurs as an acute disease. Its relatively mild and more persistent form is referred to as subacute. Recurrent disease is marked by periods of remission and exacerbation. Reference is sometimes made to chronic necrotizing ulcerative gingivitis. However, it is difficult to justify this designation as a separate entity because most periodontal pockets with ulceration and destruction of gingival tissue present comparable microscopic and clinical features. Signs and symptoms:  Typically, interdental papillae are inflamed, edematous and hemorrhagic.  Involved papillae show punched out, crater like necrotic areas covered by grayish pseudomembrane.  There is a fetid odor, extreme pain and spontaneous hemorrhage.  Associated features like lymphadenopathy, fever and malaise may also be present.  Involvement of PDL leads to necrotizing ulcerative periodontitis.  If infection spreads through mucosa to skin of face, then the infection is called “Cancrum oris” or .

Comprehension control 1. Classification of the periodontium diseases. 2. Clinical types of gingivitis. Differential diagnostics. 3. Determine the test of Shillera-Pisareva. 4. Determine the CPITN index. 5. Prescribe the additional methods of diagnostics.

Practical class № 6 Localized and general periodontitis in children. Etiology, pathogenesis, clinic, diagnostics, differential diagnosis. Teaching objective: to learn with students the causes of the periodontitis in children, peculiarities of the clinical course and differential diagnosis.

Pre-study test questions 1. Classification of the periodontium diseases. 2. Structure of the periodontium tissue. 3. PMA, PI, CPITN indexes, its characteristic. 4. Functional methods of examination of the periodontium. 5. Additional methods of diagnostics.

Contents of the class

Periodontitis  Refers to inflammation of gingival tissues in association with some loss of attachment of periodontal ligament and alveolar bone.  Due to progressive loss of attachment, destruction of PDL and adjacent alveolar bone occurs.  The sulcular epithelium shifts apically along the root surface, resulting in formation of periodontal pockets. Pathogenesis:  For more than a century, periodontitis has been associated with dental plaque. But periodontitis has been shown to be absent in patients with extensive plaque also.  Recent evidence indicates periodontitis results not from mere presence of plaque but from changes in proportions of bacterial species in plaque.  is associated with Actinobacillus actinomycetecomitans, Bacteroides forsythus and Prevotella intermedia.  The pathogenic bacteria exist inside the plaque where they are protected from host defenses.  Here they also show increased resistance to local / systemic antibiotics.  These bacteria then release lipopolysaccharides which bring about the release of catabolic inflammatory mediators as host response.  However, only presence of pathogenic bacteria is not sufficient to cause periodontitis.  Other host factors like smoking, diabetes and heredity predilection are also significant in leading to periodontitis.

Classification 1. CHRONIC PERIODONTITIS - Localized - Generalized 2. - Localized - Generalized 3. PERIODONTITIS WITH SYSTEMIC DISEASES - Associated with hematologic disorders - Associated with genetic diseases - Diabetes mellitus 4. NECROTIZING PERIODONTAL DISEASES - Necrotizing ulcerative gingivitis - Necrotizing ulcerative periodontitis 5. ABSCESSES OF PERIODONTIUM - Gingival abscess - - Pericoronal abscess 6. PERIODONTITIS ASSOCIATED WITH ENDODONTIC LESIONS

CHRONIC PERIODONTITIS

A risk factor can be defined as a state or occurrence that increases the probability of an individual developing a disease. Risk factors for periodontal disease can be classified as local or general. Local factors, for example, an instanding lateral incisor, may serve to compromise local plaque control by hindering effective cleaning and resulting in dental plaque accumulation. On the other hand, general risk factors, such as an inherited disorder may predispose an individual to periodontal disease despite a good level of plaque control.

It is important to understand that if a child possesses a risk factor for periodontal disease, it does not necessarily follow that the child will develop the condition. Conversely, a patient may appear to have no risk factors, but the disease may develop subsequently. Bearing this in mind, risk factors (both local and general) should be considered when assessing, diagnosing, treating, and maintaining child patients with periodontal disease.

These can be grouped simply into four areas. There may be overlap between these areas.

.  Following traumatic dental injuries.  Plaque retentive factors.  Ectopic eruption General risk factors for periodontal disease may have a genetic basis, with certain inherited conditions possessing periodontal manifestations (e.g. Papillon Lefevre Syndrome). The genetic conditions are dealt with previously in this chapter. There are also metabolic, haematological, and environmental risk factors within the general category. A full discussion of each is outwith the scope of this chapter, so the two most prevalent examples of general risk factors, diabetes mellitus and smoking will be discussed.

Children and adolescents can have any of the several forms of periodontitis as described in the proceedings of the 1999 International Workshop for a Classification of Periodontal Diseases and Conditions (aggressive periodontitis, chronic periodontitis, and periodontitis as a manifestation of systemic diseases). However, chronic periodontitis is more common in adults, while aggressive periodontitis may be more common in children and adolescents. The primary features of aggressive periodontitis include a history of rapid attachment and bone loss with familial aggregation. Secondary features include phagocyte abnormalities and a hyperresponsive macrophage phenotype. Aggressive periodontitis can be localized or generalized. Localized aggressive periodontitis (LAgP) patients have interproximal attachment loss on at least two permanent first molars and incisors, with attachment loss on no more than two teeth other than first molars and incisors. Generalized aggressive periodontitis (GAgP) patients exhibit generalized interproximal attachment loss including at least three teeth that are not first molars and incisors. In young individuals, the onset of these diseases is often circumpubertal. Some investigators have found that the localized form appears to be self-limiting, while others suggest that it is not. Some patients initially diagnosed as having LAgP were found to have GAgP or to be periodontally healthy at a 6-year follow-up exam.

I. Localized aggressive periodontitis

Age incidence: Begins around 11 - 13 years.

Sex predilection: Nil

Signs and symptoms:

This type of disease is localized around the incisors and first molars Typically the oral hygiene is good and there may be mild or no gingival inflammation. The rate of bone loss is 5-10 times more than chronic periodontitis.

Radiographic features: -

Radiographs usually reveal bilaterally symmetrical vertical bone loss. Similar involvement is seen around anterior teeth also. Tooth mobility and migration is common. In 1/3rd of cases, disease progresses to a more generalized pattern.

II. Generalized aggressive periodontitis:

Age incidence: Occurs before 30 years

Sex predilection: Nil

Signs & symptoms:

Compared to localized variant, more teeth are involved. Bone loss is not limited to specific areas of jaws.

Primary dentition (prepubertal periodontitis)

The disease may present immediately after the teeth have erupted. In the generalized form the gingiva appear fiery red, swollen, and haemorrhagic. The tissues become hyperplastic with granular or nodular proliferations that precede gingival clefting and extensive areas of recession. Gross deposits of plaque are inevitable as the soft tissue changes make it difficult to maintain oral hygiene. The disease progresses extremely rapidly, with primary occurring as early as 3-4 years of age. The entire dentition need not be affected, however, as the bone loss may be restricted to one arch. Children with generalized disease are susceptible to recurrent general , principally otitis media and upper respiratory tract infections.

Localized disease progresses more slowly than the generalized form and bone loss characteristically affects only incisor-molar teeth. Plaque levels are usually low, consequently soft tissue changes are minimal with gingivitis and proliferation involving only the marginal tissues.

The predominant micro-organisms that have been identified are aggressive periodontopathogens: Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Fusobacterium nucleatum, and Eikenella corrodens. This suggests that there is an infective component to the disease, although defects in the hosts' response have also been identified. Profound abnormalities in chemotaxis and phagocytosis of polymorphonuclear neutrophils and monocytes are frequently reported in these patients. These immunological defects are heritable risk factors that help to define phenotypically the disease entity. Conversely, they may also be associated with more serious and life-threatening conditions, and thus a full medical screen is indicated.

Oral hygiene instruction, scaling, and root planing should be undertaken at frequent intervals. Bacterial culturing of the pocket flora identifies specific periodontopathogens. If pathogens persist after oral debridement, an antibiotic such as metronidazole or amoxycillin (amoxicillin) should be given systemically after sensitivity testing, as a short course over 1-2 weeks. Generalized disease responds poorly to treatment. Some improvement has been achieved following a granulocyte transfusion in a patient with a defect in neutrophil function. Extraction of involved teeth has also produced an improvement in neutrophil chemotaxis, which suggests that the defect may be induced by certain organisms in the periodontal flora. Furthermore, in severe cases of generalized periodontitis, extraction of all primary teeth (and the provision of a removable prosthesis) can limit the disease to the primary dentition. Presumably, anaerobic pathogens are unable to thrive in the absence of teeth. When the permanent teeth erupt, bacterial culturing of the subgingival flora ensures that reinfection is detected early.

Comprehension control 1. Etiology and pathogenesis of the periodontium diseases in children. 2. The main clinical types of periodontitis. 3. Differential diagnosis of periodontitis. 4. Rentgenologic peculiarities of periodontitis in children. Practical class № 7 Principles of the treatment of periodontal diseases in children. Therapeutic treatment of the periodontal diseases in children of the different age. The tactics of the pedodontist. Physiotherapeutic methods of the treatment of the periodontal diseases in children. Teaching objective: to teach students to co-operate with pediatritians for choosing the plan of complex treatment of periodontitis in children.

Pre-study test questions 1. Content of the local and general treatment of the periodontium diseases in children. 2. Role of the oral cavity hygiene in the treatment of the periodontium diseases. 3. Choice of the tools and remedies for hygiene. 4. Physiotherapeutic methods of treatment.

Contents of the class Mechanical plaque control Plaque control refers to the removal of plaque from the tooth surface and gingival tissues, and prevention of new microbial growth. Effective plaque control results in resolution of gingival inflammation and is fundamentally important in all periodontal therapy. Periodontal treatment performed in the absence of plaque control is certain to fail, resulting in disease recurrence. Mechanical plaque control is performed using toothbrushes, toothpaste and other cleaning aids. Plaque-control programmes should be tailored to the requirements of individual patients. Motivation of patients to change their behavioural habits is a great challenge and patients must be educated so they understand the importance of their contribution to maintaining health and preventing disease.

Chemical plaque control Chemical agents have been incorporated into mouthrinses and toothpastes with the objective of inhibiting the formation of plaque and calculus. Antiplaque agents may also have a significant clinical effect of resolving an established gingivitis.

Scaling and root planing Non-surgical management (NSM) of periodontal diseases comprises OHI and scaling and root planning (SRP): • scaling is the removal of plaque and calculus fromthe tooth surface • root planing is the removal of subgingival plaque, calculus and necrotic cementum to leave a hard, smooth root surface. SRP is generally undertaken with various hand instruments and / or ultrasonic sealers. As a result of OHI and SRP, plaque bacteria are reduced and there is resolution of the inflammatory lesion in the periodontium. This leads to shrinkage of the gingival soft tissues (as oedema resolves), increased resistance to probe tip penetration by the tissues at the base of the pocket (as inflammation resolves) and the formation of a long junctional epithelium at the base of the pocket. All these mechanisms contribute to the reduction in probing depths observed after effective NSM, although gingival shrinkage and resolution of inflammation have the most significant effects on pocket reduction. Clinical research has shown that effective OHI alone can reduce mean probing depths by approximately 0.5 mm, and SRP results in additional reductions of about 1.0-1.5 mm. There is no initial probing depth above which NSM does not confer a benefit to patients. However, root planing performed at sites with minimal or no pocketing is detrimental rather than beneficial. Root planing of shallow sites with initial probing depths <3 mm results in loss of attachment to the root surface as a result of mechanical trauma from instrumentation

Antimicrobials The use of systemic antimicrobials in the management of periodontal disease should be restricted to the following conditions: • severe necrotising ulcerative gingivitis • multiple or severe periodontal abscesses with involvement of regional lymph nodes • some cases of aggressive periodontitis.

Host modulation The realisation that the destructive host immuneinflammatory response to the presence of plaque bacteria in the periodontal pocket is the primary cause of periodontal breakdown has led to the concept of adjunctive host modulation using systemic medication.

Surgical treatment The major limitation of closed SRP (non-surgical treatment) is that root surfaces cannot be visualised directly, and access for removal of subgingival plaque and calculus may be limited. Periodontal therapies (both surgical and non-surgical) are aimed at the removal of all plaque and calculus, and while this is seldom achieved, improvements in periodontal health are observed nonetheless. Therefore, while total elimination of causative factors is an appropriate goal for periodontists, reduction of plaque and calculus below a certain threshold acceptable to the host may be a more realistic aim. This tips the balance between the host and bacteria in favour of the host, allowing reduction in the signs of inflammation and improvements in clinical parameters. It is typical, therefore, for patients to receive a course of non-surgical therapy and then to be monitored. For those sites that do not respond favourably to treatment (e.g. because of complicated local anatomy such as grooves or furcation involvements), then a decision may be taken to expose the area surgically for further treatment. The majority of periodontal surgery is undertaken to improve access to the root surface for cleaning, generally via a flap procedure, although there are also several indications for specific surgical procedures too. It is fundamentally important that a high level of oral hygiene is maintained before and after surgery; surgical treatments will fail if plaque is not adequately controlled. Other indications for periodontal surgery: • crown lengthening to increase clinical crown length • gingivectomy for the removal of overgrown gingivaltissues • guided tissue regeneration (GTR) to regenerate periodontal supporting structures • mucogingival surgery for correction of mucogingival and aesthetic defects.

Comprehension control 1. The major group of remedies for local treatment of periodontium diseases. 2. Principles of treatment of different types of gingivitis. 3. Principles of treatment of different types of periodontitis. 4. The major groups of the remedies for general treatment of periodontium diseases. 5. Periodontal dressings. 6. Physiotherapeutic methods of treatment. 7. Role of pediatricians in treatment of periodontium diseases in children. Recommended literature

Practical class № 8 Periodontal syndrome in children. Clinic, Diagnostics, tactics of pedodontist.

Teaching objective: to teach students the peculiarities of diagnostics of the periodontal syndrome; to learn the main principles of differential diagnosis of this pathology and choosing of treatment method.

Pre-study test questions 1. Structure of the periodontium. 2. Role of the general factors in periodontium diseases in children. 3. Methods of diagnostics of periodontium diseases in children. 4. Additional methods of examination of inflammatory process in the periodontium.

Contents of the class The genetic basis for aggressive periodontitis in particular is substantiated by the definite association between the condition and a number of rare inherited medical conditions and syndromes. The pattern of inheritance reflects a single gene disorder, commonly involving inherited defects of neutrophils, enzyme reactions, or collagen synthesis.

Papillon-Lefevre syndrome (PLS)

This syndrome is characterized by palmar-plantar hyperkeratosis, premature loss of primary and permanent dentitions, and ectopic calcifications of the falx cerebri. Some patients show an increased susceptibility to infection. The syndrome is an autosomal- recessive trait with a prevalence of about 1-4 per million of the population. Consanguinity of parents is evident in about one-third of cases.

Rapid and progressive periodontal destruction affects the primary dentition with an onset at about 2 year. Exfoliation of all primary teeth is usual before the permanent successors erupt and patients may be edentulous by the mid to late teens. Cases of a late-onset variant of PLS have also been described in which the palmar-plantar and periodontal lesions are relatively mild and only become evident in the permanent dentition. An extensive family dental history supported by clinical, laboratory, and radiographic examinations confirms the diagnosis.

Neutropenias

The neutropenias comprise a heterogeneous group of blood disorders that are characterized by a periodic or persistent reduction in the number of circulating polymorphonuclear neutrophils. Neutropenias can be drug-induced or be secondary to severe bacterial or viral infections or autoimmune diseases such as . , benign familial neutropenias, and severe familial neutropenias are all heritable conditions transmitted as autosomal-dominant traits and diagnoses are often made during early childhood. The chronic benign neutropenia of childhood is diagnosed between 6 and 24 months of age and is characterized by frequent and multiple pyogenic infections of the skin and mucous membranes.

The periodontal problems associated with the neutropenias are very similar, and in many cases the patient presents with a localized or generalized aggressive periodontitis. Occasionally, the primary dentition may not be involved, and clinical signs do not appear until the permanent dentition has erupted. The gingiva are inflamed and oedematous; gingival recession, ulceration, and desquamation can also occur.

The treatment of a neutropenic-induced periodontitis involves local removal of plaque and calculus. Strict plaque control measures are difficult to achieve in younger children, so use of an antibacterial mouthrinse may prove useful.

Chediak-Higashi syndrome

This is a rare and very often fatal disease inherited as an autosomal-recessive trait. Clinical features include partial albinism, photophobia, and nystagmus. The patients suffer from recurrent pyogenic infections and malignant lymphomawhich is accompanied by neutropenia, anaemia, and a thrombocytopenia. The neutrophils show defects in migration, chemotaxis, and phagocytosis producing a diminished bactericidal capacity.

Periodontal changes associated with the syndrome include severe gingival inflammation and rapid, and extensive, alveolar bone resorption that can lead to premature exfoliation. The nature of the changes has not been fully established, but they may be plaque- induced, secondary to infection, or related to the underlying defect in neutrophil function.

Leucocyte-adhesion deficiency syndrome (LAD)

This autosomal-recessive trait is characterized clinically by a delayed separation of the umbilical cord, severe recurrent bacterial infections, impaired wound healing, formation of pus, and an aggressive gingivitis, which may be the presenting sign of the disorder. Consanguinity between the parents of affected children confirms the mode of the inheritance as autosomal-recessive.

The syndrome demonstrates the important role of leucocytes (and other white blood cells) in protecting the host against periodontal disease. Moderate pheno- types, however, may appear relatively disease-free, but then develop symptoms and progress 'downhill' extremely rapidly. The majority of patients do not survive beyond 30 years. The progressive periodontal condition is very difficult to control and is often of secondary importance to other life-threatening infections.

Ehlers-Danlos syndrome

The syndrome is an autosomal-dominant trait with nine variants that display defects in the synthesis, secretion, or polymerization of collagen. The variants of the syndrome exhibit extensive clinical heterogeneity and collectively represent the most common of the heritable disorders of connective tissues. The clinical findings are principally excessive joint mobility, skin hyperextensibility, and susceptibility to scarring and bruising of the skin and oral mucous membrane. Defective type IV collagen supporting the walls of small blood vessels predisposes to persistent postextraction haemorrhage.

Gingival tissues are fragile and have a tendency to bleed on toothbrushing. The type VIII syndrome is associated with advanced periodontal disease. Periodontitis has also been linked with the type IV variant, although other variants do not appear to be affected. Ultrastructural changes also occur in the teeth, with abnormalities of the amelodentinal junction, vascular inclusions in dentine, fibrous degeneration of the pulp, and disorganization of cementum.

Type VIII patients require a thorough preventive periodontal programme as root debridement can cause extensive trauma to the fragile soft tissues. Periodontal surgery should be avoided because of the risk of haemorrhage and the potential problems encountered with suturing soft tissue flaps.

Hypophosphatasia

Hypophosphatasia is a rare, inborn error of metabolism characterized by defective bone mineralization, a deficiency of alkaline phosphatase (ALP) activity, and an increased excretion of phosphoethanolamine in the urine. ALP plays a major part in the mineralization of hard tissues and so the absence of the enzyme predisposes to a range of bone and cartilage defects. The condition is an autosomal-recessive trait, although the inheritance pattern of some milder forms of hypophosphatasia may be autosomal- dominant.

The lesions of juvenile or childhood hypophosphatasia become apparent before 2 years of age. Bone defects are usually quite mild with bowing of the legs, proptosis, and wide-open fontanelles being prominent signs. Dental features are resorption of alveolar bone (in the absence of marked gingivitis), premature exfoliation of anterior deciduous teeth, hypoplasia or complete absence of cementum, and the presence of 'small teeth' that have enlarged pulp chambers as a consequence of defective mineralization .The aplastic or hypoplastic cementum and a weakened periodontal attachment is thought to render the patients susceptible to infection with periodontopathogens.

The diagnosis of hypophosphatasia is confirmed biochemically by low activity of serum ALP and a raised level of phosphoethanolamine in a 24-h urine sample. Down syndrome

Children with Down syndrome (trisomy 21) do not suffer aggressive periodontal disease, However, there are a significant number of local and general risk factors that may exist as a result of the syndrome. Local factors that may serve to increase dental plaque retention are:

 Angles Class III malocclusions with crowding;  Lack of an anterior seal;  Anterior open bites.

General risk factors for periodontal disease are mainly centred on leucocyte defects and may include:

 Defects of polymorphonuclear leucocyte function (chemotaxis, killing, and phagocytosis);  Reduced T-cell activity.

Comprehension control 1. Clinical course of the periodontal syndrome in patient with decompensate diabetes. 2. Clinical course of the periodontal syndrome in patient with hereditary neutropenia. 3. Periodontal syndrome in Histocytosis. 4. Papillon-Lefevre syndrome. Clinic. Diagnostics. 5. The periodontium in the immunodeficiency disorders. 6. General principles of treatment of pathologic process in periodontium. Recommended literature