PERIODONTITIS CHRONIC PERIODONTITIS AGGRESSIVE PERIODONTITIS OTHER FORMS OF PERIODONTITIS
Introduction : Chronic periodontitis is a multifactorial disease associated with local and general factors. It is the most prevalent form of periodontitis.
1-Definition: Chronic periodontitis is a common multifactorial disease of the tooth attachment system induced by pathogenic microorganisms (periodontopathogenic bacteria) contained in dental plaque. The loss of attachment is accompanied by destruction of the alveolodental ligament and the alveolar bone that support the tooth. In the absence of treatment, its continuous progression therefore results in the spontaneous loss of this tooth. It preferentially affects adults, but cases are sometimes observed in children and adolescents.
2-Etiology:
-The severity of the damage is associated with local factors.
-Moderate to high and frequent presence of plaque and subgingival tartar.
-Great variability in the composition of the biofilm.
-Association with local aggravating factors (anatomical or iatrogenic).
-Association with environmental factors such as smoking and stress resistance.
-Association with general modifying factors such as diabetes.
3-Prevalence : more prevalent in adults than in children and adolescents, but the latter can also be affected.
4-Progression : its progression is generally slow but can present episodes of rapid destruction.
5-Classification : according to the extent and severity of chronic periodontitis (Armitage).
1-Scope:
-Localized: ≤ 30% of sites are reached.
-Generalized: > 30% of sites are affected.
2- Severity:
-Slight: Continuous attachment loss of 1 to 2 mm.
-Moderate: Continuous attachment loss of 3 to 4 mm.
-Severe: Continuous attachment loss ≥ 5mm.
Clinical correspondence between pocket depth and continuous attachment loss as a function of the severity of periodontitis. Only one of these signs leads to the diagnosis of periodontitis.
PERIODONTITIS CHRONIC PERIODONTITIS AGGRESSIVE PERIODONTITIS OTHER FORMS OF PERIODONTITIS
| Pocket depth(mm) | Loss of attachment (mm) | |
| Mild periodontitis | 4 | 1 – 2 |
| Moderate periodontitis | 5 – 6 | 3 – 4 |
| Severe periodontitis | > 6 | ≥ 5 |
6-Clinical signs
1- Constant signs:
-Gingival inflammation:
- Clinical signs associated with gingivitis (alterations in the color, texture and volume of the gum)
- Bleeding on probing.
-Loss of attachment:
– Continuous increase in the level of clinical attachment over time.
-Periodontal pocket: Probing depth > 3 mm.
-Horizontal alveolysis: bone lysis resulting in an increase in the distance between the enamel-mound junction and the alveolar bone crest and a regular and continuous crestal radiological image, which is substantially horizontal.
2- Inconstant signs :
Gingival signs:
-Clinically detectable crevicular fluid exudate.
-Crevicular suppuration.
-Spontaneous gingival bleeding.
-Periodontal fistula.
-Gingival recessions.
-Periodontal abscess.
Dental signs:
-Dental mobility.
-Dental migrations.
-Spontaneous tooth loss
General signs: Halitosis.
It is interesting to note that the inconstant signs are those which motivate the consultation. The constant signs are silent.
7-Radiological signs
-Vertical alveolysis.
Bone lysis resulting in an increase in the distance between the cementoenamel junction and the alveolar bone crest and an irregular, substantially vertical crestal radiological image characterized by angular, circumferential, crater-shaped bone defects, etc.
-Tendency towards symmetry of bone lesions.
PERIODONTITIS CHRONIC PERIODONTITIS AGGRESSIVE PERIODONTITIS OTHER FORMS OF PERIODONTITIS
8-Treatment:
The treatment of chronic periodontitis is essentially based on the immediate and lasting reduction of the overall load of microorganisms through professional mechanical removal of dental plaque (scaling/scaling) combined with daily individual mechanical (brushing) and chemical (toothpastes, mouthwash) plaque control.
Controlling environmental (smoking, unbalanced/poorly controlled diabetes, etc.) and local (toothlessness, dental malposition, etc.) risk factors/indicators is essential for the long-term success of treatment.
A restorative phase of the periodontal tissues helps to finalize the treatment by creating the anatomical conditions favorable to the absence of relapse.
9-Periodontal monitoring :
Periodontal monitoring maintains a low bacterial load compatible with the absence of clinical inflammation. Compliance, inherent to daily monitoring and plaque control, is essential to the absence of recurrence.
Aggressive periodontitis
Aggressive periodontitis represents a set of clinical situations whose general characteristics differ from those of chronic periodontitis.
Localized aggressive periodontitis is very rarely preceded by gingivitis, unlike chronic periodontitis.
There is no clear and consensual definition that allows in all cases to decide between the diagnosis of severe chronic periodontitis and that of generalized aggressive periodontitis.
1-Definition : Aggressive periodontitis is a disease with a low prevalence, rare in its localized form, generally severe and rapidly progressive, most often affecting young patients, and characterized by familial aggregation.
2-General characteristics:
Constant characters
-patients with aggressive periodontitis are generally in good health. (Clinical and biological examinations do not reveal any general pathology).
-the severity of attachment loss and alveolysis is not necessarily proportional to the amount of plaque or the existence of other local factors. This allows us to evoke the notions of host susceptibility and virulence of pathogenic bacteria. Possibility of long rest periods.
-the third element common to aggressive periodontitis corresponds to the notion of genetic predisposition.
Inconstant characters
-minimal amount of plaque relative to the significant severity of periodontal destruction
– rates of A. actonomycetemcomitans and, in some populations, P. gingivalis may be elevated
-phagocytosis abnormalities
-possible spontaneous cessation of periodontal destruction
– High concentration of prostaglandin E2 and interleukin-1β
3-Etiology:
Local factors
Ethnic factor: The risk of developing aggressive periodontitis does not appear to be shared equally in the population. However, it is difficult to conclude on an independent ethnic risk factor given the impact of socioeconomic status as a confounding variable in the assessment of prevalence.
Socioeconomic conditions: Higher prevalence was associated with low socioeconomic status and some developing countries
Tobacco consumption: Compared to chronic periodontitis, tobacco consumption is little studied because of the age groups involved in the diagnosis of aggressive periodontitis. It seems nevertheless that an association is present with the generalized form, but not or little with the localized form. The response to treatment seems poor in smokers with generalized aggressive periodontitis. The same is true for the 5-year follow-up where smokers lose more attachment than non-smokers.
Plaque control: According to the 1999 classification, one of the secondary characteristics of aggressive periodontitis is the lack of correlation between the amount of plaque and the severity of periodontal destruction. However, a positive association between plaque deposits and generalized aggressive periodontitis has been shown.
Adaptation to stress: Adaptation to stress has also been mentioned among the factors of initiation/aggravation of aggressive periodontitis.
Associated conditions: According to the 1999 classification, one of the essential characteristics of aggressive periodontitis is the absence of other health problems.
PERIODONTITIS CHRONIC PERIODONTITIS AGGRESSIVE PERIODONTITIS OTHER FORMS OF PERIODONTITIS
4-Classification of aggressive periodontitis
Localized aggressive periodontitis:
Clinical signs:
-mainly affects the first molars and incisor sectors with loss of proximal attachment on at least two permanent teeth including a first molar. Alveolysis cannot affect more than two teeth other than the first molars and incisors.
-this form would begin at the time of puberty (13-14 years).
-patients have a strong serological response (antibodies directed against the infectious agent).
Generalized aggressive periodontitis:
Clinical signs :
-Proximal attachment loss involves at least three permanent teeth other than the first molars and incisors.
-These periodontitis most often affect people under 30-35 years old but can also affect older individuals.
Prevalence of A. actinomycetemcomitans rather high.
-low antibody response to infectious agents
– marked episodic character of loss of attachment and bone lysis
5-Etiopathogenesis : in generalized forms, several bacterial species seem to predominate, notably P. gingivalis, but also T.forsythensis nucleatum and, sometimes, A.actinomycetemcomitans.
An immunological reaction against P. gingivalis is often demonstrated but does not allow us to consider the notion of specificity.
6-Microbiological profile:
More than 35 years ago, the first dominant microorganisms identified in cases of localized aggressive periodontitis were Aggregatibacter actinomicetemcomitans, capnocytophaga, corrodens, prevotella and rectus.
AA is strongly associated with localized aggressive periodontitis.
This Gram-negative, non-motile, facultative aero-anaerobic bacillus is considered a major pathogen of aggressive periodontitis.
It is not possible to date to distinguish microbiologically generalized aggressive periodontitis from severe chronic periodontitis.
7-Genetics : According to the report of the consensus conference of the American Academy of Periodontology (AAP) DE 1999, familial aggregation is a major diagnostic criterion for identifying aggressive periodontitis and therefore establishing a differential diagnosis with chronic periodontitis.
The mode of transmission would be autosomal dominant.
8-Diagnosis : the clinical diagnosis of aggressive periodontitis is essentially a diagnosis by elimination. The main difficulty of the differential diagnosis will therefore lie in the exclusion of the diagnosis of severe chronic periodontitis.
PERIODONTITIS CHRONIC PERIODONTITIS AGGRESSIVE PERIODONTITIS OTHER FORMS OF PERIODONTITIS
| chronic | Generalized aggressiveness | Localized aggressiveness | |
| Other associated diseases | Possible | No | No |
| Genetic incidence | Low to non-existent | Important | Very important |
| Age of diagnosis | Rather harsh after 30-35 years | Rather before 30-35 years old | Rather before 30-35 years old |
| Evolution | Slow | Fast | Fast |
| Destruction model | None but rather horizontal and symmetrical | All teeth can be affected, rather vertical and asymmetrical | Incisors and molars mainly |
| Plate | Very abundant | Quite abundant | Not abundant |
| Gingivitis | Always | Often | Minimal but sometimes significant at the level of the sites concerned |
| Bacterial profile | Same for generalized and localized | Similar to chronic periodontitis | Rather peculiar High prevalence of Aa |
9-Screening : given the low prevalence of aggressive periodontitis in the population and the high incidence of certain forms in children and adolescents, early screening is important in order to prevent the progression to severe forms.
10-Treatment :
As with localized forms, antibiotic therapy is justified in the overall management of generalized aggressive periodontitis.
A recent systematic review indicates that treated aggressive periodontitis has a very low recurrence rate. The rate of tooth loss is 0.09 teeth per patient per year, or 1 tooth lost on average after 11 years.
Individual and professional mechanical removal of bacterial plaque is a prerequisite that does not differ from chronic periodontitis in principle.
Mechanical treatments alone, whether non-surgical or surgical, do not appear to be effective enough to result in a decrease in A. actinomycetemcomitans levels below the detection threshold of the tests.
Systemic antibiotic therapy has therefore been proposed to complement mechanical action. However, antibiotic therapy alone, in the absence of mechanical removal of plaque, cannot in any case constitute treatment.
Antibiotic treatment:
The combination of metronidazole (250mg) + amoxicillin (500mg) 3 times a day for 10 days, in association with non-surgical treatment, has proven to be the most effective in eliminating A. actinomycetems. If the latter bacteria is absent, in the presence of the red complex, metronidazole alone is sufficient. Due to the need for disruption of the biofilm to obtain maximum penetration and therefore effectiveness of antibiotics, these should be prescribed at the end of the initial therapy.
The effects of antibiotic therapy last about 3 months, there is no need to repeat it during this period, otherwise resistance may develop. Surgery could perhaps reduce the indications for antibiotic therapy.
PERIODONTITIS CHRONIC PERIODONTITIS AGGRESSIVE PERIODONTITIS OTHER FORMS OF PERIODONTITIS
Necrotic periodontal diseases
General:
Classically, necrotic periodontal diseases (NPD) include necrotic gingivitis (NG) and necrotic periodontitis (PN) (according to Armitage 1999).
They are both now considered to be the same condition, at different stages of development, because their main clinical, microbiological and immunological characteristics appear similar.
These oral cavity diseases are among the most severe infections of the periodontium in response to dental plaque.
These conditions have been known for over a century and have been described under various names including:
ulceromembranous gingivitis,
ulceronecrotic gingivitis (UGN),
ulceronecrotic periodontitis (PUN),
Vincent’s gingivitis or gingivostomatitis,
ulceronecrotic gingivostomatitis and
the mouth of the trenches.
The clinical features of MPN are significantly different from those of other periodontal diseases. They are practically the only periodontal diseases causing acute and spontaneous pain.
The distinction between the different forms of MPN, gingivitis and periodontitis, is classically based on the presence or absence of attachment loss.
The GNs are limited to the gingiva and no loss of attachment can be observed.
As with gingival disease, when lesions extend beyond the mucogingival line, the diagnosis of necrotic gingivostomatitis (NGS) will be made.
In the presence of loss of attachment following the progression of the disease, the diagnosis of PN will be made.
1-Prevalence : Despite the continuing interest in MPNs, particularly due to their high prevalence in certain general diseases, knowledge remains relatively limited regarding the prevalence, distribution and risk factors associated with this type of condition.
In summary, MPNs occur at all ages of life, but there is a different age distribution depending on the country concerned. The prevalence is higher in developing countries than in industrialized countries, particularly in children.
2-Risk factors:
Changeable factors:
Local factors
-poor oral hygiene
– plaque-induced gingivitis
-composition of dental plaque
-MPN history
General factors:
-HIV infection
-malnutrition (unbalanced diet)
-stress, fatigue, personality disorder, insomnia.
-socioeconomic conditions
-alcohol consumption
– white line damage including leukemia
-viral infections
-tobacco
Non-modifiable factors:
-age (adolescent, young adult)
-season September/October and December/January)
3-Necrotic periodontal diseases and HIV infection:
MPNs are among the seven cardinal oral lesions with a strong association with HIV infections.
The seven oral lesions associated with HIV infection (after Coogan et al. 2005)
- Candidiasis
- Hairy leukoplakia
- Kaposi’s sacoma.
- Linear gingival erythema.
- Ulceronecrotic gingivitis
- ulceronecrotic periodontitis
- Non-Hodgkin’s lymphoma.
PERIODONTITIS CHRONIC PERIODONTITIS AGGRESSIVE PERIODONTITIS OTHER FORMS OF PERIODONTITIS
4-Necrotic gingivitis :
-The onset phase is acute, classically localized to the anterior mandibular or even maxillary sextants, while the posterior sextants seem to be more slightly affected.
-Fever and lymphadenopathy are inconstant and infrequent.
-The gum is soft, crumbly, bleeding at the slightest touch due to exposure of the connective tissue.
-Bleeding may be spontaneous.
– Necrotic lesions are typically covered with a whitish-yellow coating, most often described as “pseudomembranous” which facilitates diagnosis.
-The evolution is rapid. In a few days, we observe necrosis (decapitation) of the interdental papillae which sometimes extends to the marginal vestibular and lingual/palatine gingiva.
-The necrotic lesion appears quite distinct from the healthy gingival area, from which it is separated by a linear erythema due to microvascular permeability.
-Halitosis is typically observed.
-There are rarely ulcerations on the tongue, the inner side of the lips or the cheeks (GSN).
-The amount of dental plaque, usually significant in these patients, is increased due to the difficulty of oral hygiene which is made painful.
-At this stage of GN, the situation is reversible with treatment, although there are sometimes discrete sequelae such as loss of papillary height and the presence of gingival recessions respectively associated with ulceration of the papillae and periodontal necrosis. It should be noted that recurrence is frequent, even after treatment.
5-Necrotic periodontitis:
The acute nature of GN can immediately progress to PN or, in the absence of treatment, to chronicity. The progression occurs in successive attacks, secondarily leading to attachment losses. Necrosis then extends to the underlying alveolar bone.
The presence of interproximal craters is observed.
Necrosis extends to the vestibular marginal gingiva forming a continuous necrotic line involving a group of teeth
The classic general signs are adenopathy, most often submandibular, and increased body temperature, asthenia. These signs are inconstant and related to the severity of the disease.
Evolution:
The acute nature of MPN can evolve, in the absence of treatment, towards chronicity, even at the stage of GN which then evolves by successive thrusts towards loss of attachment, i.e. PN. It should be noted that recurrence is frequent, particularly at the stage of GN, even after treatment.
6-Diagnosis:
The concomitant occurrence of the two conditions in the same patient can be ruled out. The general signs (pain, fever, malaise) are then more marked. Other non-plaque-induced gum diseases cannot be confused because of the distinctive signs that characterize them .
7-Microbiology:
The microbial composition classically comprises a constant part and an inconstant part comprising a variable proportion of microorganisms.
The constant part is dominated by spirochetes (Treponema) and by spindle-shaped bacteria (fusobacterium nucleatum, prevotella intermedia and selenomonas).
8-Treatment: treatment must be early in order to:
-quickly reduce pain
-limit the after-effects
-allow a rapid return to normal eating (especially for patients with general illnesses
In all cases, mechanical debridement is the rule.
State phase:
Absence of general signs : scaling and surface cleaning is generally sufficient to stop the disease (progressively and non-traumatically). Due to the constant associated pain, local anesthesia is the rule. Ultrasonic instrumentation allows better visualization and better debridement of the lesions due to the irrigation of the inserts. If anesthesia cannot be performed, the lesions will be very delicately cleaned by gradually eliminating the yellowish superficial soft layer. Oral hygiene must be resumed immediately (very soft toothbrush associated with the roller technique).
The first two days, the patient may not be able to brush properly due to the pain caused. This is why in the acute phase in adults, a 48-hour rinse with an equal mixture of 3% hydrogen peroxide and lukewarm water will be prescribed every 2 to 3 hours. This rinse will be followed by an alcohol-free chlorhexidine mouthwash twice a day for the next 8 days. Stop smoking and drinking alcohol for the duration of treatment. Eliminate spicy foods and prefer a semi-liquid diet rich in vitamins (fruit juice). A prescription for paracetamol (1g per dose every 6 hours until the pain stops) will be issued. Spontaneous pain usually subsides quickly within a few hours. The patient will be seen again after 2 to 5 days depending on the severity of the signs.
Mechanical debridement of the lesions will be repeated in order to remove pseudomembranous necrotic debris. In principle, a significant improvement in clinical signs is observed after 4 to 6 days.
Presence of general signs
In case of fever, malaise, adenopathy, curative oral antibiotic therapy is recommended in addition to mechanical debridement and local care.
- As a first-line treatment, monotherapy is the rule. Metronidazole (1500 mg/day in 2 or 3 doses for 6 to 8 days) is the antibiotic of choice due to the high prevalence of spirochetes (National Agency for the Safety of Medicines and Health Products, 2011). It is not necessary to combine another molecule. In case of intolerance, it can be replaced by amoxicillin (2 g/day in 2 doses for 6 to 8 days).
- As a second-line treatment, if local signs of infection do not improve, the amoxicillin-metronidazole combination (same dosage) may be prescribed, or amoxicillin-clavulanic acid at 2 g/day in 2 doses for 6 to 8 days.
Local antibiotic therapy is not indicated. Physical and sports activities should be limited for the days following the start of treatment .
Reconstructive phase: the presence of interproximal gingival craters and/or gingival recession may be observed after the acute phase. These periodontal sequelae may require, for functional reasons (plaque retention, phonation) or aesthetic reasons, surgical correction of the lesions using plastic surgery or gingival grafts. No reconstructive surgery will be considered without prior initial therapy aimed at eliminating plaque retention factors. This point is particularly important in these patients whose oral health is often poor.
Periodontal follow-up phase : it is very important because of the frequent recurrence of MPN and the key role of plaque accumulation in triggering symptoms. Following a first episode of MPN, the patient will be followed 3 times a year for the first year and then 2 times a year in the event of no recurrence and satisfactory individual plaque control.
PERIODONTITIS CHRONIC PERIODONTITIS AGGRESSIVE PERIODONTITIS OTHER FORMS OF PERIODONTITIS
Refractory periodontitis
In practice, a certain number of periodontitis cases recur or do not respond to apparently well-conducted treatment. It seems that these so-called refractory forms occur preferentially in patients with severe periodontitis or those considered to be very progressive before treatment (Haffajee et al. 1985). Other factors also seem to intervene or at least be present in these patients:
– smoking (in 82 to 90% of them)
-high levels of F. nucleatum, E. corrodens, P. gingivalis, certain genotypes of A. actonomycetans and even other unusual species in the oral flora.
-an alteration of chemotaxis and phagocytosis of polymorphonuclear neutrophils.
-A dysfunction of the immune response which can result either in a defect in the antibody response to infections or in high levels of interleukin 1, 2 and 6 in the gingival fluid.
Conclusion: the proposed classification facilitates the diagnosis of the different forms of periodontal disease by taking into account elements directly accessible during the first consultation.
bibliography:
-PHILLIPE Bouchard periodontology implant dentistry Lavoisier medicine.
-Marc DANAN Francoise FONTANEL Monique BRION Severe periodontitis and orthodontics Edition Cdp Collection JPIO.
PERIODONTITIS CHRONIC PERIODONTITIS AGGRESSIVE PERIODONTITIS OTHER FORMS OF PERIODONTITIS
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