Locoregional complications of dental origin Therapeutics and management

Locoregional complications of dental origin Therapeutics and management

1. Introduction :

• Dental infectious foci are infections that essentially originate in the teeth, characterized by their location, severity and progression.
• We mainly distinguish apical periodontitis (formerly desmodontitis) possibly complicated by an apico-dental cyst, odontogenic cellulitis which constitutes the most severe development of these infections and can, in certain cases, be life-threatening.

2. Definition :

• Primary infectious foci:

The imbalance between the proliferation of commensal flora and the integrity of the

mucous membrane leads to the penetration of microorganisms into the tissues. The following are recognized as infectious foci:

• Complications of pulp necrosis and periodontal diseases (eruption and disinclusion pericoronitis and periodontal diseases).
• Impacted or impacted teeth, mature in adults, silent, would not be infectious foci

3. Etiology:
   1. The carious lesion:

Caries is the main source of contamination of the endodontic system. The rupture of the hard tissues that protect the pulp leads to contamination of the dentin-pulp complex, causing inflammatory and infectious reactions.

2. Pulp pathologies:

Endodontic infections usually develop as a result of pulp necrosis or in cases where the pulp has been removed during treatment.

Bacteria are the main microorganisms involved in apical periodontitis. Bacteria colonizing the root pulp cavity come into contact with the periradicular tissues via the apical and lateral foramina. With microbial progression, the bacterial flora evolves due to changes in nutritional conditions and

metabolic for bacteria (anaerobes) and the absence of defense cells. Colonization of the pulp by bacteria leads to innate and acquired immune reactions in the periradicular periodontium in relation to the apical and lateral foramina(s) of the infected canals which will lead to the formation of a periradicular inflammatory lesion of endodontic origin (LIPOE), or apical periodontitis.

1. Symptomatic apical periodontitis:

The first extension of pulpal inflammation into the periradicular tissues is called symptomatic apical periodontitis (SAP). Irritants causing it include: mediators of irreversible pulp inflammation or bacterial toxins from necrotic pulps; chemical agents (e.g., irrigants and disinfectants); overbitten restorations; overhanging endodontic instruments; or root canal fillings.

2. Asymptomatic apical periodontitis:

Asymptomatic apical periodontitis (AAP) is caused by pulp necrosis and is usually a sequela of PAS. Histologically, AAP lesions are classified as granulomas or cysts.

Histologically, PAA lesions are classified as granulomas or cysts

1. Initial lesions (granulomas):

• These are lesions consisting of inflammatory tissue circumscribed by a fibrous capsule, highly infiltrated by inflammatory cells, mainly polymorphonuclear cells, macrophages, T and B lymphocytes, mast cells, osteoclasts, osteoblasts, fibroblasts, epithelial cells and cellular debris.

2. The apical (radicular) cyst:

The apical (radicular) cyst has a central cavity filled with eosinophilic fluid or semi-solid material and is encapsulated by stratified squamous epithelium.

3. Condensing osteitis:

• Condensing osteitis, a variant of asymptomatic apical periodontitis, results in an increase in trabecular bone density in response to persistent irritation.
• The main cause of condensing osteitis is the diffusing irritant from the root canal into the periradicular tissues.

3. Apical abscess:

• When the body’s defenses are overwhelmed, bacteria can invade the periapical lesion and create an apical abscess that can either progress to fistulization and resolution of symptoms, or to cellulitis when bacteria invade neighboring cellular tissue. An acute apical abscess (AAA) is a liquefaction lesion

localized or diffuse of pulp origin which destroys the periradicular tissues,

accompanied by severe inflammation in response to microbial or non-microbial irritants from the necrotic pulp.

4. Chronic apical abscess:

• Chronic apical abscess (CAA) is an inflammatory lesion of pulpal origin

characterized by the presence of an old lesion transformed into an abscess which has drained into the mucosa or to the surface of the skin by a fistula.

5. Other forms: Resistant LIPOE, cysts:

• Initial lesions are not the only forms of LIPOE. Some only appear after endodontic treatment, which is one of the most important factors.

correlated with the presence of LIPOE. The reason is always the contamination of the endodontium by bacteria. In this case, the flora may be different from that of the initial lesions since the bacteria do not come from the same selection process. Enterococcus faecalis, for example, is the most present in persistent lesions.

6.  Evolution of LIPOE:
   1. The Progress:

The persistence of the infectious agent in the endodontium, inaccessible to defensive cells, does not allow the lesion to be stopped, which therefore progresses. Bone lysis resulting from the mechanisms described above continues. Bacteria organized into biofilms can colonize periapical surfaces and extend the infectious surface. Their progression in soft tissues is slowed by inflammatory reactions.

2. Exacerbation:

• The transition from an asymptomatic to a symptomatic form is not well understood. Acute infections are generally linked to virulent bacteria in the planktonic stage, to reduced defenses or to specific bacterial properties.
• Invasion of periradicular tissues occurs after changes in microbial balance and can result in abscess formation.

4. Local-regional or remote dissemination:
   1. How?

Dissemination can be done

• by hematogenous route
• by anatomical routes: bone, sinus, vascular, nervous or along the aponeuroses of the neck
• Swallowing or inhaling products contaminated by the oral cavity can also be a cause.

2. When? :

• through an oral therapeutic gesture.
• by a latent infectious focus
• by an active focus

3. At whose home:

Field concept: The appearance of remote manifestations depends on:

• The quantity of bacteria present at the primary focus,

• The patient’s susceptibility to developing infections
• Immunosuppression (pathologies, immunosuppressive treatments).

5. LOCO-REGIONAL COMPLICATIONS OF DENTAL OUTBREAKS

In the absence of treatment or adequate treatment, the condition progresses to chronicity or to circumscribed or diffuse cervicofacial cellulitis. In this case, the prognosis may be life-threatening.

1. Maxillofacial cellulitis:

• Cellulite affects the cellular fatty tissue occupying areas of less resistance in different spaces, delimited by musculoaponeurotic insertions on the maxillary and mandibular bone cortices.
• The boundaries can be more or less clear, ranging from circumscribed cellulite to diffuse cellulite.
• Depending on the development, acute, chronic or diffuse cellulitis is described, which can become complicated locally or remotely, with a prognosis that is more or less severe.

1. Routes of diffusion of odontogenic cellulitis:

• The infection spreads through anatomical routes: bone, sinus, vascular, nervous or along the aponeuroses of the neck

The location of the infection depends mainly on four factors which are the tooth

causal, the thickness of the alveolar bone, the length of the roots and the relationship between the site of the bone fenestration and the various muscular insertions of the maxilla and mandible. This results in an infection of the cellular fatty tissues of the face.

• The location of the dental apices in relation to the bone tables and the musculo-aponeurotic insertions determines the location of cellulitis.

2. Classifications:
3. Circumscribed cellulitis:

Acute circumscribed cellulitis is divided into serous, suppurative and gangrenous cellulitis.

• Serous cellulitis : Acute serous cellulitis is the initial, purely inflammatory stage.
• We find the four cardinal symptoms of inflammation: swelling, pain, heat, redness, painful swelling with imprecise limits which fills the furrow and erases the flat spots.

• Skin tight, hot, slightly erythematous
• General signs = fever, headaches in the absence of therapy,
• Evolution: collected or suppurative cellulite.
• Suppurative cellulitis:

• In the absence of appropriate treatment, suppurative cellulitis sets in within days and is characterized by abscessation
• Red, tight, shiny, hot skin, swelling adhering to the bone.
• Fluctuation signing the collection.
• Pain++ intense, continuous, stabbing, predominantly nocturnal, causing insomnia, hindering eating, swallowing and speaking, trismus Other possible signs depending on the location and severity:
• Dysphagia, halitosis, insomnia, fever at 38–39°C, asthenia, general malaise… Evolution without treatment: Chronic cellulitis/diffuse cellulitis/complications…
• Chronic cellulite:

• Chronic cellulitis often follows poorly treated suppurative cellulitis, either due to insufficient drainage, inadequate antibiotic therapy, or insufficient etiological treatment.
• Chronic evolution can last for several months
• Clinically, we find at the cutaneous level, in relation to the
• causal tooth, a fistula present for several months, even several years

2. Diffuse cellulitis:

• Diffuse cellulite can be either secondary to circumscribed cellulitis or diffuse from the outset.
• Due to its rapidity, it leads to very serious complications early on.
• Due to its emergency nature, it requires hospitalization of the patient as quickly as possible.
• malignant toxicosis
• Hyperthermia,
• Anxiety +++
• Snowy crackle

•Extension of the cervico-mediastinal collection.

• Engages vital prognosis

2. Osteitis and osteomyelitis of the jaws:
   1. Location :

• cortical: osteitis
• medullary: osteomyelitis
• periosteal: periostitis
• Presence or absence of suppuration: suppurative or non-suppurative osteitis (primary, dry).

2. Duration :

• When acute: the onset is rapid and severe.
• When chronic: long duration (more than 4 weeks).

3. Etiology:

 The origin may be microbial or not or following treatment.

• Infectious origin by direct contamination bone exposure
• In the Neighborhood: local or regional causes: dental origin (PAA, cyst)…; Maxillofacial trauma (fracture); Iatrogenic origin (avulsion, orthopedics…) Other causes (sinus, cutaneous).
• Hematogenous (e.g. staph aureus): General cause (staphylococcus aureus ++): rare by hematogenous route:

4. General Clinical Signs:

• CLINICAL:

• Sharp pain, localized or radiating, continuous or paroxysmal.
• Edematous swelling adjacent to the inflammatory site.
• local or general infectious syndrome.
• cutaneous or mucous fistulas.
• Others: especially in the mandible++ • Trismus in the event of posterior bone involvement
• Labiomental hypoesthesia

Locoregional complications of dental origin. Therapeutics and management

5. Complications:

• Towards local extension by contiguity of the infectious process: in areas of hypovascularization leading to bone sequestra.
• If persistence: extension to soft parts with cellulitis with cutaneous fistulizations
  • In the maxilla: oro-sinuso-nasal communications, thrombophlebitis, etc.
  • towards distant extension of the infection: essentially septicemia, bronchopneumopathy, infective endocarditis.

All these unfavorable developments with local or distant extension of the infection to fragile or neglected terrain.

3. Sinusitis of dental origin:

The relationship between dental organs and sinus repercussions has been widely demonstrated (Melen et al., 1986; Abrahams and Glassberg, 1996). As early as 1943, Bauer spoke of maxillary sinusitis of dental origin (Bauer, 1943).

His studies on cadavers showed the direct relationships between lesions of dental origin and pathologies of the maxillary sinus.

• The dental origin of these chronic sinus pathologies is estimated at 40.6% (Melen et al., 1986) and healing very often occurs after endodontic treatment of the causative tooth or its extraction (Donald et al., 1995; Legert et al 2004). Sinus symptoms often erase the dental pain which,

ultimately, may not be considered the causative agent. In these cases, sinusitis is treated with antibiotics or ENT surgery. Since the dental origin is not resolved, recurrences are frequent and inevitable.

• The medical consequences are sometimes dramatic and generate regional and locoregional complications. Their medical treatment must be rapid. These include periorbital cellulitis; blindness; brain abscess; subdural empyema, cavernous sinus thrombosis; and meningitis.

6. Remote infections:

• Even minimal dental and/or periodontal infectious foci can have significant long-term repercussions on the body’s various systems. This concept was introduced at the beginning of the century under the name of focal infection.
• There is certainly a relationship between the bacterial flora of the oral cavity and general health, but how can we explain the relationship between a primary periodontal-dental focus and a secondary distant focus?

1. Pathogenesis:

Two hypotheses are mentioned:

• 1- The infectious agent from the primary focus is disseminated to the tissue of the distant organ, via the blood or lymphatic system.
• 2 – The infectious agent remains confined to the primary focus but secretes microbial toxins which are released secondarily.

1. Bacteremia:

• The first mechanism is bacteremia, which was the origin of the focal infection theory. Its scientific proof has been established for bacterial endocarditis.
• Bacteremia is the transient presence of bacteria in the circulating blood, it can be: spontaneous in origin in the presence of infectious foci or following dental treatment (dental extraction).
• Spontaneous bacteremias are more frequent (daily) and more significant over a cumulative period than during an isolated act:
• over one month, bacteremia is 900 times higher than after a single dental extraction maneuver

2. Pathology with proven oral origin:
   1. Bacterial endocarditis:

Infective endocarditis is secondary to grafting and multiplication of an infectious agent at the level of the valvular endocardium after induced or spontaneous bacteremia

1. Microbiology:

Infective endocarditis with positive cultures is the majority, representing 85% of all infective endocarditis.

The germs involved are streptococci (sanguis, mutans, salivarius, mitis), enterococci (faecalis, faecium, durans) and staphylococci (aureus).

2. Pathophysiology of infective endocarditis:

The valvular endothelium, normally resistant to bacterial colonization and infection by circulating bacteria, can become the site of fibrin and platelet deposits.

There would thus be two main situations of primary infection of a valve:

• on a physically modified endothelium, promoting infection by most microorganisms;
• on an unaffected endothelium, conducive to S. aureus infective endocarditis.

3. Procedures at risk of infective endocarditis:

• Finally, it is necessary to distinguish between at-risk patients, on the one hand, and at-risk procedures, on the other.

1. Patients at risk:

According to the ANSM, patients at risk are those:

1. who have a prosthetic valve or prosthetic valve repair material . They have a high risk of infective endocarditis, an increased risk of mortality and are exposed to particularly severe complications (Anderson et al, 2005; Lalani et al., 2006)
2. who have already had infective endocarditis ; they are also exposed to higher mortality and more severe complications than others (Renzulli et al, 2001; Chu et al, 2005)
3. who are carriers of cyanotic congenital heart disease:
   • non-operated or surgical pulmonary-systemic bypass
   • operated on, but presenting a residual shunt
   • operated with placement of prosthetic material by surgical or transcutaneous route, without residual leakage, only within 6 months following placement
   • operated with placement of prosthetic material by surgical or transcutaneous route with residual shunt.
4. Risky procedures:

Risky endodontic procedures are:

• periodontal probing for diagnostic purposes
• periapical surgery
• endodontic therapies.

4. Pathologies suspected of oral origin:

The various studies concerning these pathologies put forward a level of scientific proof of grade B, i.e. a scientific presumption.

Multiple pathologies have been associated with oral infectious foci. Those for which the level of scientific evidence is low, but for which an oral health assessment may be requested, according to consensus conferences, professional agreements or scientific associations, are:

• prematurity and/or hypotrophy
• type I and II diabetes, for which a toxic mechanism is suspected with a decrease in insulin resistance

• some dermatological pathologies such as angioedema localized to the face (consensus conference), or panarteritis nodosa and erythema nodosum whose streptococcal origin can be suspected
• brain or liver abscesses or unexplained prolonged fevers, transplanted organ infections
• Cardiovascular accidents: Cardiovascular accidents include strokes and coronary heart disease. The mechanism involved is toxic, involving bacterial endotoxins which in turn lead to the secretion of inflammatory cytokines.

Various studies suggest that the treatment of periodontal diseases, by improving endothelial function, could have a favorable effect in the

prevention of atherosclerosis and its complications.

• Facial vein thrombosis (FVT) : FVTs are, to our knowledge, a complication of maxillofacial infections.
• Pulmonary infections: Pulmonary infections whose presumed pathophysiological mechanisms are bacteremia or aspiration.

Treating oral infections would reduce the incidence of pneumonia in patients in institutions or intensive care units.

• joint prosthesis infections : joint prosthesis infections of oral origin, the incidence of which is low: 0.04%

The risk is multifactorial and complex to analyze. In summary, it depends on four factors: bacteremia, the patient’s general status, the prosthesis itself, and the nature of the microorganisms involved.

• Brain abscesses : Brain abscesses correspond to focal suppurations of infectious origin developed within the brain parenchyma. The spread of oral-dental germs to the brain can occur either by contiguity in the context of acute infection or by hematogenous route with chronic foci. In 70% of cases, streptococci are found. The search for an entry point is only carried out after the bacteriological assessment, most often with antibiotic therapy already started. The attitude to be adopted by the dentist will be

conditioned by the general condition of the patient and possible immunosuppression, the eradication of significant infectious foci must be a priority.

• uveitis of unknown etiology : The role attributed to teeth in uveal inflammations varies greatly over time and also between teams.

Its mechanism has been the subject of much discussion to explain “distant propagation” with successively the incrimination of toxins then the notion of “focal allergy” and sensitization of uveal tissue to a microbial antigen.

7. Action to take:
   1. How to deal with primary infectious outbreaks:

The approach to take in the face of LIPOE consists of ensuring effective debridement of the endodontic system by eliminating necrotic tissue, bacteria and their toxins using canal shaping and obturation techniques; The chemical action of canal disinfectants combined with the mechanical action of the instruments makes it possible to

neutralize the irritants that caused the development of the lesion.

At this stage the treatment is confined to the endodontium and its environment, conservation of the tooth is indicated if all the conditions allow its maintenance on the arch:

• coronary decay.
• absence of lesions compromising the success of endodontic treatment (perforation, resorption, fractured instrument).
• notion of land.
• oral hygiene.

2. How to deal with local-regional complications:
   1. Cellulite: treatment

• Assessing urgency: severity criteria
• Made according to the stage

3 types of treatment:

• Medical: medicinal
• Etiological: suppression of cause
• Surgical: drainage

1. Acute circumscribed serous cellulitis:

• At this stage, there is no suppuration yet. In case of pulp necrosis, antibiotic therapy is combined with trepanation of the tooth or its extraction depending on general and local parameters.
• A broad-spectrum antibiotic is chosen, prescribed orally for 7 to 10 days. The table summarizes the antibiotics used in this case.
• Surgical treatment:
• Surgical treatment consists of draining the infection, either via the root canal or by making a skin or mucosal incision. Depending on local and/or general parameters, preservation of the causative tooth may or may not be considered.

• Medical treatment:
• Antibiotic treatment : Antibiotic therapy is broad-spectrum, probabilistic and then secondarily adapted to the antibiogram if a bacteriological sample has been taken. It is necessary but not sufficient in the case of suppurative collections or areas of necrosis; surgery then proves essential.

2. Acute circumscribed suppurative cellulitis.

• Antibiotic therapy is prescribed in parallel with surgical drainage of the abscess.
• The administration of broad-spectrum antibiotics is again indicated here. The molecules used are identical to those mentioned previously. The combination of antibiotics allows for synergy, which is a valuable asset in our therapeutic arsenal.

3. Pain relief treatment:

The functional signs experienced by the patient with odontogenic cellulitis are important. This is why a prescription for analgesics, combined with an antibiotic prescription, is the rule. Most often, after assessing liver function, we are led to prescribe an analgesic

level II according to the WHO, combining paracetamol 1 g and codeine 60 mg every 4 to 6 hours.

2. Osteitis and osteomyelitis of the jaws:

The treatment consists of two approaches:

• Medical approach: Antibiotic therapy +++ Anti-inflammatories Analgesics Anticoagulants/vasodilators Oxygen therapy
• Surgical approach: Treatment of the cause if present and elimination of the affected area++

3. Sinusitis of dental origin:

The treatment of odontogenic maxillary sinusitis involves three therapeutic modalities: treatment of the dental cause, antibiotic therapy and treatment of the sinus consequence.

1. Medical treatment:

Antibiotic therapy

Antibiotic therapy is only indicated in cases of acute, uncomplicated purulent maxillary sinusitis with suspicion of a bacterial infection with at least 2 of the following 3 criteria:

• Persistence or increase in infraorbital sinus pain despite symptomatic treatment prescribed for at least 48 hours;
• unilateral nature of the pain and/or its increase when the head is tilted forward, and/or its throbbing nature and/or its peak in the late afternoon and at night
• ; increased rhinorrhea and continuous purulence.
• These signs are all the more valuable as they are unilateral: amoxicillin, 3 g/24 hours, for 7 days.
• Unilateral maxillary sinusitis associated with overt dental infection

homolateral of the upper dental arch: amoxicillin/clavulanic acid, 3 g/24 hours, for 7 days.

• In case of allergy to penicillin without contraindication to cephalosporins, the recommended treatment is: cefotiam hexetil, 400 mg/24h, or cefpodoxime proxetil, 400 mg/24h, or cefuroxine axetil, 500 mg/24h, for 5 days. – In case of contraindication to beta-lactams: levofloxacin, 500 mg/24h, or moxifloxacin, 400 mg/24h, for 7 days, pristinamycin, 2 g/24h, for 4 days

Analgesic prescription : Analgesic and antipyretic treatments are administered in parallel depending on the clinical symptoms.

Corticosteroid therapy : The relevance of using steroidal anti-inflammatory drugs remains to be evaluated, even though their prescription is widespread. If it is decided, it is prescribed for 3 to 5 days at a dose of 1 mg/kg/24 hours, equivalent to prednisone. Its discontinuation will be abrupt, without resorting to a tapering dosage.

2. Endodontic treatment:

The aim of endodontic treatment is to restore the pathological dental organ, the source of the infectious focus.

3. Surgical treatment:

Tooth extraction

When the tooth is no longer conserveable, its extraction is indicated: damage to the furcation, fracture, not conserveable for a prosthetic project, context of unstabilized periodontal diseases, concomitant of certain general pathologies (risk of infectious endocarditis), deep caries, impossibility of endodontic treatment by orthograde or surgical means (complex anatomy, significant or inaccessible root resorption, large and deep perforation by a root post), failure of endodontic treatment.

3. What to do in the event of focal infection:
4. Search for oral and dental infectious foci:

The oral cavity specialist frequently receives patients referred by practitioners from different specialties for a search for oral and dental infectious foci (ODIF).

The search for FIBD is requested by the correspondent in several circumstances: due to a particular general condition, to prevent the appearance of a secondary infection or to stabilize a general pathology to search for the starting point of a secondary infection before initiating medical therapy (chemotherapy, immunosuppressive therapies) or physical therapy (radiotherapy) Likely to promote or aggravate an infectious process to prepare the patient for a surgical intervention.

We can define:

• FIBD (active or latent) : actual presence of bacterial foci, whether it is a proven infection or there is no clinical repercussion at the time of observation
• Potential infectious risk situations (PIRS) : likely to become infectious hotspots in the future due to the conditions present at the local level.

1. Conducting the search for infectious foci

• An oral health assessment must include a clinical examination (interview, periodontal probing, vitality tests, percussion, palpation of the lymph nodes, etc.).
• The initial assessment must include a panoramic radiographic examination.
• In case of doubt when reading the panoramic examination, the radiographic examination must be supplemented by other examinations: retroalveolar images, cone beam tomography, computed tomography (scanner).

2. General attitude in patients with a particular infectious risk other than dental

• Prior contact with the physician responsible for monitoring the patient is recommended to assess the medical risk.
• In the event of an oral infection, the general medical context (radiotherapy, chemotherapy, cardiac surgery, etc.) should not delay surgical and/or medical management of the infectious emergency. In particular, an abscess must be drained.
• Therapeutic decision in patients with a particular infectious risk

• in cases of FIBD, as in SRIP, the choice of oral therapy must integrate multiple notions, in particular:
  • the patient’s vital prognosis linked to the general condition,
  • the risk associated with therapeutic abstention, depending in particular on the presumed virulence of the infectious source,
  • the morbidity inherent in each therapeutic solution,
  • the expected benefit of each therapeutic proposal for the patient’s comfort of life,
  • the patient’s predictable compliance with hygiene procedures and check-ups;
• In all cases, the different treatments must be explained to the patient and their informed consent must be obtained.

2. Classification of patients according to the risks of focal infection of oral origin.
   1. General population

For the entire population, regardless of any notion of pathology .

• It is recommended to eliminate FIBDs as well as SRIPs.
• The discovery of an FIBD must be the subject of information given to the patient, specifying the possible consequences of this infection.
• The discovery of a SRIP must be the subject of information provided to the patient, containing the assessment of the risk of developing an infection and specifying the possible consequences of this infection.

The general population includes:

• patients without pathologies (taking into account that no patient is completely free from the risk of developing an infection);
• patients with moderate-risk heart disease (other valvulopathies, other congenital heart diseases, mitral valve prolapse, etc.);
• patients with an orthopedic prosthesis. In this group of patients, no indication for prophylactic antibiotic therapy for oral and dental procedures was identified (however, this does not call into question the need to carry out a complete oral and dental examination in patients who are candidates for the fitting of a joint prosthesis, in order to eliminate local infectious foci).

2. Immunocompromised patients

The risk of infection is considered to be linked to any factor responsible for immunodepression, whether congenital or acquired.

In the absence of objective, biological or clinical criteria to assess it, the decision to include a patient in this risk category must be taken in good faith between the dental surgeon, or the stomatologist, and the doctors concerned.

3. Patients at high risk of infective endocarditis

This group includes only patients with heart disease defined as being at high risk of infective endocarditis.

It therefore excludes patients with heart disease defined as being at low or moderate risk of infective endocarditis (e.g. mitral regurgitation).

1. Procedures contraindicated in patients at high risk of infective endocarditis

• Intraligamentary anesthesia.
• Endodontic treatment of teeth with non-vital pulp, including re-treatment of root canal treatment.
• Endodontic treatment of teeth with vital pulp in several sessions or without an operating field (dam).
• Root amputation.
• Transplantation.
• Reimplantation.
• Periapical surgery.
• Periodontal surgery.
• Implant surgery and peri-implantitis.
• Installation of filling materials.
• Preorthodontic surgery for impacted or impacted teeth.

2. Endodontic care in patients at high risk for endocarditis

infectious

• They must be exceptional.
• They can only be carried out after checking the vitality of the tooth by appropriate tests, under a dam, in a single session, being sure that the entire canal lumen is accessible.
• This treatment should therefore be reserved for single-rooted teeth and, at a pinch, for the first premolar if both canals are accessible.
• Root separation is an act to be avoided as much as possible and is only permitted in the absence of any periodontal damage.
• Pulp diseases, periodontal diseases and trauma require extraction.

3. Antibiotic prophylaxis

• Prophylactic antibiotic therapy (antibiotic prophylaxis) consists of administering an antibiotic with the aim of preventing the development of a local, systemic or distant infection.
• It is therefore used in the absence of any infectious source and consists of the systemic administration of a single dose of antibiotic in the hour preceding

the invasive act.

• It is important to reserve such a prescription for the situations for which it is recommended.
• It is not indicated:

-for the performance of non-invasive procedures (examples in table 1);

– for most invasive procedures (see table 1) for the general population.

• It will depend on the clinical situation in immunocompromised patients.
• It is recommended during invasive procedures in patients at high risk of infective endocarditis.

Table 1: Examples of invasive and non-invasive procedures.

• Modalities of antibiotic prophylaxis (Table 2.)

Single dose within one hour before the procedure.

• Choice of antibiotic prophylaxis according to the type of procedure (table 3)

CI: contraindicated.

(1) In immunocompromised patients, the ratio between the benefit of the intervention and the risk of infection should be taken into account.

8. CONCLUSION :

Dental infections usually progress favorably, especially in healthy conditions. However, inadequate or nonexistent treatment never leads to a favorable outcome.

On the contrary, these infections risk developing into worsening, that is, cervicofacial cellulitis.

Locoregional complications of dental origin Therapeutics and management

  Wisdom teeth can cause infections if not removed in time.
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Clear aligners discreetly and comfortably correct teeth.
Modern dental fillings use biocompatible and aesthetic materials.
Interdental brushes remove food debris between teeth.
Adequate hydration helps maintain healthy saliva, which is essential for dental health.

Locoregional complications of dental origin Therapeutics and management