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Dental infections

 

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Dental infections usually arise from inflammation of the tooth pulpit  and associated necrotic dental pulp, that initially begins as dental caries. 

 

 

Such infections may remain localized or spread through various fascial planes. 

 

 

Dental  infection may be primary or secondary to periodontal, pericoronal, traumatic, or postsurgical procedures.

 

 

Odontogenic infections originate from caries, which cause decalcification of the protective enamel. 

 

 

Caries are caused by bacteria that erode the enamel outside shell of the tooth and the dentin underneath. 

 

 

Bacteria builds up on the surface of teeth as plaque which consists of both bacteria as well as food and saliva. 

 

 

As the starches in the mouth turn into acid, it dissolves the enamel and forms a pit that gradually grows in size.

 

 

During the  development of caries an imbalance of demineralization and remineralization of the tooth structure occurs.

 

 

There is greater demineralization of the tooth with high bacterial activity and low pH. 

 

 

There is greater remineralization with a pH higher than 5.5 and high concentrations of calcium and phosphate from the saliva.

 

 

Odontogenic infections are mixed aerobic-anaerobic infections. 

 

 

Management of dental  infections requires changing of the environment through decompression, removal of the etiologic factor and by choosing the proper antibiotic. 

 

 

Following dissolution  of the enamel, the infectious caries can travel through the dentinal tubules and gain access to the pulp. 

 

 

Infection n the pulp, may develop a track to the root apex and burrow through the medullar cavity of the mandible or maxilla. 

 

 

Such an infection may perforate the cortical bone plates and drain into the superficial tissues of the oral cavity or track into deeper fascial planes. 

 

 

If not drained, the infection will remain localized and develop into a periapical or periodontal abscess.

 

 

Serotypes of Streptococcus mutans are primarily responsible for causing oral disease. 

 

 

Lactobacilli are not primary causes, they are progressive agents of caries because of their great acid-producing capacity.

 

 

((Dental caries)) is the most common chronic disease in the world. 

 

 

The decline in caries in certain segments of the world is due to the addition of fluoride to public drinking water. 

 

 

While dental caries is not a life-threatening disease; an odontogenic infection can spread through fascial planes, create risk for sepsis, compromise the  airway- Ludwig angina, retropharyngeal abscess, and account#  for 49.1% of the deep neck abscesses.

 

 

 Patients with chemotherapy induced

 

neutropenia are at risk for certain pathogenic oral microorganisms that cause sepsis.

 

 

Odontogenic infections carry significant morbidity. with pain and cosmetic defects.

 

 

The oral cavity contains approximately 30-50% viridans group streptococci that are resistant to penicillins and macrolides.

 

 

It is estimated 60% of caries occurred in 20% of children, who were generally minorities or of lower socioeconomic status. 

 

 

Patients with superficial dental infections complaints include: localized pain, edema, and sensitivity to temperature and air. 

 

 

Patients with deep infections or abscesses that spread along the fascial planes may complain of fever and difficulty swallowing, breathing, and opening the mouth.

 

 

When tooth decay is small, patients may be asymptomatic, but as the decay grows the tooth may become sensitive.

 

 

Caries can be prevented by brushing and flossing daily as well as using antibacterial mouthwash in order to reduce the amount of bacteria in the mouth. 

 

 

Affected teeth with dental decay, generally are tender to percussion and temperature.

 

 

Infection can spread from the tooth to the apex to form a periapical or periodontal abscess. 

 

 

The infection may then elevate the periosteum and penetrate adjacent tissues.

 

 

Pericoronal infection occurs when tissue covering the tooth’s crown becomes inflamed and infected. 

 

 

Submental space infections, sublingual space infections, submandibular space infections, retropharyngeal space infection due: to  infection from the mandibular incisors, anterior mandibular tooth infections, mandibular molar infections, infections of the molars, respectively.

 

 

With spread to the deeper areas of the neck, signs and symptoms of vagal injury, Horner syndrome, and lower cranial nerve injury may be seen.

 

 

Deep neck infections are more common in children younger than 4 years.

 

 

Ludwig angina is associated  with brawny swelling from a rapidly spreading cellulitis of the sublingual, submental, and submandibular spaces with elevation and edema of the tongue, drooling, and airway obstruction. 

 

 

Ludwig angina is odontogenic in 90% of cases and arises from the second and third mandibular molars in 75% of cases. 

 

 

If infection spreads through the buccopharyngeal gap adjacent retropharyngeal and mediastinal infection is possible.

 

 

Buccal space infection is typically associated with cheek edema and is due to infection of posterior teeth, usually premolar or molar.

 

 

Masticator space infection presents with trismus manifestation and is due to infection of the third molar of the mandible. 

 

 

Canine space infection is noted with anterior cheek swelling with loss of the nasolabial fold and possible extension to the infraorbital region,

 

and potentially may spread to the cavernous sinus.

 

 

Acute necrotizing ulcerative gingivitis (ANUG), also known as Vincent angina, or trench mouth is a condition in which patients present with edematous erythematous gingiva with ulcerated, interdental papillae covered with a gray pseudomembrane.

 

 

ANUG  may be associated with fever and lymphadenopathy and may patients complain of metallic taste. 

 

 

The condition is caused by invasive fusiform bacteria and spirochetes but is not contagious.

 

 

Serotypes of S mutans are thought to cause initial caries infection. 

 

 

Infections that occur through the fascial planes usually are polymicrobial with an average of 4-6 organisms

 

 

Dominant isolates: 

 

 

Anaerobes (75%) – Peptostreptococci, Bacteroides and Prevotella organisms, and Fusobacterium nucleatum

 

 

Aerobes (25%) – Alpha-hemolytic streptococci

 

 

In the management of dental infections 

 

the source must ultimately be removed or controlled. 

 

 

Analgesics and antibiotics may be given for simple localized odontogenic infection or abscess. 

 

 

In odontogenic maxillofacial infections, extraction of the causative tooth is associated with a faster clinical and biological resolution.

 

 

Incision and drainage may be performed if a periapical or periodontal abscess is 

 

present.

 

 

Deep fascial infections of the neck have a higher chance of causing impingement on the airway directly or indirectly through trismus.

 

 

Tracheostomy or  management through fiberoptic nasoendotracheal intubation while the patient is awake is preferred.

 

 

Silver diamine fluoride (SSF) is used for arrest of tooth decay.

 

 

The silver in SDF acts as an antimicrobial killing bacteria allowing for the slowing down and stopage of tooth decay. 

 

 

The fluoride prevents further demineralization. 

 

 

SDF plugs the lesion forming a protective layer decreasing dentinal sensitivity, causing the lesion to become more shallow.

 

 

As the lesion remineralizes SDF simultaneously inhibits proteins that break down the dentin matrix.

 

 

When applied to caries, SDF plugs the lesion forming a protective layer decreasing dentinal sensitivity. 

 

 

As the lesion becomes more shallow, it gradually remineralizes while simultaneously inhibiting proteins that break down the dentin matrix.

 

 

Amoxicillin is the first-line drug of choice.

 

 

34% of Prevotella species resistant to amoxicillin, the alternatives of amoxicillin/clavulanate, clindamycin, and metronidazole need to be considered.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

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