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INFECTIONS OF THE TEETH, GINGIVAE, AND JAWS

INFECTIONS OF THE TEETH AND GINGIVAE

Dental caries, gingivitis, and periodontal diseases usually are not diagnosed and treated by physicians; however, poor oral hygiene can result in infections that are of concern to physicians. Infections of the teeth and gingivae can spread to contiguous structures (e.g., sinusitis, osteomyelitis of the jaw, aspiration pneumonia). To better care for patients with these diseases, an introductory understanding of these diseases is useful. Dental caries is a lesion of the enamel and dentine of the teeth; gingivitis is an infection of the gingivae (gums); and periodontal diseases are disorders of the supporting structures of the teeth (e.g., gingivae, periodontal ligament, and supporting alveolar bone).

 

Etiology

Streptococcus mutans is the most common cause of dental caries. Plaque-associated periodontal disease that begins as gingivitis and develops into periodontal disease is a polymicrobial process involving the organisms listed in Table TGJ-1. More severe periodontal disease is seen in patient harboring Actinobacillus actinomycetemcomitans or Porphyromonas gingivalis

 

Table TGJ-1. Bacterial Causes of Gingivitis and Periodontal Disease

Bacteria

Gram Stain and Shape

Actinobacillus actinomycetemcomitans

Gram-negative rod

Bacteroides forsythus

Gram-negative rod

Capnocytophaga

Gram-negative rod

Eubacterium sp.

Gram-positive bacillus

Fusobacterium nucleatum

Gram-negative rod

Micromonas (Peptostreptococcus) micros

Gram-positive coccus

Porphyromonas gingivalis

Gram-negative rod

Prevotella intermedia

Gram-negative rod

Selenomonas

Gram-negative curved rod

Oral spirochetes (Treponema denticola, most have not been named yet)

Unable to Gram stain; spiral shape


Manifestations

Dental caries are small pits that form on the smooth surfaces and in the fissures of the teeth; the pits can enlarge forming necrotic centers. Gingivitis causes the gums to be swollen, red, and tender and bleed during tooth brushing. A severe form of gingivitis is called acute necrotizing ulcerative gingivitis or trench mouth. It has a rapid onset. Symptoms include fever, malaise, lymphadenopathy, halitosis, and painful and inflamed gingiva with necrotic gray to black ulcerations (crateriform lesions) of the interdental papillae that bleed easily (papillae are blunted and no longer cone shaped). A gray pseudomembrane covers lesions and is easy to remove. Vincent’s angina is a spread of trench mouth to the oropharynx. It can occur rapidly (hours to days). Symptoms include; fever, swelling of lower face and neck, difficulty with speech or swallowing, membranous pharyngitis, painful ulcers on gingivae, buccal mucosa, and pharynx with hyperemic patches, and edema. Periodontal disease results in periodontal pockets forming around the roots of the teeth. People with periodontal disease will also have gingivitis.

Epidemiology

Pathogenesis

 

Dental caries is a chronic infection of enamel or dentine due to bacteria normally found in the mouth. A biofilm also called plaque, containing high numbers of Streptococcus mutans forms on the surface of the tooth. S mutans attaches to the salivary pellicle on the surface of the tooth using a 190 kDa protein adhesion called SAI/II. The bacteria in the plaque break down sugar in the saliva and produce acid that damages the enamel of the tooth and eventually forms a cavity on the surface of the tooth. If untreated, the damage can extend into the dentine and the pulp. If the pulp is infected, the tooth may die, and there is increased risk of development of periapical abscesses. Complications include pulpitis and dentoalveolar abscess.

Gingivitis results when increased numbers of normal flora grow in the gingival crevice and produce toxins that cause an inflammatory reaction in the gums. Plaque accumulates in the crevice resulting in an inflammatory reaction. The most common bacterial species involved are Actinobacillus actinomycetemcomitans or Porphyromonas gingivalis. Complications include development of periodontal disease.

Acute necrotizing ulcerative gingivitis is a severe form of gingivitis that is associated with excessive growth of organisms in the mouth. In many cases this excessive growth is due to poor dental hygiene. Immunosuppression, poor dental hygiene, and stress contribute to this disease. Vincent’s angina is seen when acute necrotizing ulcerative gingivitis spreads to the oropharynx.

Periodontal disease is an inflammation of the supporting structures of the teeth. It begins as gingivitis that spreads down to the root surface causing alveolar bone resorption and pocket formation. Build-up of calculus contributes to the chronicity of periodontal disease. If plaque is not removed, it forms a hard mass called tartar. Tartar traps the bacteria that cause gingivitis. When toxins are released from the bacteria they stimulate an immune response that increases production of collagenase. Collagenase destroys the connective tissue, making the teeth less secure, leading to periodontal disease and tooth loss. Tooth loss is associated with destruction of the periodontal ligament. It can also lead to alveolar bone loss. Other complications include periodontal abscess and osteomyelitis of the jaws.

Other causes for these diseases include; poor dental hygiene, smoking tobacco, faulty dental prosthesis, malocclusion, breathing through the mouth, local trauma (brushing too hard), dry mouth, vitamin deficiency (especially vitamin C), prementral hormonal changes, obesity, Down syndrome, medications, and malnutrition.

Diagnosis

Medical patients with dental caries, gingivitis, and periodontal disease are usually referred to a dentist for diagnosis, treatment, and preventive maintenance.

 

Therapy and Prevention

To prevent dental caries, gingivitis, and periodontal disease, patients should be encouraged to brush and floss their teeth daily, obtain professional dental examinations and cleanings twice a year, and avoid sweet and sticky foods.

Treatment of acute necrotizing ulcerative gingivitis and Vincent’s angina includes debridement and oral penicillin and metronidazole or with just clindamycin.

INFECTIONS OF THE PERIAPICAL TISSUE AND JAW

Dentoalveolar abscesses form at the end of the tooth root. Periodontal abscesses form deep in the gingivae along the tooth root following advanced periodontal disease.

Ludwig’s angina is a cellulitis of the sublingual and submandibular spaces and can rapidly become fatal without treatment.

Osteomyelitis of the jaw is an inflammation of the bone and the muscles around the jawbones and is more commonly seen in the mandible.

Etiology

Dentoalveolar and periodontal abscess, Ludwig’s angina, and osteomyelitis of the jaw are all polymicrobial infections (Table TGJ-2).

 

Table TGJ-2. Causes of Dentoalveolar and Periodontal Abscesses, Ludwig’s angina, and Osteomyelitis of the Jaw

Disease

Causative Agents

Dentoalveolar abscess

Strict anaerobes found in the oral mucosa

Periodontal abscess

Gram-negative rods, Streptococcus viridans group, anaerobic streptococci, spirochetes

Ludwig’s angina

Streptococcus, Bacteroides, Fusobacterium, Staphylococcus aureus

Osteomyelitis of the jaw

Gram-negative rods, anaerobic streptococci, Actinomyces israelii

Manifestations

Dentoalveolar abscesses usually cause pain in and around the affected tooth, and there may be swelling of the face over the site of the abscess. Periodontal abscess manifests similar to dentoalveolar abscess (i.e., pain and facial swelling over the site of the abscess); however, the patient with periodontal abscess also has signs of periodontal disease.

A patient with Ludwig’s angina is severely ill and has a fever, severe dysphagia, trismus, and dysphonia. The patient has brawny edema and erythema of the neck under the chin. The floor of the mouth is often tender to the touch. The patient will experience intense pain upon tongue movement. The mouth is usually open, and the tongue is lifted upwards and backwards so that it is pushed against the roof of the mouth and the posterior pharyngeal wall. When this occurs, acute respiratory obstruction is likely to follow. Examination shows a brawny, tense swelling of the submaxillary and submental regions with enlargement of the neighboring lymphatic glands.

Osteomyelitis of the jawbone causes restricted jaw motion, pseudoparalysis, and hyperemic, warm, edematous, and tender soft tissue around the inflamed bone. Actinomycosis of the jaw may also present with a localized swelling at the angle of the mandible.

Epidemiology

 

Pathogenesis

Dentoalveolar abscess usually follows an infection of the pulp of the tooth that extends to the base of the tooth roots. Periodontal abscesses usually are an extension of periodontal disease and form deep in the gingivae along the roots of the teeth.

Ludwig’s angina is a rapidly developing cellulitis of the sublingual and submaxillary spaces, often arising from infection of the tooth roots (molars and premolars) that extend below the mylohyoid line of the mandible. Ludwig’s angina can also occur following infections in the floor of the mouth, the base of the tongue, and the lingual tonsils, and following salivary calculi or from intravenous injection of the internal jugular vein (especially in intravenous drug users).


Diagnosis

 

Diagnosis of dentoalveolar and periodontal abscesses is usually based on the patient’s signs and symptoms. Radiographs of the affected areas can be helpful.

Ludwig’s angina is usually diagnosed based on clinical signs and symptoms. CT scans and blood cultures can be helpful. The disease can quickly become life threatening; therefore, rapid diagnosis is important to the survival of patients.

Osteomyelitis can be diagnosed using radiographs; however, radiographs are not very sensitive and usually do not detect osteomyelitis early in the disease process. It may take up to 3 weeks of infection to be detectable by radiograph. When detected by radiography a “moth-eaten” appearance of the bone is positive for osteomyelitis. CT scans are more sensitive than plane radiographs, and MRIs are more sensitive than CT scans and can detect changes even earlier. Tissue samples and culture may help to identify the causative agents. In cases of actinomycosis, needle aspiration of the abscess can be helpful. If sulfur granules are present in the aspirate, Gram stains should be performed to demonstrate gram-positive branching filamentous bacteria in the sample.

Therapy and Prevention

 

Patients with dentoalveolar abscesses should be referred to a dentist. Tooth extraction or a root canal and antibiotic therapy may be necessary. Patients with periodontal abscess should also be referred to a dentist. Tooth extraction or drainage of the abscess followed by periodontal and antibiotic treatments are usually required.

Treatment of Ludwig’s angina involves four principal components.

1.  Adequate airway management is essential.

2.  Antibiotic therapy must be designed to cover both anaerobes and Staphylococcus aureus. Clindamycin is the first-line antibiotic therapy.

3. In the past, incision and drainage of abscesses was routine. Surgical therapy now is usually reserved for cases of failure of medical treatment.

4.  Attention to adequate nutrition and hydration should be given, since both are difficult to maintain in a patient with significant oropharyngeal edema.

Treatment of osteomyelitis consists of antibiotic therapy for an extended period (4–6 weeks). The specific antibiotic therapy depends on the cause of the infection. A bone biopsy should be obtained to determine the cause of the infection; surgical debridement maybe necessary to eliminate the infection.

Dentoalveolar and periodontal abscesses, Ludwig’s angina, and osteomyelitis of the jaw can usually be prevented by encouraging good oral hygiene, regularly visiting the dentist, and treating oral and dental infections promptly.

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Send comments and mail to Neal R. Chamberlain, Ph.D., nchamberlain@atsu.edu
Revised 10/15/13
©2013 Neal R. Chamberlain, Ph.D., All rights reserved.