INFECTIONS OF THE TEETH, GINGIVAE, AND JAWS

Infections of the Teeth, Gingivae, Periodontal Ligament and Alveolar Bone of the Jaw (Dental Caries and Periodontal Disease)

Dental caries/periodontal disease 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, gingivae, periodontal ligament and alveolar bone can spread to contiguous structures (e.g., sinusitis, osteomyelitis of the jaw, aspiration pneumonia). Poor oral hygiene also contributes to cardiovascular disease. 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 dentin of the teeth. Periodontal disease includes gingivitis and periodontitis. Gingivitis is an infection of the gingivae (gums); and periodontitis is an infection/inflammation of the supporting structures of the teeth (e.g., periodontal ligament and alveolar bone). There are two basic forms of periodontitis; chronic and aggressive periodontitis.

Etiology

Dental Caries: Mutans group of Streptococcus; S. mutans and S. sobrinus, Lactobacillus casei, Actinomyces species, Bifidobacterium species, and low-pH tolerant Streptococcus species. Cariogenic bacterial species are present in healthy dental biofilm. There is not one particular bacterial species responsible for caries production, but a collection of several bacterial species that have the following abilities; acidogenicity, aciduricity, production of extracellular polymers and production of intracellular polysaccharides.

Periodontal Disease: Plaque-associated periodontal disease includes gingivitis, chronic periodontitis, aggressive periodontitis acute necrotizing ulcerative gingivitis (trench mouth) and Vincent’s angina (Plaque = subgingival biofilm adherent to tooth surfaces containing high numbers of organisms associated with periodontal disease).

All of these diseases are polymicrobial processes. Certain organisms, when present in plaque will make the chances of periodontal disease more likely. When the numbers of anaerobic Gram-negative rod-shaped bacteria and spirochetes increase compared to the other bacteria in the subgingival biofilm/plaque then periodontal disease is more likely to occur.

Patients are at high risk of developing periodontal diseases if red complex organisms (high risk) such as Porphyromonas gingivalis, Tannerella forsythia, and Treponema denticola are in the subgingival plaque.

Patients are at moderate risk of developing periodontal diseases if orange complex organisms (moderate risk): Fusobacterium nucleatum, Prevotella intermedia, Prevotella nigrescens, Parviomonas micra, Eubacterium nodatum, and various Campylobacter species (e.g., C. rectus).

Patients are at low risk of developing periodontal diseases if yellow complex organisms (low risk): Streptococcus intermedius, Streptococcus sanquinis, Streptococcus oralis, Streptococcus mitis, and Streptococcus gordonii.

Aggressive periodontitis is usually seen in patients under 30 years of age, that have plaque colonized by high numbers of Aggregatibacter actinomycetemcomitansor Eikenella corrodens in concert with Fusobacterium nucleatum.

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. Inflammation is manifest in the gingiva by swelling (edema), redness (erythema) and bleeding following brushing/flossing. Rarely, if ever, are the gingiva painful. If they are the patient may state that their gums are tender.

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.

Periodontitis causes the gingiva to recede and to form deep periodontal pockets around the roots of the teeth. Damage can extend to the periodontal ligament and alveolar bone causing the tooth to become loose and, in severe cases, fall out. There are two forms of periodontitis; chronic and aggressive. Chronic periodontitis takes years to develop. Aggressive periodontitis is an uncommon rapid detachment of the periodontal ligament and destruction of alveolar bone. It usually affects younger patients < 30 years of age (particularly adolescents) that appear otherwise healthy. It is associated with phagocyte abnormalities and hyper-responsive macrophages leading to inflammation of the tissue. People with both forms of periodontitis will also usually have gingivitis.

Epidemiology

· Dental caries, gingivitis, and periodontal disease are ubiquitous; however, with good oral hygiene and preventive dental practices, the incidence is decreasing in the Western world.

· Dental caries is the leading cause of tooth loss in children younger than age 12.

· Periodontal disease is the leading cause of tooth loss in adults and is present in 8–10% of the adult population.

· Incidence of gingivitis increases with age with a peak at 34. 50% to 90% of adults have gingivitis.

· 13% of the population is susceptible to severe periodontal disease.

· There may be a genetic susceptibility to periodontal disease. Other factors are also responsible including poor access to dental care and poor dental hygiene.

· Acute necrotizing ulcerative gingivitis is rare. It is more common in patients with immunosuppression, who use tobacco or are under physical or emotional stress. The disease was common in the trenches during World War I and is why it is called trench mouth. It is also seen in college dorms and in other stressful conditions.

· Acute necrotizing ulcerative gingivitis is more common in persons with poor dental hygiene.

· Acute necrotizing ulcerative gingivitis is NOT spread person to person.

· Vincent’s angina is the spread of acute necrotizing ulcerative gingivitis to the oropharynx and is less common.

Pathogenesis

A diverse collection of oral microorganisms is found in dental biofilms. A small sample of dental biofilm yields cultures containing between 12 and 27 bacterial species. After a thorough cleaning to remove dental biofilm on the tooth surface it only takes about 24 hours for dental biofilm to form again. If not removed by brushing two times a day and daily flossing the biofilm can accumulate to form plaque. If plaque is mineralized it becomes calculus (tartar). Plaque formation and its mineralization to calculus takes on average about 12 days (range of 10 to 20 days). Calculus is difficult to remove and REQUIRES professional cleaning to remove it. If plaque and calculus are not regularly removed patients are much more likely to develop dental caries and/or periodontal disease. Plaque and calculus can form on the supra- and sub-gingival surfaces of the teeth.

Dental caries is a chronic infection of enamel and/or dentin due to bacteria normally found in the mouth. A biofilm also called plaque, containing high numbers of gram-positive cariogenic bacteria forms on the surface of the tooth by attaching to the salivary pellicle on the surface of the tooth. When dental biofilm becomes visible, this biofilm is called plaque. Plaque and mineralized plague (calculus/tarter) can produce dental caries in a sucrose-rich environment when enriched with cariogenic bacteria.

Four microbial characteristics, or cariogenic abilities, are common in cariogenic bacterial inhabitants of dental plaque;

1. Acidogenicity- rapid uptake and fermentation of carbohydrates to lactic acid or other acidic byproducts

2. Aciduricity- the ability to tolerate, grow, and continue to make acid in acidic (low-pH) environments

3. Extracellular polymers- the synthesis of extracellular polymers or EPS from sucrose to consolidate attachment of the plaque to the surface of the tooth

4. Intracellular polysaccharides- the production of intracellular polysaccharides during periods of excess carbohydrate availability which can be converted to acid during times when carbohydrates are not available.

The bacteria in the plaque break down sucrose in the saliva and produce lactic acid that damages the enamel of the tooth and eventually forms a cavity on the surface of the tooth. At pH’s of 5.5 or below the tooth demineralizes and cavities can result. Cavity formation depends on how long and how frequently the pH goes to 5.5 or below. If the times of low pH are short and infrequent, cavity production is less likely. If the times of low pH are long and frequent, cavity production is more likely.

If sucrose intake stops, the pH of the plaque will rise and remineralization of the enamel occurs. Caries will result if the acidification-demineralization phase is more damaging and more frequent than the repair phase (alkalinization-remineralization phase). If untreated, the damage can extend into the dentin 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.

Periodontal disease includes gingivitis, acute necrotizing ulcerative gingivitis (trench mouth), chronic periodontitis and aggressive periodontitis.

Gingivitis: The more sub-gingival plaque that accumulates on the teeth the more likely a patient will develop gingivitis. Gingivitis does NOT occur following any specific pathogen being present in the dental plaque. More anaerobic Gram-negative rod-shaped bacteria and spirochetes are present in the sub-gingival plaque when compared to supra-gingival plaque that can cause dental caries. When the numbers of anaerobic Gram-negative rod-shaped bacteria and spirochetes increase compared to the other bacteria in the sub-gingival plaque then gingivitis is more likely to occur. The organisms in this plaque contains large numbers of gram-negative proteolytic and hemolytic bacteria that cause inflammation of the gingiva. The sub-gingival plaque bacteria produce proteases and hemolysins to obtain nutrients by damaging host tissues. As a result, the host immune response produces an inflammatory reaction in the gingiva. Inflammation is manifest in the gingiva by swelling (edema), redness (erythema) and bleeding following brushing/flossing. If the biofilm/plaque is not removed the gingiva may detach from the tooth and allow the biofilm/plaque to extend further down the tooth’s surface. Plaque accumulates in the crevice resulting in an inflammatory reaction. Complications include development of periodontitis.

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.

Chronic Periodontitis is an infection and inflammation of the supporting structures of the teeth and is the most common form of periodontitis. It is an infection and inflammation of the periodontal ligament and of the alveolar bone. It causes destruction of the ligament and alveolar bone resorption. Build-up of plaque contributes to the chronicity of periodontal disease. If plaque is not removed, it becomes mineralized and forms a hard mass called tartar or calculus. 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.

Aggressive Periodontitis is a less common but rapid infection and inflammation of the supporting structures of the teeth. It usually affects younger patients < 30 years of age (particularly adolescents) that appear otherwise healthy. It is associated with phagocyte abnormalities and hyper-responsive macrophages leading to inflammation of the tissue. The plaque microflora in aggressive periodontitis is similar to chronic periodontitis. However, the presence of certain bacteria in the plaque increases the risk for this disease to develop (Aggregatibacter actinomycetemcomitans or Eikenella corrodens in concert with Fusobacterium nucleatum). Sparse amounts of biofilm/plaque are generally found relative to the degree of periodontal destruction.

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), premenstrual hormonal changes, obesity, Down syndrome, medications, and malnutrition.

Diagnosis

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

Therapy and Prevention

To prevent dental caries 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, Prevotella, 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

· With the advent of good oral hygiene, most infections of the periapical tissue and jaw are relatively uncommon.

· Ludwig’s angina is the most commonly encountered infection of the neck space. It is uncommon, but if not treated has a mortality rate of about 50%.

· Most cases of Ludwig’s angina occur following a dental infection.

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.

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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