Infections of the
Teeth, Jaw and Mouth
Diseases
of the Teeth and Supporting Structures
Dental caries- a lesion of the enamel and dentine of the teeth.
Periodontal Diseases- disorders of the supporting structures of the teeth
(gingiva, periodontal ligament and supporting alveolar bone).
Overview
These diseases are outside of the field of medicine and are diagnosed and treated by dentists. Poor dental hygiene can result in infections that are of concern to physicians. Infections of the teeth and the gums can spread to contiguous structures (sinusitis, osteomyelitis of the jaw, aspiration pneumonia). To better care for these sorts of patients an introductory understanding of these diseases is useful.
Etiology
Dental caries- Streptococcus mutans (most
common cause; initiates dental cavity), Lactobacillus sp. (appear to be
important in progression of lesion deep into enamel and the dentine).
Plaque-associated periodontal disease-
gingivitis/periodontal disease- is a polymicrobial process. The following are
commonly seen in these infections: Eubacterium sp., Peptostreptococcus
micros, Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis,
Bacteroides forsythus, Fusobacterium nucleatum, Prevotella intermedia,
Capnocytophaga sp., Selenomonas sp., Spirochaetes.
Epidemiology
Dental caries is ubiquitous. However, with
good dental hygiene and prevention practices the incidence in the Western world
is falling. It is the leading cause of tooth loss in children under the age of
12.
Gingivitis/periodontal disease is also very
common and with good dental hygiene and prevention practices is decreasing in
incidence in the Western world. It is the leading cause of tooth loss in adults
and is present in 8-10% of the adult population.
Pathogenesis
Dental caries- is a chronic infection of
enamel or dentine due to bacteria normally found in the mouth. A biofilm
(plague; high numbers of Streptococcus mutans) forms on the surface of
the tooth. The bacteria in the plaque breakdown sugar in the saliva and produce
acid that damages the enamel of the tooth eventually forming a cavity on the
surface of the tooth. If untreated the microbes can extend the lesion into
dentine and then into the pulp. If the pulp is infected the tooth may die and there
is an increased risk of periapical abscesses forming. Complications include
pulpitis and dentoalveolar abscess.
Gingivitis (plaque associated)- increase numbers of normal flora organisms (Streptococcus,
Capnocytophaga, Actinomyces, etc.) grow in the gingival crevice producing
toxins that cause an inflammatory reaction in the gums. Plaque accumulates in
the crevice resulting in an inflammatory reaction. Complications include
development of periodontitis.
Periodontitis- An inflammation of the supporting
structures of the teeth. It starts out as gingivitis that then spreads down to
the root surface causing alveolar bone resorption and pocket formation. Can
eventually lead to alveolar bone loss and damage to the periodontal ligament
then can result in tooth loss. Other complications include periodontal abscess
and osteomyelitis of the jaws.
Manifestations
Dental caries- small little pits form on the smooth surfaces
and in the fissures of the teeth that can enlarge forming necrotic centers.
Gingivitis- Swollen, red, tender gums that bleed during brushing of the teeth.
Periodontitis- periodontal pockets with gingivitis.
Diagnosis
Refer to a dentist.
Therapy
Refer to a dentist.
Prevention
Refer to a dentist. Encourage good dental
hygiene.
Diseases
of the Periapical Tissue and Jaw
These diseases include infections around the end of the tooth roots and the contiguous tissues surrounding them as well as the jawbone and the muscles in that area.
Dentoalveolar abscess
Periodontal abscess
Ludwig’s angina
Osteomyelitis of the jaw
Overview
Dentoalveolar abscess- an abscess that forms at the end of the tooth root.
Periodontal abscess- an abscess that forms deep in the gums along the tooth root following advanced periodontal disease.
Ludwig’s angina- a cellulitis of the sublingual and submandibular spaces (floor of the mouth).
Can rapidly become fatal without treatment (mortality rate before the antibiotic era was 50%)
Osteomyelitis of the jaw- an inflammation of the bone (medullary space) and the muscles around it. More commonly affects the mandible.
Etiology
Dentoalveolar abscess- polymicrobial, usually an endogenous infection, strict anaerobes are very important in the formation of the abscess (obligate anaerobes, Streptococcus milleri).
Periodontal abscess- polymicrobial including Gram-negative rods, streptococcus viridans, anaerobic streptococci, and spirochaetes.
Ludwig’s angina- Streptococci, Bacteroides, Fusobacterium, Staphylococcus aureus
Osteomyelitis of the
jaw- polymicrobial (Gram-negative rods, anaerobic streptococci, Actinomyces
israelii)
Epidemiology
With the advent of good dental hygiene most
of these infections are relatively uncommon.
Ludwig’s angina is the
most commonly encountered neck space infection.
Pathogenesis
Dentoalveolar abscess- usually follows an
infection of the pulp of the tooth that extends to the base of the roots.
Periodontal abscess- usually an extension of
periodontal disease deep in the gums along the roots of the teeth.
Ludwig’s angina- is a rapidly swelling
cellulitis of the sublingual and submaxillary spaces, often arising from
infection of the tooth roots (molars and pre-molars) that extend below the
mylohyoid line of the mandible. Most abscesses in the spaces are caused by
dental infections (90%). They can also
occur following infections in the floor of the mouth, the base of the tongue,
the lingual tonsils, and following salivary calculi or from intravenous
injection of the internal jugular vein especially in drug abusers. There is a
high incidence of associated systemic illnesses including diabetes mellitus,
AIDS and HIV seropositivity
Manifestations
Dentoalveolar abscess- pain in and around the
affected tooth. Swelling of the face over the site of the abscess.
Periodontal abscess- as above for
dentoalveolar abscess. The patient also has signs of periodontal diseases.
Ludwig’s angina- severely ill, severe dysphagia, trismus, cervical tenderness, swelling, limited range of motion, dysphonia. Patients may appear quite toxic, sitting upright, drooling and tachypneic. The patient has edema (brawny) and erythema of the neck under the chin and often of the floor of the mouth. There is intense pain on tongue movement and the patient may be severe dehydrated due to an inability to take anything by mouth. The mouth is 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 occur. Examination shows a brawny tense swelling of the submaxillary and submental regions with enlargement of the neighboring lymphatic gland. The patient has a fever and there is considerable salivation because the patient is unable to swallow (dysphagia).
Osteomyelitis- Restricted jaw
motion, pseudoparalysis; Soft tissue around the inflamed bone, which is
hyperemic, warm, edematous, and tender. Actinomycosis may also present with a
localized swelling at the angle of the mandible.
Diagnosis
Dentoalveolar and periodontal abscesses-
usually determined clinically, radiographs of the affected areas could be of
help.
Ludwig’s angina- This disease can be diagnosed clinically. CT scans and blood cultures can be helpful. This disease can rapidly become life threatening. Rapid diagnosis is important to the survival of these patients.
Osteomyelitis- Radiographs can take up to 3 weeks to be positive and yield a “moth eaten” appearance. CT scans are more sensitive. MRI can detect early changes. Bone scans with gallium to detect early disease. Tissue samples and culture may help in identifying the causative agents. In the case of actinomycosis needle aspiration of the abscess can be helpful. Look for the presence of sulfur granules in the aspirate following by Gram stains to show Gram-positive branching filamentous bacteria.
Therapy
Dentoalveolar abscess- refer to dentist
(tooth extraction or root canal. Antibiotic therapy may also be required).
Periodontal abscess- refer to dentist (tooth
extraction or drainage of the abscess followed by periodontal treatment,
antibiotics).
Ludwig’s angina- there is four principal components in the treatment of Ludwig’s angina. First, adequate airway management is essential. Second, antibiotic therapy must be designed to cover both anaerobes and Staphylococcus aureus. Penicillin with or without metronidazole is the first line therapy. Clindamycin or amoxicillin/clavulanic acid is considered highly effective. Empiric antibiotic treatment in the immunocompetent host is considered safe; however, medical therapy must be guided by cultures and sensitivities in the immunocompromised host. Third, in the past, incision and drainage of abscesses was routine. Now, surgical therapy is usually reserved for cases of medical treatment failure. Finally, adequate nutrition and hydration can be a challenge in patients with significant oropharyngeal edema.
Prevention
Dentoalveolar
periodontal abscess- encourage good dental hygiene, regular visits to the dentist, and prompt treatment of oral/dental
infections.
Ludwig’s angina- encourage good dental hygiene, regular visits to the dentist, and prompt treatment of oral/dental infections.
Osteomyelitis of the jaw- encourage good dental hygiene, regular visits to the
dentist, and prompt treatment of oral/dental infections.
Infections
of the Tongue and Mouth
Disease
Stomatitis is an inflammation of the mucosal surfaces in the
mouth and on the tongue. HSV 1 and 2 viruses and Candida albicans are
the most common causes of this inflammation. If inflammation includes the
gingivae (gums) then it is called gingivostomatitis (common with herpes
infections).
There are basically three different types of candidosis; pseudomembranous, erythematous, and hyperplastic. These types are further divided into 4 types;
(1) Acute pseudomembranous candidosis (thrush),
(2) Acute erythematous (atrophic) candidosis,
(3) Chronic hyperplastic candidosis,
(a) Chronic oral candidosis (candidal leukoplakia),
(b) Endocrine candidosis syndrome,
(c) Chronic localized mucocutaneous candidosis
(d) Chronic diffuse candidosis.
(4) Chronic erythematous (atrophic) candidosis.
Thrush (acute pseudomembranous candidiasis) is the term used for the multiple white-fleck appearance of acute candidiasis. Erythematous candidosis is the term used for the red lesions of candidiasis.
Etiology
The most common causes of this infection are Herpes Simplex viruses 1
and 2 (gingivostomatitis or cold sores) and Candida albicans (oral
candidosis). Other species of Candida (ex. C. krusei),
have been isolated from severely immunocompromised patients with candidosis.
Epidemiology
Oral herpes- is a very common infection affecting nearly 60% of
the population by 15 years of age. Oral herpes is most commonly seen in young
children however, it has also occasionally been observed in adults. HSV-1 and
HSV-2 is transmitted person to person by touching infected saliva, mucous
membranes, or skin and by sharing of cups or utensils. HSV-1 causes
around 80% of the oral herpes infections. HSV-2 is usually transmitted to the
oral cavity via oral sex. These viruses become latent and remain with the host
for life. Recurrences in the mouth are uncommon. Asymptomatic shedding occurs
periodically and even people without any herpetic lesions can infect others.
The herpes simplex viruses infect humans only.
Candidosis - a very common endogenous disease in patients with
certain predisposing conditions. Candida albicans is a common inhabitant
of the oral flora (50% of population) and any disturbance of this flora can
result in overgrowth of the yeast. Is acquired during passage down the birth
canal, by sharing cups and eating utensils, breast-feeding and sharing saliva.
Candidosis may predispose individuals to esophageal spread. The percentage of
carriers is higher in women than in men.
Predisposing factors:
§
Infants and neonates
§
Patients on
broad-spectrum antibiotic treatment
§
Patients taking
steroids (inhaled and systemic; Children on inhaled steroids also have
increased incidence of oral candidiasis.)
§
Patients with
polyendocrine disorders (diabetes)
§
Smokers (30-70% more
likely to carry Candida)
§
Denture wearers
§
Drugs with xerostomic adverse
effects are associated with oral candidosis.
§ Xerostomia (dry mouth; Sjögren syndrome and after radiotherapy)
§ Patients with underlying immune dysfunction (HIV infection)
Acute
pseudomembranous candidosis (Thrush)-Up to 37%
of newborns develops thrush. It is usually a mild and self-limiting disease. It
is uncommon during the first week of life. It is most commonly seen around the
fourth week of life. Thrush is uncommon in infants older than 6-9 months.
Thrush can occur, however, at any age in predisposed patients.
Pathogenesis
Oral herpes- the virus causes painful sores on lips, gums, tongue, roof of the mouth, and inside the mucous membranes lining the cheeks. It also can cause symptoms that include fever and muscle aches. Mouth sores most commonly occur in children aged 1-2 years, but it can affect people at any age and any time of the year.
After the herpes virus infection it has the ability to proceed to the following stages.
1. Primary infection: The virus enters the skin or mucous membrane and reproduces. During this stage, oral sores and other symptoms, such as fever, may develop. The virus may cause asymptomatic infections. Asymptomatic infection occur twice as often as symptomatic disease.
2. Latency: From the infected site, the virus moves to nerves in the region. There the virus reproduces and becomes inactive.
3. Recurrence: During certain stresses, emotional or physical, the virus may reactivate and cause new sores and symptoms.
Three different
types of candidosis:
Acute pseudomembranous candidosis (Thrush) - During some disturbance of the normal oral flora Candida albicans will overgrow causing various signs and symptoms described below. Overgrowth of the yeast on the oral mucosa leads to desquamation of epithelial cells and accumulation of bacteria, keratin, and necrotic tissue. This debris combines to form a pseudomembrane, which may adhere closely to the mucosa. Neonates are colonized when they pass down the birth canal. Neonates can also acquire this organism during breast-feeding and from improperly cleaned bottle nipples. The organism also resides in the lower GI tract. Candidal diaper rash is oftentimes observed in conjunction with thrush.
Erythematous candidosis- There are both acute and chronic conditions. It is an inflammatory response to Candida overgrowth without the pseudomembrane forming or is the infection post pseudomembrane shedding. May arise due to a number of different factors and local conditions:
§ Follows acute pseudomembranous candidosis after the white plaques have shed yet the infection persists;
§ de novo in AIDS patients;
§ in patient receiving prolonged drug therapy: topical steroids or broad spectrum antibiotics;
§ most commonly related to wearing dentures.
There are varying degrees of inflammation starting with localized pinpoint hyperemia (type 1), diffuse erythema and edema (type 2), and inflamed hyperplastic epithelium (type 3).
Hyperplastic candidosis (candidal leukoplakia)- Is characterized by areas in the mouth of parakeratinization, marked hyperplasia with candidal hyphae invading the parakeratinized layer at right angles and superficial to the surface. In some cases can develop into malignancies.
Manifestations
Oral herpes- The incubation period is 2-12 days. Most people average about 4 days.
Duration of illness: 2-3 weeks. Fever, tiredness, muscle aches, and irritability may occur.
Pain, burning, tingling, or itching occurs at the infection site before the sores appear. Then clusters of blisters erupt. The blisters break down rapidly and when seen, appear as tiny, shallow, gray ulcers on a red base.
Oral sores: The most intense pain caused by these sores occurs at the onset and make eating and drinking difficult. The sores may occur on the lips, the gums, the front of the tongue, the inside of the cheeks, throat, and the roof of the mouth. They may also extend down the chin and neck.
The gums may become red, mildly swollen and may bleed. Neck lymph nodes often swell and become painful. In people in their teens and 20s, herpes may cause a painful throat with shallow ulcers and a grayish coating on the tonsils.
The
3 basic types of candidosis:
Acute pseudomembranous candidosis (Thrush) – Is characterized by the presence of creamy-white plaques (pseudomembranes) that consist of superficial mucosal cells, neutrophils and yeast cells. These plaques can be found on the tongue, soft palate, cheek, gingivae and/or pharynx. Lesions often start as tiny focal areas that enlarge to white plaques (patches). When scraped with a tongue blade, lesions are difficult to remove and leave behind an inflamed base that may be painful and may bleed.
In neonates and infants, parents usually notice a white coating in the child's mouth. The child may have trouble feeding in severe cases. Candidal infection in the diaper area may accompany thrush. A thorough physical examination is important for patients with recurrent thrush infections and for older children.
Erythematous candidosis- these lesions consist of red areas of varying sizes that can occur on any part of the oral mucosa. If present on the tongue the lesions can be painful, fiery red and shiny with evidence of depapillation. This disease can be acute or chronic in nature.
Hyperplastic candidosis (candidal leukoplakia)- Usually an individual lesion on the oral mucosa of the cheek near the commissure, at the angles of the mouth, or on the surface of the tongue. They are chronic, discrete, raised lesions that may vary from a small, palpable, translucent, or whitish area to a large, dense, opaque plaque that is hard and rough to the touch. Homogeneous or speckled areas, which do not rub off (nodular lesions), can be seen. Speckled, red-white, areas account for 3-50% of the lesions and have a higher change of malignant transformation.
Diagnosis
Herpes gingivostomatitis- culture for virus, serology, Tzanck test positive.
Candidosis- swab lesions for culture, scrap some of the lesions smear on slide and use periodic acid-Schiff (PAS), Gridley stain, or Gomori methenamine silver (GMS) stain to reveal the pseudohyphae of the yeast, biopsy hyperplastic conditions for histology. Remember pseudomembranous lesions are removable but hyperplastic lesions are not.
Treatment
Herpes gingivostomatitis- usually is self-limiting and does not usually require treatment however if severe penciclovir or valacyclovir can be given. Treatment will not cure and recurrences can occur.
Candidosis- Fluconazole or Itraconazole
Disease
Angular Cheilitis (angular stomatitis, perlèche) is an inflammation of the angles of the mouth.
Etiology
Most common cause is Candida albicans. If yellow crusting appears then Staphylococcus aureus is likely to also be involved.
Pathogenesis
Angular stomatitis describes erythema and maceration of the skin adjacent to the angle of the mouth. It is often seen in the elderly where it is predisposed to by sagging facial muscles and ill-fitting dentures, which produce a fold in the angle of the mouth. Angular stomatitis also may be seen in individuals with HIV infection.
Angular stomatitis commonly is an isolated initial sign of anemia or vitamin deficiency, such as vitamin B-12, and resolves when the underlying disease has been treated. Iron deficiency anemia and other vitamin deficiencies have been cited as other predisposing factors.
Manifestations
Lesions affect the angles of the mouth; soreness, erythema, and fissuring are characteristic; diagnosis usually is associated with ill-fitting denture-induced stomatitis.
Diagnosis
Usually done clinically however you can swab the lesion and culture the organisms.
Treatment- hydrocortisone 1%, clioquinol 3%
Miscellaneous others
Neisseria gonorrhoeae can cause erythema, edema, vesicles, ulcers and pain in the mouth. Usually following oral sex with an infected partner. These patients are more likely to develop systemic gonorrhea.
Treponema pallidum infections can occur in the mouth resulting in chancre formation. Secondary syphilis can result in mucous patch formation on the tongue or in the mouth.
Varicella-Zoster Virus- just before the rash of chickenpox a patient may have ulcers with an erythematous halo on the roof of their mouth.
Hand, foot, and mouth disease- usually caused by Coxsackievirus A16 this disease begins with a mild fever, poor appetite, malaise, and frequently a sore throat. One or 2 days after the fever begins, sores develop in the mouth. They begin as small red spots that blister and then often become ulcers. They are usually located on the tongue, gums, and inside of the cheeks. The skin rash develops over 1 to 2 days with flat or raised red spots, some with blisters. The rash does not itch, and it is usually located on the palms of the hands and soles of the feet.
Herpangina- another disease caused by Coxsackievirus A that causes small papulovesicular lesion to develop on the mucosa of the anterior pillars of the fauces, soft and hard palate, tongue, uvula, pharyngeal wall and tonsils.
Measles- oral lesions called Koplik’s spots occur following this viral infection.
Papilloma viruses- can produce warty lesions on the mucous membranes in the mouth and on the lips. These can include the common wart (verruca vulgaris) or the venereal wart (condyloma acuminatum).