Disorders of the mouth

Pathophysiology and clinical features

In developed countries, dental caries (dental decay) is a common bacterial disorder. First, the surface enamel of the tooth is breached by the demineralising action of lactic acid generated by commensal oral bacteria as a byproduct of carbohydrate metabolism, particularly of refined sugar. The most vulnerable sites for decay are just below the contact points of adjacent tooth crowns and the pits and fissures on the biting (occlusal) surface of molars and premolars. These sites are inaccessible to natural oral cleansing mechanisms and to tooth brushing.

Once enamel is breached, proteolytic bacteria enter the less calcified dentine beneath and cause progressive destruction. The enamel remains intact until the dentine is undermined and the enamel fractures. Thus, dental caries may be well advanced but invisible, even to a dental mirror and probe, and detectable only on X-ray. The decay process is asymptomatic until close enough to the dental pulp to cause inflammation and pain and, eventually, bacterial invasion and abscess formation. The pathological process and corresponding symptoms are outlined in Figure 48.1.

Once the pulp is exposed, inflammation and bacterial invasion usually destroy it, then spread to the periapical region forming an abscess. This causes painful oral and facial swelling, and if untreated, eventually drains into the mouth or occasionally onto the face. However, the initiating cause, the necrotic pulp, remains, so a chronic abscess flares up intermittently or continues with a persistent discharge.

The pain of dental caries is usually well localised and recognised as a ‘toothache’. Dental pain is sometimes poorly localised and causes non-specific facial pain. In the upper jaw, this may simulate sinusitis. Dental caries should always be considered before rarer diagnoses. Overall, a surprising amount of dental caries, even with periapical infection, is asymptomatic.

Management of dental caries

Provided the dental pulp has not been invaded by infection (i.e. become ‘exposed’), a dentist can usually drill out the carious enamel and dentine and restore it (Fig. 48.2) with synthetic resin, silver amalgam or gold, with a sedative insulating lining. Once exposed, the necrotic tissue must be removed by endodontic treatment, and the pulp cavity filled; this is ‘root filling’ (Fig. 48.2). In this way, the tooth can often be preserved.

Management of dental abscesses

A periapical abscess is the most common manifestation of caries seen by general practitioners or casualty officers. Primary treatment, as for other abscesses, is drainage of pus. Extracting the offending tooth is most effective, but better to preserve the tooth by draining the abscess via the root canal then root filling it later. Patients with periapical abscesses should ideally be referred to a dentist.

Large acute abscesses ‘pointing’ within the mouth can be drained by incising at the site of greatest fluctuation. Oral penicillin should be prescribed for spreading infection. Antibiotics have no part in managing toothache unless there is swelling or other signs of an acute abscess. A dental abscess occasionally presents on the face but usually settles with extraction of the offending tooth. Dental abscesses are rarely complicated by osteomyelitis.

Bleeding tooth socket after extraction

A small amount of blood mixed with saliva may look like severe haemorrhage. The extraction site should be inspected. A normal socket should be filled with firm clot with some ooze from the gingival margin. This is aggravated if the anxious patient disturbs the clot by rinsing or ‘exploring’ the socket with the tongue. Aspirin may also promote bleeding.

Oozing or minor bleeding is easily controlled by the patient biting on a small dry pack such as a folded gauze swab and maintaining pressure for 10–15 minutes. Persistent bleeding can usually be controlled by inserting sutures through the gingival margins across the socket (Fig. 48.3) then biting on a dry gauze pad. Suturing requires local anaesthesia infiltrated into the gingiva on each side of the socket. Absorbable polyglactin sutures are preferred as they do not leave irritating sharp ends and dissolve in 5–10 days. If bleeding continues after these simple measures, the patient should be investigated for a coagulation or platelet abnormality.

Pain after tooth extraction

Forceps extraction or surgical tooth removal may lead to pain soon afterwards. Removal of lower molar teeth may cause trismus (spasm of the muscles of mastication), making jaw movements painful and restricted. If there is no sign of infection, treatment is with analgesia, not antibiotics. Pain appearing several days after extraction is usually due to a superficial osteitis of exposed socket bone caused by failure to fill with organised clot. This condition, known as a dry socket, is intensely painful and requires dental treatment. Antibiotic therapy is not helpful.

Swelling after tooth extraction

Soft tissue swelling is uncommon after extraction, with the exception of surgically removed teeth, especially lower third molars (‘wisdom teeth’). Extraction of these often causes swelling around the angle of the mandible, with trismus and pain. This represents a normal inflammatory response plus interstitial haemorrhage rather than infection. The swelling subsides within a week or so and does not warrant antibiotic therapy.

Gingivitis and periodontitis

Teeth are embedded in bony alveolar ridges in both jaws. A thin layer of cementum (a bone-like material) on the root connects to the socket bone by a tough periodontal membrane or ligament. Oral mucosa (gingiva or gums) is bound to the alveolar bone and normally forms a tight cuff around the tooth neck, protecting alveolar bone from bacteria and trauma. The gingival crevice extends down to the cemento-enamel junction where the tough stratified oral epithelium becomes a thin vulnerable layer.

If oral hygiene is inadequate, commensal bacteria colonise the gingival margin and form a white gelatinous plaque (Fig. 48.4). If allowed to persist, plaque becomes adherent to the tooth and becomes mineralised. This is known as calculus, and cannot be removed by tooth brushing. Bacterial toxins then cause gingival inflammation or marginal gingivitis. This appears as swelling and redness of the gums and bleeding during tooth brushing.

Figure 48.5 shows gingivitis causes eversion of the gingival margin. This encourages more plaque and calculus to form and results in greater gum trauma from food, both leading to more inflammation. If untreated, inflammation extends to deeper tissues causing progressive resorption of alveolar bone and destruction of periodontal membrane, known as periodontitis. By this stage, the gingiva is thickened and inflamed with a purulent discharge. This explains the old term ‘pyorrhoea’ or flowing of pus. Despite this, the patient is remarkably pain free, although halitosis is obvious.

As periodontal inflammation progresses, more alveolar bone is destroyed and gums recede. The root surface becomes exposed to view, giving rise to the expression ‘long in the tooth’. Teeth gradually become more mobile until they fall out or can be extracted with the fingers! Periodontal disease is an insidious process commencing in early adulthood. It was once thought to be inevitable with advancing age, but is almost entirely preventable. In adults, periodontitis (not dental decay, as is commonly supposed) is responsible for most lost teeth. Inflammatory destruction of alveolar bone makes it difficult to construct satisfactory dentures for many of these patients, due to the lack of a retaining alveolar ridge.

Sometimes an acute periodontal abscess may complicate periodontitis.

Pericoronitis

This occurs when a lower third molar (wisdom tooth) is impacted against the second molar or the ramus of the mandible so that its eruption is prevented (see Fig. 48.6). If a flap (operculum) of gingiva partly overlies the impacted tooth, this creates a space around the buried tooth crown (Fig. 48.6b). Food and bacterial plaque collect and cause acute infection, which may extend outwards, even into the parapharyngeal area.

The patient complains of severe, poorly localised pain near the mandibular angle. Pain is aggravated by chewing because the opposing tooth bites on the swollen gingival flap. On examination, the pericoronal tissues of the affected tooth are red and swollen with a purulent discharge from beneath the flap. Oral examination may be difficult because of trismus. Externally, the submandibular and upper cervical lymph nodes are enlarged and tender.

Acute ulcerative gingivitis (vincent's infection)

This is an acute inflammatory condition with necrotising ulceration of the gingival margin. It is caused by a mixture of Gram-negative organisms which are normal oral commensals. The most prominent are Fusobacterium fusiformis, Borrelia vincentii and Bacteroides melaninogenicus. Acute ulcerative gingivitis most commonly occurs in young adults who ‘burn the candle at both ends’ and become run down. Poor oral hygiene, pericoronitis and smoking may contribute. Acute ulcerative gingivitis is now uncommon, but was widespread in the First World War when it gained the name ‘trench mouth’.

There is an abrupt onset of gingival pain and bleeding, accompanied by a foul, often metallic taste and marked halitosis. Cervical nodes are enlarged and tender, and there may be fever, malaise and anorexia. Oral examination reveals characteristic ragged ulceration of the gingiva, especially between the teeth. In severe cases, the pharyngeal mucosa becomes inflamed and ulcerated (Vincent's angina). Acute ulcerative gingivitis is easily distinguished from herpetic gingivo-stomatitis, as the former is confined to the gingival margin, whereas herpetic ulcers are scattered all over the oral mucosa.

Pathophysiology and aetiology

The oral cavity and tongue is invested by stratified squamous epithelium. Oral squamous cell carcinoma (SCC) accounts for about 3% of all malignancies, and is the commonest cancer on the Asian subcontinent. Like their skin counterparts, these usually occur in older people, though this trend is changing as a result of human papillomavirus-induced SCC. Men are affected twice as often as women, but in HPV cancers the ratio is more even.

Tobacco products are the more usual cause, with pipe and cigar smokers and tobacco chewers at greatest risk in the West. The tongue and lower lip are the common sites, each accounting for about 25%. Chronic irritation by ill-fitting dentures, jagged tooth restorations or alcohol abuse may contribute to the aetiology.

In India, Sri Lanka, Papua New Guinea and other countries, the habit of chewing paan, a stimulant package of betel leaf, areka nut, cured tobacco and slaked lime, causes a very high incidence of buccal carcinoma, and submucous fibrosis which results in trismus and is itself pre-malignant.

Leukoplakia is a premalignant dysplasia found in 50% of patients with oral carcinoma.

Clinical features of oral cancer

Oral cancer usually presents as a slowly enlarging chronic indurated ulcer which fails to heal (Fig. 48.7b and c). An early lesion may present as a mucosal swelling. Lesions are usually painless unless secondarily infected, although advanced lesions may cause pain as they invade deeply. Carcinoma of the tongue, for example, may cause pain referred to the ear or pharynx via the lingual nerve or chorda tympani.

Oral SCC invades locally and usually metastasises initially to submandibular and upper cervical lymph nodes. Even small tumours can cause metastases. Spreading tumours of the posterior floor of mouth and tongue interfere with speech, mastication and swallowing and are particularly distressing symptoms.

Management of oral cancer

A chronic oral ulcer which fails to heal after removing aggravating factors (such as ill-fitting dentures) should undergo urgent incision biopsy to exclude cancer.

Oral cancers are excised with at least a 1 cm margin of normal tissue. This may not be possible anatomically or cosmetically and often necessitates major reconstructive surgery. Involved lymph nodes are removed by neck dissection, aiming to preserve vital structures such as the accessory nerve and great vessels.

Some cancers, particularly tongue base and oropharynx are best managed with radiotherapy. Induction chemotherapy is often used as a single modality but is never curative. Radiotherapy is usually via external beam, and rarely with radioactive implants. A disadvantage of radiotherapy is that it damages salivary glands, resulting in xerostomia (dry mouth) which can be debilitating. Apart from discomfort, this predisposes to salivary gland infection.

Carcinoma of the lip has the best prognosis. The crude 5-year survival rate of oral cancer is around 50%, with small tumours having the best prognosis. Regional node involvement reduces the chance of cure by half.