Infection and inflammation of the teeth and jaws

Overview

The common clinical problems in dentistry are related to infections and inflammation. The most prevalent dental diseases, dental caries and the periodontal diseases, are not included here. However, the sequelae of these diseases are frequently infection and inflammation of the bone. This chapter deals with these, along with other associated conditions of importance to the dentist.

5.1 Pulpitis

Learning objectives

You should:

• recognise the symptoms and management of acute and chronic pulpitis

• understand the pathological changes involved in pulpitis.

Pulpitis is inflammation of the pulp of a tooth and, in its acute form, is one of the most frequent emergencies facing the dentist. In general, there is a poor correlation between the patient’s clinical symptoms and the findings when the pulp is examined histologically. The division of pulpitis into the acute and chronic forms, documented below, is based predominantly on clinical symptoms. It should be remembered that the pathological processes occurring in pulpitis may be completely asymptomatic.

The pulp is infiltrated by variable numbers of chronic inflammatory cells, particularly lymphocytes and their derivatives and macrophages (Fig. 5.2). Fibrosis may occur and an acute phase with fluid and leukocyte emigration may occur. The chronic inflammatory process may spread into the periapical tissues. In internal resorption, osteoclasts line the internal surface of the dentine, which becomes scalloped in outline.

Fig. 5.2 Histopathology of chronic pulpitis as seen in a section through the pulp.

Management

Endodontic therapy or extraction of the affected tooth. Pulpectomy will, obviously, also arrest internal resorption, as any cells capable of producing resorption will have been removed.

Pathological mechanisms in acute and chronic pulpitis

Using pulpitis arising in response to caries as our example, the earliest changes in the pulp are observed beneath the carious lesion. A chronic inflammatory infiltrate is seen beneath the odontoblast layer. As the carious lesion develops and bacteria advance towards the pulp, the classic features of acute inflammation are seen with vasodilatation and the development of an inflammatory exudate. As oedema increases, the fact that the pulp is contained within a solid-walled compartment, the pulp chamber makes expansion impossible. The rise in pressure results in the collapse of the local microcirculation, leading to hypoxia and necrosis. Abscess formation may occur involving the whole or part of the pulp. In low-grade chronic pulpitis, the odontoblasts respond to irritation from the advancing carious lesion by producing reactionary dentine and this function offers some protection to the pulp.

An uncommon finding, occurring in deciduous teeth or permanent molars with open apices, is the pulp polyp. This lesion develops in grossly carious teeth where a substantial portion of the pulp has been exposed. Granulation tissue forms that protrudes into the carious cavity in the form of a red or pink (if epithelialised) fleshy polyp.

5.2 Periapical inflammation

Learning objectives

You should:

• know how to diagnose periapical inflammation

• understand the management of acute and chronic periodontitis.

A necrotic pulp, with or without the presence of infection, will provoke an inflammatory response in the periapical periodontal ligament. Diagnosis of periapical inflammation is made by interpretation of a combination of symptoms and clinical and radiological signs.

Acute periapical periodontitis

Clinical features

The classic symptom is of a dull throbbing ache, usually well localised to a heavily restored or grossly diseased tooth. It may be difficult for the patient to determine whether an upper or lower tooth is affected as the pain is experienced particularly when the teeth are occluded. However, the affected tooth is painful to touch. The tooth should be non-responsive to sensitivity tests (as the periapical inflammation is usually provoked by a dead and/or infected pulp) although, particularly with multirooted teeth, some response may still be elicited, as well as tenderness on percussion.

Acute periapical periodontitis may also occur after trauma or endodontic treatment to a tooth. In such cases, the history should lead to the diagnosis.

Radiology

The basic radiological sign accompanying acute inflammation around the apex of a tooth is localised bone destruction. Where there is little or no previous chronic inflammation, this will appear as loss of the lamina dura (Fig. 5.3). Where the periapical periodontal ligament was previously widened or a granuloma was present, acute inflammation will appear as a poorly defined radiolucency, termed a rarefying osteitis (Fig. 5.4).

Fig. 5.3 Radiograph of loss of lamina dura on the fractured central incisor.

Fig. 5.4 Radiograph of rarefying osteitis associated with the lower right central incisor.

Pathology

Acute periapical periodontitis may arise de novo or develop against a background of pre-existing chronic periapical periodontitis. In the former, the periodontal ligament is infiltrated by neutrophil leukocytes and macrophages, while in the latter, they accumulate within a periapical granuloma. In both cases, suppuration may occur, leading to the development of a periapical abscess.

Management

Endodontic therapy or extraction of the affected tooth is required. In cases of post-traumatic acute periapical periodontitis, the inflammation may resolve with splinting and time.

Chronic periapical periodontitis (periapical granuloma)

Clinical features

There may be few or no symptoms.

Radiology

The initial sign is widening of the periodontal ligament space with preservation of the radio-opaque lamina dura (Fig. 5.5). This naturally progresses with time to form a rounded periapical radiolucency with a well-defined margin – a granuloma (Fig. 5.6). Ultimately, this may undergo cystic change (radicular cyst; see Chapter 10). Differentiation between a large granuloma and a small radicular cyst is not possible on purely radiological grounds, but lesions greater than 1 cm diameter are often assumed to be cysts until histopathological diagnosis is established.

Fig. 5.5 Radiograph of widened periodontal ligament on the lateral incisor with intact lamina dura.

Fig. 5.6 Radiograph of granuloma on a central incisor.

A further radiological sign frequently seen in chronic periapical periodontitis is sclerosing (or condensing) osteitis (Fig. 5.7). This appears as a fairly diffuse radio-opacity, usually around the periphery of a widened periodontal ligament or a periapical granuloma.

Fig. 5.7 Radiograph of condensing (sclerosing) osteitis relating to the grossly carious molar.
The vertical radiolucent line is a vascular channel.

Pathology

Chronic periapical periodontitis is characterised by the formation of granulation tissue derived from the periodontal ligament, the periapical granuloma, surrounding the apex of a tooth (Fig. 5.8). Chronic inflammatory cells infiltrate the granuloma in variable numbers. Often plasma cells predominate because of multiple antigenic stimulations from pulpal infection. Foamy macrophages, cholesterol clefts often rimmed by multinucleate giant cells and deposits of haemosiderin are also frequent findings. Remnants of Hertwig’s root sheath, the cell rests of Melassez, may proliferate as a result of release of inflammatory mediators. Neutrophil infiltration within this epithelium may be one factor leading to cavitation and formation of a radicular cyst.

Fig. 5.8 Histopathological section of apical granuloma showing cholesterol clefts.

Management

Endodontic therapy or extraction of the affected tooth is required. Should the lesion persist following orthograde endodontic therapy, apicectomy should be considered (Box 5.1 and Fig. 10.12 on p. 95).

Box 5.1 Apicectomy surgical procedure

The procedure is also known as apical surgery or surgical endodontics.

1. A mucoperiosteal flap is raised (Fig. 5.9).

Fig. 5.9 Typical flap design for apicectomy.

2. Bone is removed over the buccal aspect of the tooth root in the area of the apex and associated pathology using an irrigated round surgical bur. The bone is thin and careful superficial sweeping movements are necessary to avoid removing tooth root tissue.

3. Pathological soft tissue about the root apex is removed with curettes and sent for histopathological examination.

4. At least 3 mm of the root apex should be removed using an irrigated fissure bur. The cut is made as close as possible to 90° to the long axis of the root to reduce the number of exposed dentinal tubules (Fig. 5.10).

Fig. 5.10 Apicectomy of tooth and retrograde restoration.

5. A cavity is prepared in the root end using an ultrasonically powered tip.

6. The cavity is isolated and packed with a biologically compatible material such as mineral trioxide aggregate (MTA), super EBA, intermediate restorative material (IRM), composite resin with a dentine bonding agent or reinforced zinc oxide-eugenol. Any excess material is removed and the area is irrigated to check this. Amalgam is no longer recommended.

7. The soft tissues are closed with a suture material such as vicryl.

Pathoses associated with periapical inflammation

Hypercementosis

Hypercementosis is usually identified on radiography. Affected roots of teeth become bulbous because of accretion of cementum. The cause may be unidentifiable, but it is frequently associated with teeth affected by periodontal disease or periapical inflammation (hence its inclusion here). It is also seen in Paget’s disease (Chapter 7), when multiple teeth are often affected. No treatment is indicated for hypercementosis per se, but its recognition is obviously important if extractions are planned.

External resorption

Resorption of the root surface, particularly apically, is occasionally seen on teeth with periapical inflammation, although there are a number of other known causes (e.g. trauma, iatrogenic (orthodontic), re-implanted teeth, adjacent cysts/tumours). Successful treatment of the periapical lesion by endodontic therapy often arrests the resorption.

5.3 Pericoronal inflammation

Learning objective

You should:

• be able to diagnose and manage pericoronal inflammation.

When a tooth is partially erupted, the pericoronal space is connected to the oral cavity. Accumulation of food debris and plaque, along with mechanical trauma from mastication and trauma from an opposing tooth, favour the development of infection. Lower third molars are most frequently affected. Acute and chronic pericoronitis can both occur (Fig. 5.11).

Fig. 5.11 Radiograph of hypercementosis affecting the premolar tooth.

Clinical features

Early symptoms are of pain and swelling, localised to the operculum (gum flap) overlying the crown of the tooth (Fig. 5.12). In more severe cases the patient may complain of limitation of mouth opening and facial swelling.

Fig. 5.12 Clinical photograph of pericoronitis (intraoral).

On examination, there may be extraoral swelling and lymphadenopathy. Trismus may be present. Intraoral examination will reveal a swollen, tender operculum overlying the tooth. In chronic pericoronitis, pus may be seen exuding from beneath the operculum. A frequent finding with lower third molars is evidence of trauma from an opposing, often overerupted, upper tooth. Spread of infection may occur to deeper tissues.

Radiology

Apart from the appearance of a partially erupted, possibly impacted, tooth (Chapter 6), there are few radiological signs of pericoronitis. Soft tissue swelling of the operculum may be identifiable and an overerupted opposing tooth may be more easily seen radiologically than clinically when trismus is severe. The only specific radiological signs that are seen, in longstanding chronic pericoronitis, are an enlargement of the pericoronal space and sometimes, a sclerosing osteitis in the bone immediately adjacent to the pericoronal space (Fig. 5.13).

Fig. 5.13 Radiograph showing sclerosing osteitis around the follicle of the third molar.
The patient had chronic pericoronitis.

Management

Irrigation beneath the operculum with saline or 0.2% chlorhexidine solution cleans and reduces infection. Grinding the cusps (or extraction) of any opposing tooth will prevent further trauma. Where there is lymphadenopathy or severe trismus, antibiotic therapy is usually given. Advise the patient to frequently use hot salt mouthwashes and to maintain oral hygiene as best as they can (chlorhexidine mouthwash is sometimes prescribed as an aid to hygiene when normal hygiene procedures are difficult). Review is necessary to assess the partially erupted tooth and to determine its long-term management.

5.4 Soft tissue infections of the face

Learning objectives

You should:

• know how to recognise an alveolar abscess and be able to treat it

• understand how infections can spread through the lymphatics and the tissue spaces of the face

• understand the management of infections about the face.

Infection sited at a tooth

Acute alveolar abscess

A common dental emergency facing the dentist is a patient with an acute alveolar abscess. There are a number of possible conditions that may lead to an abscess, including:

• periapical periodontitis

• periodontal disease

• pericoronitis

• infection of a cyst of the jaws.

Epidermoid (sebaceous) cysts in the facial skin may become infected and be confused with infections of dental origin, according to their site, although a punctum marking the blocked keratinous outflow may be obvious.

Clinical features

There is severe pain that is not well localised, although the affected tooth is painful to touch when the abscess follows periapical periodontitis. The tooth is non-responsive to sensitivity tests and a history of trauma to a tooth may be implicated. More commonly, the tooth is carious on examination. Without treatment, the infection spreads through bone and periosteum producing a soft fluctuant swelling, which may be present in the buccal sulcus or occasionally in the palate. As soon as the abscess spreads out of bone and into soft tissues, there is a reduction in the pain experienced.

An abscess following periodontal disease is likely to result in a mobile tooth that is tender to percussion. The tooth may remain responsive to sensitivity tests and any swelling is often nearer the gingival margin rather overlying the periapical region. Pus may exude from the gingival margin.

Trismus and cervical lymphadenopathy are signs of local spread of infection. Pyrexia and tachycardia are signs of systemic toxicity.

Radiology

While the acute abscess may be very obvious clinically, radiological signs vary enormously depending upon the pre-existing pathosis. An abscess may develop from a tooth with no previous chronic periapical lesion; here the most that may be visible is a loss of periapical lamina dura. Where a periapical granuloma or radicular cyst was present beforehand, the well-defined margin of the radiolucency tends to be lost. Such an ill-defined periapical radiolucency would be described as a rarefying osteitis.

Pathology

An abscess may be defined as a pathological cavity filled with pus and lined by a pyogenic membrane (Fig. 5.14). The latter classically consists of granulation tissue but in a rapidly expanding lesion it may simply be a rim of inflammatory cells. The soft tissue surrounding an alveolar abscess may become swollen as a result of the inflammatory exudation and reactive to bacterial products, which have diffused from the abscess.

Fig. 5.14 Histopathological section of a dental abscess showing pyogenic membrane and necrosis (lower centre of picture).

Management

The principle of treatment is to establish drainage of pus. In the case of a periapical abscess, this may be accomplished via the root canal after opening this up through the crown of the tooth with an air-rotor drill. This does not require local anaesthesia as the tooth is non-responsive to sensitivity tests, although it is important not to apply pressure to the tooth (as it may be exquisitely tender to percussion) by cutting tooth tissue slowly with a sharp bur. Alternatively, the tooth is extracted to gain adequate drainage. This may be undertaken under regional local anaesthesia, with or without conscious sedation, or using general anaesthesia.

Spread of infection to facial tissues

Lymphatic spread of infection

The lymphatic system is frequently involved in infections and gives an indication as to the pattern of spread. Enlargement and tenderness of nodes, described as lymphadenitis, is common, although inflammation of the lymphatic vessels, described as lymphangitis, may occur and can be seen as thin red streaks through the skin. The lymphatic drainage of the head and neck is described in more detail in Chapter 2.

Spread of infection through tissue spaces

In addition, to spread through the lymphatic system, infection in the soft tissues of the face also spreads along fascial and muscle planes. These potential tissue spaces usually contain loose connective tissue and can be described anatomically (Fig. 5.15).

Fig. 5.15 Potential tissue spaces about the floor of the mouth.

Floor-of-mouth tissue spaces

The mylohyoid muscle divides the sublingual and submandibular spaces, although they are continuous around its posterior free edge (Fig. 5.16). The submental space is situated below the chin and between the anterior bellies of the digastric muscles. There are no restrictions on the spread of infection between the two submandibular spaces and the submental space; consequently, it can spread across the neck below the inferior border of the mandible.