5: Infection and inflammation of the teeth and jaws

Infection and inflammation of the teeth and jaws

5.1 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.

Acute pulpitis

Chronic pulpitis


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.

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

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

Chronic periapical periodontitis (periapical granuloma)


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.

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.


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.


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).

Pathoses associated with periapical inflammation

5.3 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).

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:

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.


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.

Spread of infection to facial tissues

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).

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.

Other tissue spaces of importance

Types of facial infection

Jan 9, 2015 | Posted by in Oral and Maxillofacial Pathology | Comments Off on 5: Infection and inflammation of the teeth and jaws
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