Infection and inflammation of the teeth and jaws
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.
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.
Severe, sharp pain or throbbing pain is usually of several minutes (10–15) duration. The pain is poorly localised and often radiates away from the site of origin, but it only crosses the midline when anterior teeth are involved. The pain is precipitated particularly by heat, but also sometimes by cold and sweet stimuli. The symptoms are often relieved by analgesics.
The pulp may show only hyperaemia but may show both fluid and leukocyte emigration in more severe disease. A coronal pulp abscess may form. Sometimes acute pulpitis is superimposed on longstanding chronic pulpitis. Microbial factors are important in this respect.
Clinical management depends on whether the pulpitis is deemed to be reversible or irreversible. This distinction encompasses a consideration of symptoms, findings on examination and the results of sensitivity testing and radiographic examination. For example, in some cases, removal of caries may bring about resolution of symptoms, while in others, endodontic therapy or extraction of the affected tooth may be the most appropriate treatment.
There are no radiological signs associated with chronic pulpitis per se apart from the detection of the cause, most commonly caries. However, an uncommon finding is internal resorption. This typically appears as a localised enlargement of the pulp chamber or root canal (Fig. 5.1).
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.
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.
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.
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.
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).
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.
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.
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.
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.
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).
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.
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.
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).
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.
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.
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.
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.
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.
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.
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.
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).
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.
Fig. 5.16 Inferior view of the floor of the mouth.
Buccal spaces: These are located in the cheek on the lateral side of buccinator muscle. Submasseteric tissue spaces lie between the masseter muscle and the ramus of the mandible. The pterygomandibular spaces lie between the medial surface of the mandible and the medial pterygoid muscle (Fig. 5.17). The infratemporal space is the upper part of the pterygomandibular space and closely related to the upper molar teeth. The parotid space lies behind the ramus of the mandible and about the parotid gland.
Pharyngeal tissue spaces: Of these, the parapharyngeal spaces are the most important in terms of spread of infection from the teeth and jaws. These spaces lie lateral to the pharynx and are continuous with the retropharyngeal space, to where infection may spread. The retropharyngeal space lies behind the pharynx and in front of the prevertebral fascia. The peritonsillar space lies around the palatine tonsil between the pillars of the fauces.
The spread of periapical infection may be predicted by the relationship of the buccinator muscle attachment to the teeth. Infection from molar teeth usually spreads buccally or labially into the sulcus but may spread above the muscle into the superficial tissues of the cheek, where it can spread over a wide area with little to contain it. Infection frequently spreads to the palate from lateral incisors because of the palatal inclination of the root. Occasionally, infection may also spread palatally from a palatal root of a molar or premolar. The canine root is long and infection may spread superficially to the side of the nose rather than intraorally.