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4 • Control of Pain and Anxiety
Haemoglobin saturation (%)
63
c. True. Intraligamentary or periodontal ligament an-
aesthesia is most often used as a supplementary
method to conventional injection techniques. The
solution is injected slowly under high pressure using
a specially designed syringe. The technique may
cause the tooth to be tender to percussion, which is a
consideration when used for conservative dentistry
but not when removing the tooth.
d. True. Ethyl chloride is supplied as a liquid in a glass
container. It is sprayed onto the oral mucosa where it
evaporates, cooling the surface sufficiently to cause
freezing and consequent anaesthesia. This technique
has been traditionally used to anaesthetise mucosa
over an abscess prior to its incision to permit drainage. The method is technique sensitive and less popular now. Ethyl chloride is also used on cotton wool
pledgets to investigate the vitality of teeth.
e. False. Topically applied local anaesthetics such as li-
docaine produce anaesthesia of the oral mucosa to a
depth of about 2–3 mm, which is not sufficient to
prevent the pain of needle penetration through
deeper tissues during an inferior alveolar nerve block.
3. a. True. Adrenaline (epinephrine) could precipitate a
thyroid crisis in a hyperthyroid patient. However,
there is no problem in patients who are taking thyroid replacement therapy.
b. False. It is important to prevent large increases in heart
rate in patients with ischaemic heart disease as this may
precipitate cardiac ischaemic pain (i.e., angina) or a
myocardial infarction. However, adrenaline (epinephrine) in a dental cartridge of local anaesthesia is not
absolutely contraindicated. An aspirating technique
should always be used for all patients, whether they suffer from ischaemic heart disease or not, and this will
reduce the likelihood of inadvertently injecting adrenaline (epinephrine) intravenously. The maximum dose
should be limited to about three cartridges, particularly
if the heart disease is not well controlled. The patient
should be managed with as much care as possible to
ensure that they remain relaxed during the treatment.
It is sometimes sensible to sedate these patients to ensure that they do not become physiologically stressed,
although this should be undertaken in a hospital setting. Inhalational sedation is particularly useful for this
group of patients. Adrenaline (epinephrine) should be
avoided in patients with refractory arrhythmias and in
those who have had a recent myocardial infarction
when plain 4% prilocaine is recommended.
c. True. A patient who has used cocaine in the 24 hours
before receiving a dental local anaesthetic containing adrenaline (epinephrine) is at risk of greatly increased adrenergic responses. The tachycardia may
be significant enough to lead to a cardiac arrhythmia
such as ventricular tachycardia.
d. False. High doses of felypressin may result in vaso-
constriction of the coronary vessels and precipitate
ischaemic cardiac pain. The maximum dose should
be limited to about three cartridges in patients with
ischaemic heart disease.
e. False. Tricyclic antidepressants prevent the presynap-
tic reuptake of noradrenaline (norepinephrine) and
5-HT (serotonin) and work by potentiating the effects
of these neurotransmitters. Theoretically, exaggerated adrenergic effects such as hypertension could
result when patients also receive adrenaline (epinephrine) in a dental injection. However, there is no
evidence that this occurs in practice.
4. a. False. When excessive water, blood or debris are
anticipated to collect in the mouth, then it may be
advisable to protect the oropharynx with, for example,
a rubber dam or a butterfly sponge with a tie extraorally. When carrying out oral surgery such as the
removal of wisdom teeth, it is not possible to place a
barrier behind the surgical area without triggering
a pharyngeal gag reflex. Adequate high-velocity
aspiration must always be available whether or not
a physical barrier is employed.
b. False. Should reversal with flumazenil be necessary,
an initial dose of 200 mg should be administered intravenously over 15 seconds. If the desired level of consciousness is not obtained within 60 seconds, further
doses of 100 mg may be injected every minute as necessary up to a maximum total dose of 1 mg. The usual
dose required is 300–600 mg. The dose of flumazenil
should be titrated against the individual response and it
may be preferable to maintain a degree of sedation during the early postoperative period rather than bring
about complete arousal, particularly in very anxious
patients or those with coronary artery disease.
c. False. It should be remembered that because of the
nature of the affinity of oxygen for haemoglobin, the
relationship between the partial pressure of oxygen
in blood and haemoglobin saturated is represented by
a sigmoid rather than linear graph (Fig. 4.8). This
means that at the upper end of the curve, a reduction
of 2% in the oxygen saturation of haemoglobin represents a fall in the partial pressure of oxygen of
about 15%. In other words, small changes in haemoglobin saturation represent large changes in the partial pressure of oxygen. However, the partial pressure
100
97.5
75
50
25
Mixed venous
0
5.3 13.3 14
Oxygen pressure (kPa)
Fig. 4.8 The haemoglobin dissociation curve.
64
Master Dentistry
of oxygen has to fall to 10 kPa (75 mm in figure) before the amount of oxygen carried in the blood falls
noticeably. Below an oxygen saturation of 90%, the
oxygen carriage of the blood falls off drastically and
correction of the fall is required to prevent hypoxia occurring. This may be achieved by asking the patient to
take larger breaths or by lifting the chin to improve the
airway. However, should these measures fail, then one
should consider administering supplemental oxygen
or reversing the sedation. Some consider an oxygen
saturation of 94% an indication of impending clinical
hypoxia. Haemoglobin provides an effective oxygen
reserve, such that about 75% of the haemoglobin of
mixed venous blood is saturated with oxygen.
d. True. It has been suggested in some reports that all
patients sedated intravenously should have supplemental oxygen administered. While this may be helpful in
some situations, such as sedation of elderly patients for
endoscopy, it is not necessary for all dental patients, the
majority of whom are young, fit and healthy, and where
hypoxic episodes are best prevented by careful technique rather than universal oxygen administration.
e. True. Changes in cardiovascular parameters brought
about by midazolam are slight but can induce a decrease in mean arterial pressure, cardiac output,
stroke volume and systemic vascular resistance. It is
useful to have a baseline measure of systemic arterial
blood pressure with which to compare any later measurement that may be required in a sensitive patient or
in an overdose situation. It is also an important part of
the preoperative assessment. Arterial blood pressure
may be measured indirectly by using a sphygmomanometer. Semi-automatic electrical sphygmomanometers are now readily available and inexpensive. These
have a small piezocrystal, which is positioned over the
artery to detect arterial pulsations.
5. a. True. Immediately following the administration of
high concentrations of nitrous oxide, a diffusion hypoxia may occur, as both nitrogen and nitrous oxide
occupy space in the alveolar gas at the expense of oxygen. This may be harmful to those who have respiratory or cardiovascular compromise and so should be
prevented by the administration of 100% oxygen to
the patient for a few minutes following treatment.
There is no evidence that this mild hypoxia has any
clinical significance in healthy patients.
b. True. Nitrous oxide is compressed and up to four-
fifths of the contents of a full cylinder is in the liquid
state, so the valves must be elevated above the horizontal. The amount of nitrous oxide present in a cylinder can only be determined by weighing, as the gas
pressure above the level of the liquid remains constant as long as any liquid remains.
c. True. All inhalational machines must be fitted with a
fail-safe system so that, should the oxygen supply be
cut off or the oxygen cylinder become empty, the nitrous oxide alone will automatically cut out, making it
impossible to deliver nitrous oxide alone to the patient
and render them hypoxic. Machines are also designed
so that they cannot deliver less than 30% oxygen.
d. True. Recovery is normally complete within 30 min-
utes of discontinuation of nitrous oxide and patients
can then leave without an escort.
e. False. Nitrous oxide provides good analgesia, such
that the pain on injection of local anaesthesia can be
prevented completely. This is particularly useful for
children.
Single Best Answers
1. b. Seven cartridges (2.2 mL) of lidocaine is the maximum recommended dose of local anaesthetic for a
healthy adult.
2. c. This limited mouth opening is likely to have resulted
from inflammation in muscles of mastication associated
with a haematoma following an inferior alveolar nerve
block. Patients experiencing this complication need antibiotics if diagnosed early, so there would be no benefit
in this case. Explanation of the problem and reassurance is important.
3. a. Unselective NSAIDs are associated with this relatively
high likelihood of gastric erosion. Also, 10%–30% patients taking unselective NSAIDs have gastroduodenal
ulceration but clinical events are less common. For this
reason, the COX-2 NSAIDs were developed with the intention of selectively inhibiting COX-2 only and affording mucosal protection.
4. e. The central inhibition of paracetamol on CNS cyclooxygenase reduces the production of prostaglandins
and, therefore, the central sensitisation that results from
inflammation.
5. a. Morphine is the standard opioid analgesic for severe
pain after surgery and for cancer pain and neuropathic
pain that is poorly responsive to conventional analgesics.
Case Histories Answers
CASE HISTORY 1
Reasonable cooperation for dental extractions could be expected of a 14-year-old child. However, if there are four to
undertake and the patient has had little previous experience of dentistry, then the child may find it difficult to cope
with. If proceeding using local anaesthesia alone, then two
treatment appointments would be reasonable. It may be appropriate to consider the use of inhalational sedation to
ensure that undertaking this surgical treatment does not
damage the child’s confidence in dentistry. The sedation
would ensure comfort of the local anaesthetic injections,
particularly as two palatal infiltrations will be required during the course of treatment. Whether the child has sedation
or not, the issue of consent is complicated by the fact that
the parents may not attend with the child given the child’s
residency status at a school perhaps some distance from
home. It is important that the parents are informed that the
child requires the removal of four teeth, understand the
reasons for the treatment, and that they provide their permission to go ahead.
4 • Control of Pain and Anxiety
65
CASE HISTORY 2
1. Neglect of oral health and other health issues is not unexpected in a patient who has an opioid dependence. If
the patient requires multiple extractions and potential
surgical removal of some of these, and is anxious about
any sort of dental treatment, then it would be appropriate to arrange for these procedures to be undertaken at
one treatment session using GA. The patient is likely to
attend only when in pain and such a plan to remove all
unrestorable teeth will reduce suffering in the future.
Attempts should be made to educate the patient to the
advantages of oral care, and the opportunity to receive
restorative treatment should be offered.
2. The use of a sedation technique may facilitate the latter.
Intravenous induction of general anaesthesia may be
complicated by difficult venous access as may the use of
sedation using an intravenous agent. Inhalational sedation can be a good choice in this situation.
5
Infection and Inflammation
of the Teeth and Jaws
CHAPTER OUTLINE
Overview‚ 66
5.1 Pulpitis, 66
5.2 Periapical Inflammation, 67
5.3 Pericoronal Inflammation, 71
5.4 Soft Tissue Infections of the Face, 72
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.
5.5 Other Infections and
Inflammations, 75
Self-Assessment: Questions, 79
Self-Assessment: Answers, 80
Radiology
No specific features (see chronic pulpitis, later).
Pathology
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 long-standing chronic pulpitis. Microbial
factors are important in this respect.
Management
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.
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 later is based predominantly on clinical symptoms. It should be remembered
that the pathological processes occurring in pulpitis may be
completely asymptomatic.
ACUTE PULPITIS
Clinical Features
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.
66
CHRONIC PULPITIS
Clinical eatures
A dull throbbing pain arises spontaneously and lasts for
several hours. A tooth is likely to be heavily restored,
grossly carious or have a history of trauma.
Radiology
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).
Pathology
The pulp is infiltrated by variable numbers of chronic inflammatory cells, particularly lymphocytes and their derivatives and macrophages. Fibrosis may develop 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
5 • Infection and Inflammation of the Teeth and Jaws
67
A B
Fig. 5.1 Radiograph of internal resorption in a lateral incisor as shown on (A) periapical radiograph and (B) small volume CBCT examination.
the internal surface of the dentine, which becomes
scalloped in outline.
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
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.
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
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
68
Master Dentistry
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 welllocalised 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,
which may be detected radiographically. Where there is little
or no previous chronic inflammation, this will appear as loss
of the lamina dura (Fig. 5.2). 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. 5.3).
Pathology
Acute periapical periodontitis may arise de novo or develop
against a background of pre-existing chronic periapical
Fig. 5.3 Radiograph of rarefying osteitis associated with the lower
right central incisor.
periodontitis (see later). 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
(Fig. 5.4).
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.
Fig. 5.2 Radiograph of loss of lamina dura on the fractured central
incisor.
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.
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 5.4 Radiograph taken with a gutta-percha point inserted into the
buccal sinus confirms the upper left central incisor to be the source of
suppuration.
5 • Infection and Inflammation of the Teeth and Jaws
Fig. 5.6 Radiograph of granuloma on a central incisor.
69
Fig. 5.5 Radiograph of widened periodontal ligament on the lateral
incisor with intact lamina dura.
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. Chronic inflammatory cells infiltrate the granuloma in variable numbers (Fig. 5.8A). Often plasma cells
predominate because of multiple antigenic stimulations
Fig. 5.7 Radiograph of condensing (sclerosing) osteitis relating to the
grossly carious molar. The vertical radiolucent line is a vascular channel.
from pulpal infection. Foamy macrophages, cholesterol
clefts often rimmed by multinucleate giant cells, and deposits of haemosiderin are also frequent findings (Fig. 5.8B).
Apical granulomas may mature to form apical scars and
these often contain foreign material (Fig. 5.8C). Remnants
of Hertwig’s root sheath, the cell rests of Malassez 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 (Chapter 10).
Management
Endodontic therapy or extraction of the affected tooth is required. Should the lesion persist following orthograde endodontic therapy, apicectomy may be considered (Box 5.1).
70
Master Dentistry
A BA B
C
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).
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 degrees to the long axis of the root to reduce the number
of exposed dentinal tubules (Fig. 5.10).
5. A cavity is prepared in the root end using a small round bur
or, better, an ultrasonically powered tip.
6. The cavity is isolated and packed with a biologically compatible
material such as mineral trioxide aggregate, super EBA, glass
ionomer, 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.
Fig. 5.8 Histopathological appearances of apical granuloma. (A) Hyperaemic granulation tissue with chronic active inflammation, (B) cholesterol clefts
and (C) mature apical granuloma showing collagenous tissue containing
pigmented foreign material.
PATHOSES ASSOCIATED WITH PERIAPICAL INFLAMMATION
Hypercementosis
Hypercementosis is usually identified on radiography.
Affected roots of teeth become bulbous because of continuous deposition of cementum (Fig. 5.11). The stimulus
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, 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 • Infection and Inflammation of the Teeth and Jaws
71
Fig. 5.9 Typical flap design for apicectomy.
Fig. 5.10 Apicectomy of tooth and retrograde restoration.
5.3 Pericoronal Inflammation
LEARNING OBJECTIVE
You should:
• be able to diagnose and manage pericoronal
inflammation.
Fig. 5.11 Radiograph of hypercementosis affecting the premolar
tooth.
Fig. 5.12 Clinical photograph of pericoronitis (intra-oral).
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.
On examination, there may be extra-oral swelling and
lymphadenopathy. Trismus may be present. Intra-oral
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 (see later).
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. Both acute and chronic pericoronitis can occur.
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 radiographically than
72
Master Dentistry
Fig. 5.13 Radiograph showing sclerosing osteitis around the follicle of
the third molar. The patient had chronic pericoronitis.
clinically when trismus is severe. The only specific
radiological signs that are seen, in long-standing 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).
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 use frequent 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
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:
n
periapical periodontitis
n
periodontal disease
n
pericoronitis
n
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 nonresponsive to sensitivity tests and a history of trauma to
the 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. This is known clinically as a parulis. 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 than 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 preexisting 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. If a draining parulis is present, it may be possible to identify the source of
pus by introducing a gutta-percha point into the sinus
tract as far as possible and taking a periapical radiograph
(Fig 5.4).
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.
Pathology
An abscess may be defined as a pathological cavity filled
with pus and lined by a pyogenic membrane. 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.