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Periapical periodontitis
Inflammation in the periapical part of the periodontal ligament is similar to that occurring
elsewhere in the body a particular feature of inflammation in this site is that the adjacent
bone and occasionally the root apex may resorb. the periapical vascular network has a rich
collateral circulation. greatly enhancing the ability of the tissue to heal if the cause of the
inflammation is removed. This potential for complete periapical healing & is the basis of
endodontic treatment; In this respect periapical periodontitis differs from pulpitis where the
potential for healing is limited, symptoms also differ from pulpitis in that they are generally
well located by patient to a particular tooth, stimulation of the proprioceptive nerve endings
in the periodontal ligament facilitating this accurate location.

Whether the response to irritation in the periodontal ligament is principally an acute or

chronic inflammation depends on factors such as the number and virulence of any
microorganisms involved, the type and severity of any mechanical or chemical irritant. and
the resistance of the patient. While it is convenient to describe acute and chronic periapical
periodontitis as separate conditions. it must be realized that the tissue reaction to irritation is a
dynamic response. often vacillating with time between acute and chronic inflammation.

ETIOLOGY

1. pulpitis and pulp necrosis

if pulpitis is untreated bacteria, bacterial toxins, or the products of inflammation extend

down the root canal and through the apical foramina to cause periodontitis. When pulp
necrosis follows other causes for example trauma to the tooth damaging the apical vessels.
chemical substances released from the necrotic tissue may diffuse through the apex and also

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cause periodontitis. However. when apical periodontitis is accompanied by bone resorption.
bacteria are invariably present in the root canal system.

2. Trauma

Occlusal trauma. either from a high restoration or less frequently associated with bruxism
may result in periapical periodontitis. Undue pressure during orthodontic treatment. a direct
blow on a tooth insufficient to cause pulp necrosis. and biting unexpectedly on a hard body in
food may all cause minor damage to the periodontal ligament and localized inflammation.

3. Endodontic treatment

Mechanical instrumentation through the root apex during endodontic treatment as well as
chemical irritation from root-filling materials. may result in inflammation in the periapical
periodontium. Instrumentation of an infected root canal. may be followed by periapical
inflammation. due to bacterial proliferation in the root canal or bacteria being inadvertently
forced into the periapical tissues. Clinically. this may be mistaken for periodontitis caused by
mechanical or chemical irritation and may lead to incorrect treatment.

Acute periapical periodontitis

characterized by vascular dilatation. an exudate of neutrophil leucocyres. & oedema in the
periodontal ligament in space between root apex and the alveolar bone. Pain is elicited when
external pressure is applied to the tooth because the pressure is transmitted through the fluid
exudate to the sensory nerve endings. Even light touch may be sufficient to induce pain, the
tooth is elevated in its socket. Hot or cold stimulation of the tooth does not cause pain as in
pulpitis. The radiographic appearances are often normal as there is generally insufficient time
for bone resorption to occur . If radiological changes are present. they consist of slight
widening of the periodontal ligament and the lamina dura around the apex

The inflammation may be transient if it is due to acute trauma rather than infection and the
condition soon resolves. If the irritant persists the inflammation becomes chronic and may be

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associated with resorption of the surrounding bone.Suppuration may occur if there is severe
irritation and tissue necrosis associated with bacterial infection and the continued and
massive exudation of neutrophil leucocytes leading to abscess formation. Such an abscess is
called an acute periapical or alveolar abscess and. although such abscesses may develop
directly from acute apical periodonitis or because of acute exacerbation of area of chronic
inflammation

CHRONIC PERIAPICAL PERIODONTITIS (PERIAPICAL

GRANULOMA)
characterized by an inflammatory cell infiltrate rich in lymphocytes, plasma cells and
macrophages. and the production of granulation tissue. Persistence of the inflammation is
associated with resorption of the adjacent bone which is replaced by this chronically inflamed
granulation tissue to form a periapical granuloma. Deposits of cholesterol and haemosiderin
are often present and both are probably derived from the breakdown of extravasated red
blood cells. Cholesterol crystals in the granulation tissue are represented in routine histolo-
gical sections as empty needle-like spaces or clefts multinucleate foreign-body giant cells are
grouped around the cholesterol clefts . Foci of lipid-laden macrophages-foam cells-may also
be seen . Epithelial cell rests of Malassez frequently become incorporated within the
granulation tissue and the chronic inflammatory may stimulate their proliferation .
Neutrophil leucocytes in varying stages or degeneration are often seen .

Collagen fibres may become condensed around the periphery of the lesion, separating the
granulation tissue from the surrounding bone. Occasional osteoclasts may be present in areas
where bone resorption is in progress. the organisms present are anaerobes such as Prevotella
species predominate with smaller number of facultative anaerobes such as Strepwcoccus
milleri and Streptococcus sanguis Periapical granulomas tend to be asymptomatic. but may
be associated with occasional tenderness of the tooth to palpation and percussion. percussion
may produce a dull note because of the lack of resonance caused by the granulation tissue

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around the apex. Radiological examination at first shows a widening of the periodontal
ligament space around the apex and later a definite periapical radiolucency may develop. In
some instances this radiolucency is well circumscribed and clearly demarcated from the
surrounding bone by a corticated margin. while in others the border is poorly defined . the
chronic inflammatory stimulus may lead to bone apposition and the formation of a zone of
sclerosis around the lesion . Histological evidence of external resorption of the apical
cementum and dentine is frequent

Sequelae

1. The granuloma may continue to enlarge and be associated with resorption of the bone and
the root apex. the whole process being symptomless.

2. Although a granuloma is principally a chronic inflammatory lesion. acute exacerbations are

common and the patient may present with symptoms of acute periapical periodontitis.

3. Suppuration may occur in the granuloma to form an acute periapical (alveolar) abscess.
This may be evidenced clinically by the rapid onset of pain, redness, and swelling of the
adjacent soft tissues. tenderness of the affected tooth to percussion and palpation. and tooth
mobility. A chronic periapical abscess may also develop. this being a well-circumscribed area
of suppuration and tendency to enlarge or to spread .

4. Proliferation of the epithelial cell rests of Malassez associated with the inflammation may
lead to the development of inflammatory radicular cyst.

5.low-grade irritation to apical tissues may result in bone apposition (osteosclerosis) rather
than resorption . The process is clinically asymptomatic and shows as an opaque area of bone
on radiographs. In occasions. the opacity is well-circumscribed while on others it shows no
dear line of demarcation from the normal surrounding bone.

6. low-grade irritation to the apical tissues may also result in the apposition of cementum on
the adjacent root surface to produce hypercementosis

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 ACUTE PERIAPICAL ABSCESS & SPREAD OF INFLAMMATION
Aetiology and microbiology

acute periapical abscess may develop either directly from acute periapical
periodontitis or more usually from a chronic periapical granuloma . anaerobes (for example
Prevotella and Porphyromonas and anaerobic streptococci) are usually the predominant
organisms .

Routes of spread

if the cause of the abscess is not removed, for example by extraction of the tooth, endodontic
treatment or antibiotic therapy. Suppuration will continue and the abscess continues to
enlarge . It may drain through the root canal if this is open to the mouth or occasionally it
may track through he periodontal ligament to discharge into the gingival sulcus. More
commonly, the pus tends to track through the cancellous bone and eventually perforates the
cortex. Most abscesses point buccaIly as the root apices lie closer to the buccal than to the
lingual or palatal cortical plates. However the apices of the maxillary teeth. particularly
lateral incisors and the palatal roots of the molars and premolars. often track towards the
palate. Once the cortical plate is perforated the pus strips up and may result in the formation
of a subperiosteal abscess. More frequently it penetrates the periosteum after which it may
track in various directions. Although the apices of the roots of the mandibular second and
third molars lie close to the lingual cortical plate. the bone in this area is very dense and
rarely penetrated.

Possible outcomes are

1. The pus may discharge directly into the oral cavity through a sinus following local
penetration of periosteum and mucosa. This may occur with little or no pain and only a
small swelling may develop on the oral mucosa before the pus breaks through. On other
occasions the pus may accumulate beneath the mucosa and the patient may complain of a

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gumboil before a sinus develops

2. The palatal mucoperiosteum is resistant to penetration by pus& may spread under the
mucoperiosteum posteriorly to the junction of the hard and soft palate and present as a palatal
abscess

3. Abscesses in the molar region of either jaw may penetrate the buccal cortical plate above
(in the maxilla or below in the mandible) the attachments of the buccinator muscle. In such
cases acute inflammatory oedema and suppuration spread into the soft tissues of the face or
neck, This may present as a cellulitis or less frequently as a localized soft-tissue abscess .
Such an abscess may track towards the overlying skin to discharge through a sinus on the
skin surface.

4. Abscesses related to anterior maxillary teeth may perforate the labial bone above the
attachment of the levator anguli oris muscle. The infection may then pass medially and
upwards towards the inner canthus of the eye. obliterating the nasolabial fold and into the
loose connective tissue of the lower eyelid. Alternatively. the infection may pass into the
upper lip

5. Abscesses developing at the root apices of maxillary molars and premolars are very close
to the floor of the maxillary sinus and consequently may discharge into the sinus. Periapical
inflammation may account for up to 20 % of all cases of sinusitis.

6. Pus from an abscess associated with a mandibular incisor or canine may track labially and
perforate the bone below the insertion of the mentalis muscle and pass downwards to present
as a subcutaneous abscess .

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 Cellulitis

Cellulitis is a rapidly spreading inflammation of the soft tissues particularly associated with
streptococcal infections and the rapid spread is most likely related to release of large
amounts of streprokinase and hyaluronidase which are produced by most strains of
streptococci.

Clinically: there is diffuse. tense. painful swelling of the involved soft tissues usually
associated with malaise and an elevated temperature. Much of the swelling is due to
inflammarory oedema: suppuration and abscess formation occur later if treatment is
neglected or delayed. Cellulitis associated with maxillary teeth initially involves the upper
half of the face towards the eye is a potentially serious complication because of the risk of
cavernous sinus thrombosis as a result of infection involving veins at the inner canthus of the
eye which communicate with the cavernous sinus. Cellulitis associated with mandibular teeth
initially involves the lower half of the face into the submandibular and cervical tissues may
cause respiratory embarrassment called Ludwig's angina .