Periapical diseases

(Lecture)
 Sequelae Of Pulpitis

Pulpitis
Acute chronic

Apical periodontitis
Acute chronic

Periapical abscess Periapical granuloma

Acute ↔ chronic
Periapical cyst

Osteomyelitis
 Osteomyelitis
Acute Chronic

Periostitis

Cellulitis Abscess

Space infection

Intra cranial Ludwig's angina

Complications & Death

Normal Periapical tissues
 Diseases of periapical tissues

• Apical periodontitis
• Periapical abscess
• Periapical granuloma
• Periapical cyst
• Osteomyelitis
 Apical periodontitis
 Inflammation of periodontal ligament around the apical portion of tooth

 Acute / Chronic:
1) Virulence of the microorganisms.
2) Type & severity of physical or chemical irritant.
3) Host response

 Etiology –
1) Pulp necrosis 2) Occlusal trauma from high restorations or sudden biting

on hard object 3) Inadvertent endodontic procedures. eg.

Overinstrumentation
or chemical irritation from root canal medicaments.
 Apical periodontitis

 Usual history is of pulpitis.

 No response to thermal stimulus as in pulpitis.

 Collection of inflammatory edema, the tooth is slightly elevated

 Pain during mastication due to external pressure that forces the edema fluid
against the already sensitized nerve endings.
 Radiographic features:

Slight widening of PDL space.

Class I caries

Widening of PDL space

 Histopathological features:

1) PDL shows signs of inflammation. Vascular dilatation and leukocytes

infiltration.

2) Inflammation is transient if it is caused by acute trauma. If the irritant

is not removed it progresses to resorption of the surrounding bone.

3) If due to bacterial infection, abscess formation may occur and is

known as acute peri-apical abscess or alveolar abscess.
 Treatment:

1) Selective grinding if caused by occlusal trauma

2) RCT / Extraction – drain the exudate if caused by bacterial infection.

 Chronic apical periodontitis
( Periapical granuloma)

 One of the most common of all the Sequelae of pulpitis or acute apical
periodontitis.

 Acute is a exudative response whereas chronic one is proliferative.

 Localized mass of chronic granulation tissue formed in response to

infection.

 Lateral grnuloma in case of lateral or accessory root canals.

 Etiopathogenesis:

1) Pulpal / periodontal inflammation

2) Occlusal trauma

3) Orthodontic treatment

4) Endodontic treatment
 Clinical features:

1) Involved tooth is non-vital and is slightly tender to percussion. It is due to

hyperemia and inflammation of the periodontal ligament.

2) Mild pain on chewing

3) Tooth – slightly elongated.

4) Mostly asymptomatic. There is no perforation of overlying bone and oral

mucosa (Fistula) unless there is acute exacerbation of the lesion.
 Radiographic features:

1) Initial – widening of PDL space

2) As proliferation of granulation tissue and bone resorption continue, the

periapical granuloma appear as a radiolucent area of variable size and
seemingly attached to root apex.
3) Radiolucency is well-circumscribed. Sometimes zone of sclerotic bone
may be seen outlining the radiolucency, indicating a long standing lesion.

Periapical granuloma

4) Sometimes there is diffuse blending of the radioloucent area with the

surrounding bone. This is due to difference in the cellular activity around
the margins of the lesion.
Periapical granuloma

Epithelial proliferation
 Histopathological featues:

1) Begin as hyperemia and edema of the periodontal ligament with

infiltration
of chronic inflammatory cells.

2) Due to inflammation and increased vascularity, there is resorption of the

surrounding bone.

3) As the bone is resorbed, there is proliferation of fibroblasts and endothelial

cells with formation of connective tissue fibrils and vascular channels.

4) Formation of Granulation tissue consisting of fibroblasts, endothelial cells

& numerous immature blood capillaries and Chronic inflammatory cells -

macrophages, lymphocytes, plasma cells.
5) Cholesterol crystals appear as clear needle like spaces or cleft due to the
dissolving of the cholesterol by agents used in histologic preparations.

Cholesterol clefts

6) Foam cells- lipid laden macrophages.

7) Bundles of collagen fibers become condensed at the periphery to form a

capsule.

8) Presence of stratified squamous epithelium in sheets or anastomosing

cords. It originates from cell rests of Malassez.
 9) Initially the epithelium is non-proliferative. In due course of time, it
undergoes proliferation due to continuous inflammation in an attempt to
seal the apical foramen.

10) In occasional cases inflammatory cells, collection of foreign body giant

cells and ring like structures known as Rushton bodies (hyalinized

collagen) are seen. Peri-apical granuloma. This condition is termed as
giant
cell hyalin angiopathy.

11) Bacteria- streptococci, staphylococci and pneumococci.

12) Root resorption & hypercementosis like reaction.

 Treatment:

1) RCT – apicectomy

2) Extraction

3) If left untreated- transform into cyst.

Periapical
Periapical abscess
abscess
 Definition:

1) Accumulation of acute inflammatory cells at the apex of a nonvital tooth.

2) Localized collection of pus in the alveolar bone at the root apex of the
tooth following death of the pulp.

 It may develop from acute apical periodontitis or from periapical granuloma.

 Etiology:

1) Carious involvement of the tooth and pulp infection.

2) Trauma.

3) Endodontic procedures.
 Clinical features:

1) Symptoms of acute inflammation of apical periodontium.

2) In the initial stage mere tenderness of the tooth that is relieved by applying

pressure.

3) With progression, the tooth is extremely painful, sensitivity to percussion

and slightly extruded from the socket.

4) Regional lymphadenitis and fever may be present.

5) The abscess spreads along the path of least resistance.

6) Pus may extend through medullary spaces resulting in osteomyelitis or

spread through the overlying soft tissue causing cellulitis.
7) The cortical bone may be perforated in intraoral location. In such a case,
pus may reach the gum surface and present as a ‘gum boil’ / parulis.

Focal
collection of
neutrophils

8) After sinus tract formation the abscess becomes chronic and asymptomatic.
 Diagnosis:

1) History

2) Clinical examination
Early stages – difficult to locate the tooth( pain is diffuse)
Pulp testing: Offending tooth does not respond.

3) Radiographic examination: demonstrate thickening of the apical

periodontal ligament or illdefined radiolucency.

 Differential diagnosis: Periodontal abscess

 Histopathological features:

1) Central area of disintegrating leukocytes surrounded by viable leukocytes,

some lymphocytes, cellular debris, necrotic material and bacterial colonies.

Abscess formation

Focal collection of neutrophils

 Treatment:

1) Establishing drainage & controlling systemic reaction

2) Endodontic treatment

 Prognosis:-

1) Generally favorable

2) Depends on the amount of periodontal destruction

 Acute exacerbation of a
chronic abscess – (Phoenix abscess)

 Definition:
Acute inflammatory reaction superimposed on an existing chronic lesion.
 Etiology:
Sudden influx of bacteria & necrotic material into a chronic lesion.

 Symptoms:
Symptoms of acute periapical abscess.

 Diagnosis:
Long standing carious lesion (asymptomatic).
Associated with the initiation of RCT in an asymptomatic tooth.
 Radiographic view:
Well defined periradicular lesion.

 Differential diagnosis: Acute periapical abscess.

 Treatment:
Same as acute periapical abscess.