 It is a localized or generalized condition of tissue characterized by the presence of pulp stone in the pulp tissue in the form of calcified bodies.  Site: coronal or radicular dentine.  Size: variable  Sign and symptoms: painless  Radiographic features: Radio opaque mass of variable size in pulp chamber and pulp canal.

HISTOLOGICAL TYPES  True pulp stone: consist of dentinal tubules.  False pulp stones: consists of concentric calcified rings.  Free pulp stones: is freely located in pulp chamber and pulp canals.  Attached pulp stone: is adherent to dentine wall.  Embeded pulp stone: is surrounded by secondary dentine. complications  It can interferes with .  Causes pain if it impinges on major nerves of pulp.  It is an irreversible condition of pulp tissue characterized by dead pulp tissue and degeneration (necrosis). Aetiology  Severely irritant agent.

Sign and symptoms:  painfull

Duration:  10-15min, severe and short.

 Precipitating factors of pain: hot and cold agents

 Nature of pain:  Throbbing, continuous and radiating.  Pain stops as precipitating factors are removed. Periapical lesions  Periapical abscess  Periapical granuloma  Aetiology of periapical pathosis  Presence of open or closed  Virulence of involved organisms  Extent of sclerosis of detinal tubules  Competency of the host immune response. Periapical granuloma  It refers to a mass of chronically inflammed granulation tissue at the apex of a non vital .

 May arise either after an acute condition like periapial abscess becomes quiet or may arise denovo.

 Importance: These lesions are not static and may transform into periapical cyst or undergo acute excerbation. Clinical features  Mostly asymptomatic.  Pain and sensitivity developes if it undergoes acute excerbation.  No mobility or sensitivity to percussion of involved tooth.  Pulp vitality tests are negative.

Radiographic features  Lesions can be either ill/well defined.  Variable size from small to large.  Loss of apical lamina dura.  Root resorption is common.  Cannot distinguish periapical granulaoma from periapical cyst on radiograph. Histopathological features  The lesion shows inflammed granulation tissue containing dense lymphocytic infiltrate mixed with PMNL’s, plasma cells amd macrophages.  Epithelial rest of Malassez may be seen in the granulation tissue.  Cholesterol clefts may be seen along with associated multinucleated giant cells.  Areas of extavasation of RBC’s and hemosidren pigmentation are also soon in granulation tissue.

Radiclar cyst (peiapical cyst, Apical peiodontal cyst)  By definition periapical cyst arises from epithelial rest of melessez located in the periodontal ligaments as a result of inflammation.  Often, radicular cyst remains behind in the jaws often removal of infected tooth- then called residual cyst. Clinical features:  Age incidence: peak in 3rd, 4th and 5th decades of life.

 Sex incidence: slightly more in males.

 Site predilection: maxillary anterior region.

 Frequency: most common cyst of jaw. Sign and symptoms:  primarily painless

 discovered during routine x ray examination.  Slightly enlarging hard bony swelling initially. Later, if cysts breaks through cortical plates, lesions become fluctuant.  Diagnostic criteria- associated teeth are nonvital. Rare in deciduous teeth.

Radiological features  Classsically presents as round/ovoid radiolucency with sclerotic borders and associated with pulpally effected tooth/teeth.  If infection supervenes, the margins become indistinct, making it impossible to distinguish it from periapical granuloma. Differential diagnosis  Following lesions should be distinguished from other periapical radiolucencies.  Periapical granuloma  Peiapical cemento osseous dysplasia (early lesions) Pathogenesis Phases of initiation:  accepted generally that rest of malassez included within a developing periapical granuloma proliferates to form lining of radicular cyst.  How these cells are stimulated is not clear.  Some products of non vital pulp can be responsible which simultaneously evokes an inflammatory response in CT.  Immune system also seem to be responsible as numerous plasma cells are seen in periapical granulomas.

 Phase of cyst formation:  can occur in two possible ways.  One theory demonstrates that epithelium proliferates and covers the bare connective tissue surface of abscess cavity.  Another theory- cyst cavity forms with in proliferating epithelium as the cells in centre moves away from their nutrient source. Phase of enlargment:  Enlargment occurs by the accumulation of fluid within the lumen of cyst.  Osmosis plays an important role as the cyst wall appears to have the properties of semi permeable membrane. Histopathological features  Lined partly or completely by non keratinizing stratified squamous epithelium of varying thickness.  Epithelium usually shows arcading around the connective tissue.  The connective tissue wall shows inflammatory infiltrate in the form of lymphocytes and plasma cells.

 Hyline/Rushton bodies are found in epithelium and rarely in the CT wall.  These are curved or linear structure with eosinophilic properties.  Cholesterol crystals in the form of clefts are present in the CT wall inciting a foreign body giant cell reaction.  Originate from degenerating RBC’S in the presence of inflammation.  Different type of dystrophic calcifications are seen in CT wall.  Mucus cell metaplasia and respiratory cells are also seen in epithelial lining.  Keratinization if present may be due to metaplasia and must not be confused with OKC. PERIAPICAL ABSCESS  Collection of acute inflammatory cells at the apex of non vital tooth is called periapical abscess.  Acute lesions may arise as an initial pathosis or an acute exacerbation of chronic periapical pathology (). Clinical features  Initial stage – tenderness of effected tooth.  later- pain become severe and tooth become sensitive to percussion.  Extrusion of tooth in its socket.  Systemic findings-fever, malaise and chills.  Abscess may spread along the path of least resistence through medullary spaces causing osteomyellitis.  Can also perforate cortical bone and spread to soft tissues causing cellulitis.  It can also drain through sinus tract.opening of such tract is covered by a granulation tissue – parulis.  Periapical abscess can also channelize through skin and drain via cutaneous sinus.  If an abscess begins to drain it becomes symptomless due to lack of pus in cavity.

Radiographic features  In initial stages- thickening of periodontal ligament.

 Later- ill defined radiolucency. Histopathological features  Microscopic sections are not made as specimen is fluid.  Abscess contain PMN’s mixed with cellular debris and histiocytes.  Phoenix abscesses may also contain soft tissue components comprising of granulation tissue mixed with areas of abscess.