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Pulp Calcification

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Pulp Calcification It is a localized or generalized condition of pulp 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 root canal treatment. Causes pain if it impinges on major nerves of pulp. Pulp necrosis 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 Periapical cyst Aetiology of periapical pathosis Presence of open or closed pulpitis 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 tooth. 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 (phoenix abscess). 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..
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