Hypercementosis is an idiopathic, non-neoplastic condition characterized by the excessive buildup of normal cementum (calcified tissue) on the roots of one or more teeth. A thicker layer of cementum can give the tooth an enlarged appearance, which mainly occurs at the apex or apices of the tooth. Signs and symptoms
It is experienced as an uncomfortable sensation in the tooth, followed by an aching pain.It may be shown on radiographs as a radiopaque (or lighter) mass at each root apex. Cause
Can be caused by many things. A way to remember the causes is "PIG ON TAP"Local factors- 

Occlusal Trauma
Trauma
Non-functional tooth
Unopposed tooth (and impacted teeth, embedded teeth, teeth without antagonists)Systemic factors-

Idiopathic
Pituitary Gigantism
Pagets Disease
Acromegaly
Periapical granuloma
Arthritis
Calcinosis
Rheumatic feverIt may be one of the complications of Pagets disease of bone in the form of generalized hypercementosis. It may also be a compensatory mechanism in response to attrition to increase occlusal tooth height. Complications
Such deposits form bulbous enlargements on the roots and may interfere with extractions, especially if adjacent teeth become fused (concrescence). It may also result in pulpal necrosis by blocking blood supply via the apical foramen. References


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The nucleotide substitutions were discovered in the late 1990s by classical linkage analysis and are now known as p.R122H and p.N29I respectively, according to the amino acid substitution and position in the protein sequence. These mutations are rarely identified in general screens of patients with idiopathic disease and the phenotype of p.R122H and p.N29I is now well characterised with the p.A16V mutation recently characterised for the first time. There are many other rare mutations or polymorphisms of PRSS1 which remain less well understood and not all HP families have had the responsible genetic mutation identified. The mechanism by which these genetic mutations cause pancreatitis is not yet known; but is likely to be the result of increased autoactivation or reduced deactivation of trypsinogen. However, a novel mechanism has recently been identified in a p.R116C kindred. Diagnosis
Families are defined as having HP, if the phenotype is consistent with highly penetrant autosomal dominant inheritance. In simple terms, this would require two or more first degree relatives (or three or more second degree relatives) to have unexplained recurrent-acute or chronic pancreatitis in two or more generations. It is an autosomal dominant disease with penetrance that is generally accepted to be ≈80%. Management
Treatment of HP resemble that of chronic pancreatitis of other causes. Treatment focuses on enzyme and nutritional supplementation, pain management, pancreatic diabetes, and local organ complications, such as pseudocysts, bile duct or duodenal obstruction. (PMC1774562)

Prognosis
A 2009 study which followed 189 patients found no excess mortality despite the increased risk of pancreatic cancer. References


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