Potential Correlation Between Statins and Pulp Chamber Calcification

Statins, such as Lipitor, Zocor, and Crestor, are a class of drugs used to lower cholesterol levels by inhibiting the enzyme HMG-CoA reductase, which plays a central role in the production of cholesterol in the liver.  255 million adults worldwide are prescribed statins to reduce the risks of cardiovascular disease and have revolutionized the treatment and prevention of this disease.

Statins have multiple systemic effects including anti-inflammation, the induction of angiogenesis, and the improvement of vascular endothelial cell function.  They also enhance osteoblast function and suppress osetoclastic function resulting in enhanced bone formation.

As with most drugs, statins have side effects which adversely affect the muscular system and elevate liver enzymes in some recipients.  Recent evidence in the dental literature has shown compelling evidence that statins affect odotontoblast differentiation and dentin formation.  In the adult tooth this may lead to increased calcification of the pulp.

Khan et al, JOE 39:9, tested the hypothesis that the systemic administration of statins would result in increased dental pulp calcification.  This retrospective study looked at 45 subjects over the age of 60, on systemic statins.  The included mandibular molar teeth had no caries or large restorations and high quality posterior BW radiographs.  Subjects with a history of bruxing and clenching were excluded.  An equal number of matched subjects not on systemic statins but otherwise identical, were used as controls.  Volumetric analysis was done of the available pulp chamber in both mesio-distal and apical-coronal dimensions.

Khan et al found that there was a significant reduction in the vertical dimension of the pulp chamber in the mandibular molars studied.  In the test group the pulp chamber was reduced by 40% when compared to controls.  There was no difference in the mesial-distal dimension.

There are many etiologies for pulpal calcification.  Bruxing/clenching, large restorations, pulp capping, and trauma are the main culprits while there is an overall increase in in calcification seen with age in general.  Other authors have found increased pulpal calcifications in patients diagnosed with atherosclerosis.

Pulpal calcifications are of importance to the dental practioner.  Histologic evaluation of calcified pulps show dystrophic changes in the pulp tissues with decreased cellular and extracellular components and increased inflammatory cell infiltrates.  The pulp is unique in that the connective tissue is surrounded by the unyielding walls of dentin.  When the pulp receives an insult inflammatory changes occur.  This starts with capillary leakage and movement of both inflammatory cells and fluid from the vascular system into the pulp space.  In non-pulpal connective tissue this leads to swelling of the tissue.  In the pulp, with its rigid dentin walls, the result is a rapid increase in tissue pressure.  This increased tissue pressure collapses the thin walled venules draining the pulp and pulpal circulation comes to a halt.  Hypoxia and cell death follows quickly.

Pulpal calcifications make endodontic treatment more difficult.  Calcifications make it challenging to find the entrance to canals, especially minor canals such as MB2 and lingual canals of lower anterior teeth.  Calcifications also reduce the existing canal dimensions restricting access with path finding instruments and canal shapers to the all-important apical third of the tooth.  In addition the anti-inflammatory aspect of the statins may also mask or reduce pulpal necrosis symptoms in teeth which are severely calcified making diagnosis and treatment planning decisions more challenging.

Overall, the degree of calcification of the root canal system and the ensuing increased complexity of treatment are important factors to be considered in the dentist’s ability to obtain a successful endodontic result.

 

http://gallery.mailchimp.com/09e291e6ff4a6a6bef524fee7/images/de61220c-c048-45ab-8e68-b71a3477cd12.jpgABOUT THE AUTHOR: DR. HOWARD BITTNER, DMD, CAGS

Dr. Bittner was born and raised in the Surrey/Langley area. Following his pre-dental training at Simon Fraser University, he received his Doctor of Dental Medicine from the University of British Columbia in 1982 and his Certificate in Advanced Graduate Studies in Endodontics from Boston University’s Goldman School of Dental Medicine in 1995.

Dr. Bittner was in private practice in general dentistry for 11 years in Langley prior to his Endodontic specialty training. He has been practicing the Dental Specialty of Endodontics since 1995.

In his free time, Dr. Bittner loves to participate in a variety of sports including most recent, golfing! He also enjoys being a new grandfather, which if you ask him is just the best!

On August 25, 2014, posted in: News for Doctors by