Research Projects

1.

Dental Erosion in Swimmers

What is Dental Erosion?

                      

 

Dental erosion is defined as the loss of tooth substance by a chemical process that does not include bacteria. It is an irreversible damage.

Objective: To show correlation between frequency in swimming in chlorinated pools and  dental erosion.

The purpose of this research is to bring awareness to dental professionals and the general public of low pH chlorinated pool water and its correlation to dental erosion.

What does dental erosion cause?

  • Tooth sensitivity
  • Reduced thickness of enamel,which can cause fractures
  • Change in texture, shape andappearance of teeth
  • Translucency

 

What helps acid levels neutralize?

Saliva helps to neutralize acidity, it is a slow process but will slowly harden enamel. However, because the tooth’s recovery is slow, if acid attacks happen frequently, the tooth enamel does not have the chance to repair

.

This chart shows other factors that contribute to dental erosion.

The research shows that pH levels are not well controlled in chlorinated pool waters. The general population is not aware until after erosion has advanced. The required pH level range is from 7.2- 7.8. The lower the pH number, the more acidic and the more harmful it is to your tooth enamel. The frequency of time spent in a swimming pool contributes to amount of erosion seen. Anything below a pH level of 5.5 causes tooth decay.

2.

Drug Related Gingival Hyperplasia

Drug related gingival hyperplasia is an abnormal growth and enlargement of the gingiva due to an adverse reaction of the drug a patient is taking. Patients that are taking anticonvulsants, calcium channel blockers, and immunosuppressant’s may experience gingival hyperplasia while taking some of the medications prescribed under these categories. Drugs that have been found to induce gingival hyperplasia are Phenytoin, Cyclosporine, Nifedipine. While not all people taking some of these medications will experience gingival hyperplasia, patients with pre-existing plaque and inflammation tend to be more at risk. The enlargement of the gingiva is throughout the entire mouth, but is more severe in the anterior regions.
Gingival enlargement generally is clinically seen 1-3 months after the patient has been taking the medication. The gingival growth is progressive, starting with the interdental papilla and gradually spreading to the facial and lingual margins. If left unattended to and untreated the gingiva may become so enlarged that it covers the crown of the tooth. Plaque control becomes extremely difficult to control in the presence of gingival hyperplasia, which can initiate a secondary inflammatory response. This secondary inflammatory response adds to the size of the enlarged gingiva, produces a discoloration, and increases bleeding. Drug related gingival hyperplasia does not only involve the epithelial tissue; it is actually a response of the connective tissue. A histopathology of the lesion shows an excessive accumulation of extracellular matrix proteins and collagen, as well as an increased number in fibroblasts.
As of now the full etiology of drug induced gingival hyperplasia is unknown and multifactorial. The three major drug groups that have been found to cause gingival hyperplasia all have a similar mechanism of action on the effects on the intracellular calcium ion influx. They inhibit the calcium ion influx causing an inflammatory response on the gingival connective tissue. Patients taking these drugs with pre-existing plaque and pre-existing inflammation exacerbate the drug induced gingival hyperplasia. The presence of dental plaque has been found to provide a reservoir for the accumulation of cyclosporine and phenytoin. There has been no age, sex, or race predilection linked to drug induced gingival hyperplasia.
A thorough medical and dental history evaluation is needed to properly diagnose drug induced gingival hyperplasia. Differential diagnosis of drug induced gingival hyperplasia include inflammatory enlargement, idiopathic gingival enlargement, systemic diseases causing gingival enlargement, neoplastic gingival enlargement, and false enlargement. Inflammatory enlargement can be due to the onset inflammatory response of an abscess. Idiopathic gingival enlargement can be due to pregnancy gingivitis or puberty gingivitis. Systemic diseases such as leukemia and tuberculosis can cause gingival enlargement. Neoplastic gingival enlargements can be caused by underlying tumors and tend to be hard on the gingival surface. False enlargements are not true enlargements of the gingival tissue, but are a result of the underlying osseous and dental tissues. Patients with drug induced gingival hyperplasia may have a different clinical appearance from one another depending on the drug being taken. Patients taking anticonvulsants show a uniformed enlargement of the gingiva without lobulations of the interdental papilla. Immunosuppressed patients taking cyclosporine exhibit larger lobulations of the interdental papilla, which have been linked to the presence of Candida hyphae in the gingival tissue.
The main goal for patients that suffer from drug induced gingival hyperplasia is to reduce the inflammatory response. Treatment for this type of gingival hyperplasia is to first take effective oral hygiene measures. Meticulous oral hygiene care is needed from patients with there at home care and a three-month professional cleaning are recommended. If possible, the patient should consider discontinuing or switching medications with confirmation from their physician. Chlorhexidine 12% mouthwash is also recommended to help with the inflammation. For persistent gingival enlargement, after all other efforts have failed, surgery is recommended. This surgery can include a gingivectomy, periodontal flap surgery, electro surgery, and laser excision. This is done on a case-by-case basis and there are many things that have to be taken under consideration. There is a high chance of recurrence after surgery as early as 3-6 months. Chlorhexidine 12% mouthwash is prescribed which may help the degree at which the recurrence occurs. Fitted night guards may be worn at night to also assist in the degree of recurrence.
The prevalence and severity of drug induced gingival hyperplasia is a widespread unwanted adverse effect of systemic medications on the periodontal tissues. Drug induced gingival hyperplasia effects 15-50% of patients taking these medications. The etiology of this gingival hyperplasia is unknown making it difficult to manage and treat. Identifying risk factors involved in drug induced gingival hyperplasia is the best way to manage patients suffering from this adverse effect of the medications they are taking. Meticulous home care routines and frequent dental hygiene cleanings are the most effective way to manage drug induced gingival hyperplasia. It is important for the dental hygienist to be aware of the clinical appearance and symptoms of drug induced gingival hyperplasia. Having knowledge of this will help with providing the patient with optimum oral health care.

REFRENCES

Mavrogiannis M1, Ellis JS, Thomason JM, Seymour RA. The management of drug- induced gingival overgrowth. J Clin Periodontol. 2006 Jun;33(6):434-9.

Dongari-Bagtzoglou A. Drug-associated gingival enlargement.
Research, Science and Therapy Committee, American Academy of Periodontology. J Periodontol. 2004 Oct;75(10):1424-31

Bhardwaj Amit, & Bhardwaj Verma Shalu. GINGIVAL ENLARGEMENT INDUCED BY ANTICONVULSANTS, CALCIUM CHANNEL BLOCKERS AND IMMUNOSUPPRESSANTS: A REVIEW. International Research Journal of Pharmacy, (2012); 3(7), 116-119.

Guggenheimer, James. “Oral Manifestations of Drug Therapy.” Dental Clinics of North America 46.4 (2002): 857-68. Web.

Lina M Mejia, DDS, MPH; Chief Editor: William D James, MD. Drug-Induced Gingival Hyperplasia. Updated: Sep 29, 2014
http://emedicine.medscape.com/article/1076264