The Journal of the American Dental Association
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J Am Dent Assoc, Vol 139, No 2, 131.
© 2008 American Dental Association

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LETTERS

Author’s response

We appreciate Dr. Shapira’s comments on our article, which raise some interesting points regarding elevated cytokines due to sleep apnea.1,2 Specifically, removing dentures at night may predispose to sleep apnea3 and thus increase cytokines. This points to a possible association between edentulism, sleep apnea, inflammation and short-term memory loss. However, we were unable to determine what role, if any, inflammation played in our findings. We simply found a relationship between the number of teeth and risk of dementia.

In fact, our most significant findings were not in the edentulous group, which comprised only 25 (17.4 percent) of the 144 subjects; instead, the highest odds ratio of dementia was found in the group with one to nine teeth when compared to the group with 17 to 28 teeth.

Although systemic inflammatory markers may increase with sleep apnea induced by denture removal, one also might make a case for chronic inflammation secondary to continued denture wear. Continuous denture wear is significantly related to prevalence of denture stomatitis.4 It has been suggested that cytokines associated with inflammatory papillary hyperplasia of the palate, a type of denture stomatitis, may be related to increased cell-cycle regulators, considered by many researchers to be markers of malignant transformation.5

Regarding the relationship between short-term memory loss and sleep apnea, a 2005 study in Neurology demonstrated a decline in memory in subjects with sleep apnea and the presence of the apolipoprotein E allele, but not in those without it.6 T h e presence of this allele, the major genetic marker for Alzheimer disease, may render people with sleep apnea more susceptible to cognitive impairment.

We agree with Dr. Shapira that the relationship between sleep apnea and edentulism warrants further study. Unfortunately, we do not have sufficient information on sleep apnea to conduct such an investigation in the Nun Study population.


   REFERENCES
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  1. Punjabi NM, Beamer BA. C-reactive protein is associated with sleep disordered breathing independent of adiposity. Sleep 2007;30(1):29–34.[Medline]

  2. Vgontazas AN, Bixler EO, Chrousos GP. Sleep apnea is a manifestation of the metabolic syndrome. Sleep Med Rev 2005;9(3):211–24.[Medline]

  3. Bucca C, Carossa S. Pivetti S, Gai V, Rolla G, Preti G. Edentulism and worsening of obstructive sleep apnoea. Lancet 1999; 353(9147):121–2.[Medline]

  4. Zissis A, Yannikakis S, Harrison A. Comparison of denture stomatitis prevalence in 2 population groups. Int J Prosthodont 2006;19(6):621–5.[Medline]

  5. Kaplan I, Vered M, Moskona D, Buchner A, Dayan D. An immunohistochemical study of p53 and PCNA in inflammatory papillary hyperplasia of the palate: a dilemma of interpretation. Oral Dis 1998;4(3):194–9.[Medline]

  6. O’Hara R, Schröder CM, Kraemer HC, et al. Nocturnal sleep apnea/hypopnea is associated with lower memory performance in APOE epsilon4 carriers. Neurology 2005; 65(4):642–4.[Abstract/Free Full Text]



Pamela Stein, DMD, Assistant Professor

Anatomy and Neurobiology, College of Medicine, University of Kentucky, Lexington



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