Stephen K. Shuman

Patterns of tooth loss in older adults with and without dementia: A retrospective study based on a Minnesota cohort

OBJECTIVES: To study tooth loss patterns in older adults with dementia.

Patterns of tooth loss in older adults with and without dementia

OBJECTIVES: To study tooth loss patterns in older adults with dementia.

Dental Caries in Older Adults in the Last Year of Life

To examine dental caries severity (measured by number of carious teeth) in older adults in the last year of life.

Predicting tooth loss for older adults with special needs.

OBJECTIVES Older Adults with Special Needs (OASN) have more oral health needs compared with healthy, independent elders. Currently, little is known about tooth loss, a key indicator of oral function loss, among OASN. Risk assessment is primarily based on clinical experience rather than scientific evidence, raising concerns for quality of care. The studys objective was to develop an evidence-based model to quantitatively predict tooth loss for OASN. METHODS Four hundred ninety-one dentate older adults, including 235 from long-term care facilities, were retrospectively recruited. Subjects were treated and brought to a state of oral health before enrollment. Medical and dental assessments were abstracted from dental records and used to predict risk of tooth loss. Tooth loss events were recorded for subjects during follow-up. Multivariate negative-binomial regression was used, starting with 27 risk factors and removing variables using Akaikes Information Criterion. Pearsons correlation was then conducted to evaluate the overall fit of the final fitted model. RESULTS The final fitted model included eight predictors. Among them, age, number of decayed/broken teeth at arrival, anticholinergic burden of medications and physical mobility were associated with risk of tooth loss in OASN (P ≤ 0.05). Internal validation indicated satisfactory fit of the final fitted model. CONCLUSION An evidence-based model with eight predictors was developed to quantitatively predict risk of tooth loss for OASN at the individual level.

Oral health and dementia: Current evidence and recommendations

AD risk for those identified with the APOE4 allele. Methods:Using an APOE knock-in mouse model, we sought to identify differences in brain biochemistry accompanying the APOE risk genotype (APOE4 mice) compared to the absence of this risk factor (APOE3 mice). Results:APOE4 mice had significantly more APOE in Tris buffered saline(TBS-) relative to TBS with triton X (TBSX)-soluble brain fractions, and a threefold higher level of brain ABCA1, compared to APOE3 mice. APOE4 mice also had impaired spatial memory and reduced dendritic spine density in the entorhinal cortex compared to APOE3 mice, as we had previously reported. These measures provided tractable, novel targets for analyzing compounds to reduce APOE-associated effects in the brain. Epidemiological studies repeatedly found non-steroidal anti-inflammatory drugs (NSAIDs) reduce AD risk, and we tested whether one such NSAID, ibuprofen, affected these newly identified APOEassociated biomarkers in mice. Two months of ibuprofen significantly shifted the distribution of APOE and ABCA1 levels to the patterns seen in APOE3 mice. Ibuprofen also rescued spatial learning deficits and dendritic spine density in 6-month-old APOE4 mice. Conclusions:These studies indicate ibuprofen significantly reduces differences in three measures between normal APOE3 and APOE4 mice, which could serve as biomarkers for increased AD risk associated with the APOE4 risk factor. We are currently investigating whether other NSAIDs have similar effects on these biomarkers of APOE4 to determine the molecular mechanism of their protective effects.

Oral cancer: to screen or not to screen?

To the Editor:-I very much enjoyed the comprehensive review by Drs. Katzman and Jackson on advances in Alzheimer’s disease.’ 1 was, however, disappointed with their treatment of the question as to whether neuroimaging was required for the diagnosis of all patients with dementia. Dr. Katzman has eloquently presented his side of the argument elsewhere,’ and to their credit, Katzman and Jackson did point out that “some geriatricians have argued that a very typical case of AD may be diagnosed without the use of scans.” Unfortunately, they do not reference this statement and so the interested reader cannot easily be directed to the appropriate literature dealing with this point of view. I and a colleague3 and others (hardly only ”some geriatrician~“)~, have argued that, as for all laboratory tests, there are specific conditions suggesting referral for neuroimaging. These include: (1) age < 60 years, (2) the use of anticoagulants and/or history of bleeding disorders, (3) recent head trauma, (4) previous history of carcinoma (from sites that metastasize to brain-eg lung, breast), (5) unexplained neurological symptoms (eg new onset headaches, seizures), (6) rapid unexplained decline (eg over 1-2 months) in cognition and/or function status, (7) ”short” duration of dementia (<2 years), (8) history of urinary incontinence and gait disorder early in the course of dementia, suggestive of NPH, (9) localizing physical signs, (1 0) ataxia. As has been pointed out; there are dangers to scanning all patients, not to speak of the costs involved. Whatever one’s position on this particular question, we believe that it is important for both sides of the issue to be exposed. Otherwise, we are dealing in a world of caveat lector.