Here we provide some Oral Care Resources to you and your family from our family dentistry. Please contact us if you have questions or are in need of other dental information.
(ANSWER KEY AT BOTTOM OF QUIZ)
1. A full set of permanent teeth contain how many teeth?
A. 26, including 4 wisdom teeth
B. 30, including the 4 wisdom teeth
C. 32, including 4 wisdom teeth
2. George Washington wore false teeth made out of what materials?
A. Carved stone
3. It is generally recommended that you should brush your teeth
A. 2 times a day
B. Once a day
C. Before your dental appointment every 6 months
4. What famous person had an emerald chip put in the middle of their upper right incisor and later changed it to a diamond?
A. Michael Jackson
C. Mick Jaggar
5. It is generally recommended that you should floss your teeth how many times?
C. Immediately before your dental appointment
6. The first permanent molar usually erupts at what age:
A. 3 years olD
B. 6 years old
C. 9 years old
ANSWER KEY: 1. C 2. B 3. A 4. A 5. A 6. A
A question often asked by parents is, “what are sealants?” Sealants were not available when some of us were children. Simply put, dental sealants are a plastic covering that acts as a barrier, protecting the teeth against decay-causing bacteria. The sealants are usually applied to the chewing surfaces of the back teeth (premolars and molars) where decay occurs most often in grooves of the teeth.
Since the 1970s, in the United States, the incidence of tooth decay on the smooth surfaces of teeth has declined, in part because of fluoridation becoming widespread in public water supplies as well as improved dental hygiene among the public. However, because the teeth in the back of the mouth have numerous pits and fissures (grooves) on their biting surfaces, certain areas of these teeth are often difficult to clean even with proper brushing. To help address this, research into dental sealants began in the 1960s and by the early 1970s, the first generation of sealants became available and were approved by the Federal Drug Administration (FDA). In the history of tooth decay prevention, the two breakthroughs that stand out are fluoride and sealants. Dentists learned that balanced fluoride treatments could help defend the teeth against decay and that the application of sealants could further offer protection for the teeth. Sealants do not replace fluoride. Rather, they add to the benefits of fluoride.
Children should get sealants on their permanent molars as soon as the teeth come in. The first permanent molars (called “6 year molars”) generally erupt between the ages of 5 and 7. The second permanent molars (called “12 year molars”) generally erupt between 11 and 14 years old.
Serious tooth decay in children impact their fundamental well-being and general health. Children with unmet dental needs suffer the daily distraction of toothaches.
The application of dental sealants requires the dentist to first clean the teeth, dry them and apply a solution that is designed to help the sealant bond to the tooth surface. Then, each tooth is “painted” with a very thin layer of the sealant coating. Since the coating is tooth colored, it is not easily seen. A high-intensity curing light is used to harden the sealant after it has been painted on the teeth. Sealants can last for many years, but they should be checked regularly and assessed for possible re-application.
Most people would agree that the relatively inexpensive fees for sealants compared to restoring a decayed tooth is a good investment.
Many dental insurances cover the costs of sealants or a portion of the cost. However, be aware that insurances will often deny coverage for children over a certain age. If you have dental insurance check with your company about what they will cover and the age limit.
Resources: American Dental Association, American Journal of Public Health
By Kenneth Bueltmann, DDS; Naomi Stillman, DDS, MPH
A growing body of evidence suggests that periodontal disease (PD) is associated with a number of oral and systemic conditions of particular relevance to women, including sex-hormone-induced changes in periodontal health, adverse pregnancy outcomes, and osteoporosis. In addition, PD has been linked with diabetes mellitus (DM) and cardiovascular disease (CVD). Although PD may be accompanied by obvious signs and symptoms such as halitosis, painful periodontal abscesses, or the mobility and loss of teeth, it is often an asymptomatic, “silent” infection that goes undetected by both patient and physician. Because the systemic health outcomes associated with PD can be serious and costly, it is essential to understand the possible relationships between periodontal and systemic health, and to recognize the importance of appropriate periodontal diagnosis, referral, and treatment.
Periodontal disease is a chronic, infectious condition estimated to affect 35% of the adult US population. Research shows that nearly one in three US adults aged 30 to 54 years, and 50% of adults aged 55 to 90 years have some form of periodontitis. In males, the number increased from 34% to 56% in these age categories and from 23% to 44% in females, suggesting that periodontitis is more prevalent in males than females. It is characterized by inflammation of the supporting structures of the teeth with destruction of the periodontal ligament and alveolar bone, and is the most common cause of tooth loss in adults. For most of the twentieth century, scientists believed that PD had a nonspecific bacterial etiology that was best treated by mechanical and surgical elimination of accumulations of bacterial plaque and calculus from the crown and root surfaces of teeth. Today, PD is known to be a multifactorial disease; specific pathogenic bacteria, host defense mechanisms, and genetic and acquired risk factors all play a part in PD pathogenesis. Mechanical treatment is still the mainstay of periodontal therapy, but a more comprehensive medical approach is required to address the many contributing etiologic factors of PD.
Periodontal bacteria form a biofilm that is resistant to host defenses and to antibiotics.3 This periodontal biofilm (plaque) can release gram-negative bacteria and bacterial lipopolysaccharides (LPS) into the circulation, and/or induce production of inflammatory mediators. Among the mediators implicated in PD pathogenesis are prostaglandin E2 (PGE2), interleukin-1a (IL-1a), IL-1b, IL-6, and tumor necrosis factor-a (TNF-a). In addition, recent studies have shown that C-reactive protein (CRP), an inflammatory marker and risk predictor for CVD, is elevated in the presence of specific periodontal bacteria. Chronic inflammatory insult stemming from plaque build-up could help explain why patients with PD may be more susceptible to certain systemic conditions.
Host risk factors also influence individual susceptibility to PD. Risk factors include cigarette smoking, DM, and acquired or inborn abnormalities in neutrophil function. Genetic IL-1 polymorphisms have been strongly associated with adult periodontitis.
The existence of an association between PD and sex-hormone-associated tissue changes, adverse pregnancy outcomes, osteoporosis, DM, and CVD supports a growing recognition of the complex pathogenesis of many prevalent disorders. Common underlying pathogenic processes may account for the connections between these seemingly disparate diseases.
Changes in a woman’s hormonal milieu are reflected in her periodontal tissues throughout her life. The gingiva has specific high-affinity estrogen receptors, so elevated estrogen levels are associated with gingival edema and increased gingival crevicular fluid flow. Sex hormones may also affect host defense mechanisms against bacterial plaque; elevated androgen levels have been shown to cause a decrease in IL-6 production, thus compromising resistance to bacterial insult. Finally, hormonal fluctuations can alter the gingival bacterial microenvironment.
The Oral Cancer Foundation http://oralcancerfoundation.org/
American Dental Association http://www.ada.org/