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What did McKay do?
- observed "CO brown stain" (90% fluorosis)
- consulted GV Black
- 1916: Mottled enamel: developmental imperfection
- other reports seemed geograpically localized
- McKay suspected H20
- Oakley, Idaho - new pipeline coincided w/ fluorosis (1908), 1923 McKay suggest new H2O source 10 years later no more fluorosis (still didn't know it was Floride though)
What was the initial dilemna of mottled enamel?
Hypocalcified yet not susceptible to decay
What happened in Bauxite, Arizona?
- ALCOA, Bauxite kids w/ mottled enamel, 5 miles away normal
- ALCOA chemist-> HIGH FLORIDE CONTENT (seemed normal to McKay)
What did Dean do?
- recorded prevalence and severity of mottled enamel relative to [F] in H2O
- discovered dose-response relationship
- [F] up to 1ppm, mottling isn't a concern
What did they do in Grand Rapids, MI?
1945: adjust it's water supply [F]
What are some dental controversies?
- Fluoridated H2O
- Hg in amalgam
- Bis-Phenol A in sealants
What does scientific evidence say about Floridated water?
- safe & effective
- single most effective public health measure to prevent decay
- benefits everyone espicially w/o access
What is optimal Fluoride range?
- 0.7 ppm
- ok for environment and people
- mild to very mild fluorosis, cosmetic concern
- severe and moderate is rare (well water, outside US)
What is fluorosis prevalence in 6-49 yr olds?
- less than 1/4
- prevelence in younger is higher(multiple F sources) yet still mild/very mild
What are the issues with Fluoridated Water?
- Ethics, safety, efficacy
- compulsory mass meds
- potent poison
- brain damage/ reduced IQ
- inc fracture, bone CA
- thyroid activity
- topical not systemic
What is the pathogenesis of fluorosis?
- Normal pre-eruption enamel:
- 1. protein rich, 20% mineralized, seeded w HA crystals
- 2. matrix proteins break down->replaced by Ca & PO4
- 3. Matures slowly into highly (96%) mineralized tissue via crystalization (years)
- Excess Fluoride:
- 1. slows breakdown of matrix proteins or removal of proteins by by-products
- 2. Retards crystal growth
- 3. Hypomineralized enamel (normal ameloblasts & proteins)
- 4. NO HYPOPLASTIC CHANGES (pitting occurs post-eruption)
- Porosity in outer zones of enamel
How does hypomineralized enamel resist decay?
- Post-eruption maturation: enamel takes up additional Ca & PO4 fromsaliva
- Fluoroapatite is more resistant to dissolution than HA
Why is Fluorisis brown?
exogenous (foods/porous enamel stain prior to post-eruption maturation)
What is the difference between fluorosis and white spot caries lesions?
NOT limited to areas of plaque accumulation
What is the THylstrup Fejerskov (TF) index?
ID the spectrum of mildest(TF1) to most severe(TF9) fluorosis.
What are the CDC descriptors?
- Very mild & mild: scattered white flecks, occasional white spots, frosty edges, barely noticeable
- Moderate: large white spots
- Severe: roug, pitted(brown) spots
What are some treatments for Fluorosis?
- Enamel Microabrasion
- Remineralization (CPP-ACP)
What is the enamel Microabrasion process?
- Dr. Croll
- Abrasive paste: pumice & HCL
- controlled removal of outer enamel
- Products: Opalustre (Ultradent), Prema (Practicon)
- technique: patient eye protection, rubber dam, prophy cup (low RPM), 60 sec, rinse, assess contour, repeat
- Zacatecas Mx patient
- (brighter when dehydrated)
How does demineralization affect optical properties of enamel?
less transluscent & more reflective = white spot
What is MI paste?
- Amorphous Calcium Phospate stabilized by Casein Phosphopeptides (CPP-ACP)
- drives minerals deep into white spot to regain natural coloring/optical properties
- may be used with microabrasion