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Biomedical subjects

C M Flaitz

Publications and source records attributed to C M Flaitz.

At least 37 records · Page 2Linked to original sources

Resin-modified glass-ionomer restorations and in vitro secondary caries formation in coronal enamel.

OBJECTIVE: The purpose of this laboratory study was to compare the effects of a resin-modified glass ionomer and a resin composite restorative material on secondary caries formation in coronal enamel. METHOD AND MATERIALS: Twelve caries-free molars were sectioned into tooth quarters. Coronal cavities were prepared and then restored with either a resin-modified glass-ionomer material (mesiobuccal and mesiolingual tooth quarters), or a resin composite (distobuccal and distolingual tooth quarters). Caries like lesions were created, and secondary caries was examined by polarized light microscopy following lesion initiation and progression periods. RESULTS: The resin-modified glass-ionomer specimens had significantly shallower primary surface lesions at both the lesion initiation (35% shallower) and progression (45% shallower) periods than did the resin composite specimens. There were significantly fewer wall lesions (3-fold and 2-fold fewer following lesion initiation and progression, respectively) in the resin-modified glass-ionomer group than in the resin composite group. CONCLUSION: Resin-modified glass-ionomer restorations reduce the susceptibility of unrestored adjacent enamel surfaces and cavosurfaces to a constant cariogenic challenge. The caries resistance imparted to the surface enamel and cavosurface is most likely due to the fluoride release from the resin-modified glass-ionomer material.

Composite Resins↗

Fluoride-releasing sealant and caries-like enamel lesion formation in vitro.

OBJECTIVE: The aim of this laboratory study was to evaluate the effects of a fluoride-releasing pit and fissure sealant (FS) and a conventional non-fluoride-containing pit and fissure sealant (CS) on caries-like lesion formation in enamel. DESIGN: Twelve extracted, macroscopically caries-free human molar teeth underwent fluoride-free prophylaxis and were sectioned into toothquarters. Cavity preparations were placed in buccal and lingual surfaces of the toothquarters, acid-etched and filled with sealant material (per the manufacturer's instructions) as follows: 1) mesiobuccal and mesiolingual quarters--FS (Fissurit-F, VocoChemie); and 2) distobuccal and distolingual quarters--CS (Fissurit, VocoChemie). Prior to caries formation in an acidified gel, the toothquarters were thermocycled (500 cycles) in artificial saliva. Sections were taken following caries initiation (6 week gel exposure) and caries progression (9 week gel exposure), and examined by polarized light microscopy to determine mean primary surface lesion depth and presence or absence of wall lesions. RESULTS: Mean surface lesion depths were significantly different between FS and CS groups following caries initiation (FS = 119 microns; CS = 157 microns, p < 0.05, paired t-test) and progression (FS = 169 microns; CS = 221 microns, p < 0.05, paired t-test). Wall lesions were reduced in FS (14% initiation; 25% progression) when compared with CS (19% initiation; 35% progression); however, this was not significantly different (p > 0.05, paired t-test). CONCLUSION: A pit and fissure sealant containing releasable fluoride provided a caries inhibiting effect with a significant reduction in lesion depth in the surface enamel adjacent to the fluoride-releasing sealant and a tendency toward reduction in the frequency of wall lesions. CLINICAL SIGNIFICANCE: Fluoride release by pit and fissure sealants may provide additional protection against caries formation in cuspal incline enamel and smooth surfaces adjacent to sealed pits and fissures, and act as a fluoride reservoir with long-term release of fluoride into the immediately adjacent oral environment.

Acid Etching, Dental↗

PD 098059, an inhibitor of ERK1 activation, attenuates the in vivo invasiveness of head and neck squamous cell carcinoma.

Increased mortality of patients with oral cancer largely reflects the local and regional spread of the disease. The invasiveness of these tumours requires hydrolases which are regulated through AP-1-dependent transcriptional mechanisms. Since the amount/activity of transcription factors bound to the AP-1 motif are regulated partly through the extracellular signal-regulated kinases (ERK1/ERK2), we determined the effect of PD 098059, an inhibitor of ERK1/ERK2 activation, on the in vivo invasiveness of a human squamous cell carcinoma cell line (UM-SCC-1) derived from the oral cavity. We utilized the floor of mouth musculature consisting of the mylohyoid, geniohyoid and genioglossus muscle (which are sequentially arranged), as a natural barrier to assess tumour spread in vivo in the nude mouse. Mice were inoculated with tumour cells superficial to the mylohyoid muscle. After 18 days, tumours were injected with either empty liposomes (control) or liposomes containing 5 microM PD 098059 and, after an additional 22 days, the jaws of mice examined histologically. Highly infiltrative tumours, which had penetrated the genioglossus muscle, were evident in 10/12 control mice. In contrast, in 9/12 mice in which the tumours were injected with PD 098059, tumours did not extend beyond the mylohyoid or geniohyoid muscles. Tumours penetrated bone nutrient canals in 7/12 control mice but in only 3/12 PD 098059-treated mice. Neurotropism, characteristic of aggressive oral squamous cell carcinoma, was evident in 6/12 control mice but was completely abolished (0/12 mice) in the PD 098059-treated mice. Using a staging system based on the muscle layer involved, neurotropism, as well as bone involvement, we found the inhibition of invasion to be statistically significant (P < 0.01). The reduced invasiveness of the PD 098059-liposome-treated oral cancers was associated with diminished 92-kDa type IV collagenase and ERK1/ERK2 activities but was not a consequence of a slower tumour growth rate. This is the first study to demonstrate reduced in vivo invasiveness of a malignancy brought about by an inhibitor of ERK1/ERK2 activation. These results raise the exciting possibility that second generation PD 098059 congeners may reduce the spread of the disease in patients afflicted with oral cancers.

1,2-Dipalmitoylphosphatidylcholine↗

The molecular epidemiology and evolution of Epstein-Barr virus: sequence variation and genetic recombination in the latent membrane protein-1 gene.

The phylogeny and evolution of Epstein-Barr virus (EBV) genetic variation are poorly understood. EBV latent membrane protein-1 (LMP-1) gene sequences are especially heterogeneous and may be useful as a tool for EBV genotype identification. Therefore, LMP-1 sequences obtained directly from EBV-infected human tissues were examined by PCR amplification and cloning. EBV genotypes were defined as "strains" from among 22 identified LMP-1 sequence patterns. Three molecular mechanisms were identified by which genetic diversity arises in the LMP-1 gene: point mutation, sequence deletion or duplication, and homologous recombination. The rate of LMP-1 gene evolution was found to be accelerated by coinfection with multiple EBV strains. The results of this study refine our understanding of LMP-1 sequence variation and enable accurate discrimination between independent EBV infection events and the consequence of intrahost EBV evolution. Thus, this LMP-1 sequence-based approach to EBV molecular epidemiology will facilitate the study of intrahost EBV infection, coinfection, and persistence.

Amino Acid Sequence↗

Combined effects of acidulated phosphate fluoride and argon laser on sound root surface morphology: an in vitro scanning electron microscopy study.

OBJECTIVE: The purpose of this in vitro scanning electron microscopy (SEM) study was to evaluate the effects of combining low fluence argon laser (AL) irradiation and acidulated phosphate fluoride (APF) treatment on the surface morphology of sound human root surfaces. SUMMARY BACKGROUND DATA: Previous in vitro investigations have shown that combined APF and AL irradiation of root surfaces provided a protective effect against cariogenic challenges. MATERIALS AND METHODS: Twelve extracted human molars were sectioned into quarters, and each quarter assigned to 1 of 4 treatment groups: (1) no treatment/control; (2) low fluence (11.5 J/cm2) AL irradiation; (3) 1.23% APF for 4 minutes; (4) APF treatment followed by low fluence AL irradiation. Surface morphology alterations were compared among groups using SEM techniques. RESULTS: AL irradiation alone produced irregular textured surfaces with adherent globular material and fine microporsities in the background. APF treatment, alternatively, only created relatively smooth surface coatings that masked the original underlying root surface. Combining APF treatment followed by AL irradiation resulted in a surface coating composed of relatively small (2 to 3 microns) spherical to avoid precipitates, morphologically resembling calcium fluoride. CONCLUSION: Combining APF with AL irradiation may create a more reactive surface that possesses fluoride-rich mineral deposits and protects the underlying root surface from cariogenic challenges.

Acidulated Phosphate Fluoride↗

An aggressive peripheral giant cell granuloma in a child.

An 11-year-old boy was evaluated for a maxillary lesion that had been increasing in size over a six-month period. Intraoral examination revealed a firm ulcerated lesion on the maxillary posterior alveolus, which was displacing teeth. The lesion was painful and easily bled during mastication. An incisional biopsy of the lesion resulted in the diagnosis of peripheral giant cell granuloma. The patient was taken to the operating room for excision of the lesion and extraction of involved teeth. The patient was followed for a period of six months with no recurrence.

Child↗

Molecular piracy: the viral link to carcinogenesis.

The vast majority of the human experience with viral infections is associated with acute symptoms, such as malaise, fever, chills, rhinitis and diarrhea. With this acute or lytic phase, the immune system mounts a response and eliminates the viral agent while acquiring antibodies to that specific viral subtype. With latent or chronic infections, the viral agent becomes incorporated into the human genome. Viral agents capable of integration into the host's genetic material are particularly dangerous and may commandeer the host's ability to regulate normal cell growth and proliferation. The oncogenic viruses may immortalize the host cell, and facilitate malignant transformation. Cell growth and proliferation may be enhanced by viral interference with tumor suppressor gene function (p53 and pRb). Viruses may act as vectors for mutated proto-oncogenes (oncogenes). Overexpression of these oncogenes in viral-infected cells interferes with normal cell function and allows unregulated cell growth and proliferation, which may lead to malignant transformation and tumour formation. Development of oral neoplasms, both benign and malignant, has been linked to several viruses. Epstein-Barr virus is associated with oral hairy leukoplakia, lymphoproliferative disease, lymphoepithelial carcinoma, B-cell lymphomas, and nasopharyngeal carcinoma. Human herpesvirus-8 has been implicated in all forms of Kaposi's sarcoma, primary effusion lymphomas, multiple myeloma, angioimmunoblastic lymphadenopathy, and Castleman's disease. Human herpesvirus-6 has been detected in lymphoproliferative disease, lymphomas, Hodgkin's disease, and oral squamous cell carcinoma. The role of human papillomavirus in benign (squamous papilloma, focal epithelial hyperplasia, condyloma acuminatum, verruca vulgaris), premalignant (oral epithelial dysplasia), and malignant (squamous cell carcinoma) neoplasms within the oral cavity is well recognized. Herpes simplex virus may participate as a cofactor in oral squamous cell carcinoma development by enhancing activation, amplification, and overexpression of pre-existing oncogenes within neoplastic tissues. Because of the integral role of viruses in malignant transformation of host cells, innovative antiviral therapy may prevent tumour development, involute neoplastic proliferations, or arrest malignant progression.

Cell Division↗