Diffuse optical localization of blood vessels and 3D printing for guiding oral surgery.

Diffuse optical imaging through centimeters of tissue has emerged as a powerful tool in biomedical research. However, applications in the operating theater have been limited in part due to data set requirements and computational burden. We present an approach that uses a small number of optical source-detector pairs that allows for the fast localization of arteries in the roof of the mouth and has the potential to reduce complications during oral surgery. The arteries are modeled as multiple-point absorbers, allowing localization of their complex shapes. The method is demonstrated using a printed tissue-simulating mouth phantom. Furthermore, we use the extracted position information to fabricate a custom surgical guide using 3D printing that could protect the arteries during surgery.

Oral Squamous Cell Carcinoma Mimicking Peri-Implantitis.

INTRODUCTION: Peri-implantitis is inflammation and alveolar bone loss around a dental implant. Published case reports have described squamous cell carcinoma (SCC) development around dental implants. CASE PRESENTATION: A 60-year-old female presented with two small fistulas on the alveolar ridge of missing tooth #18. The mucosa around the fistulas appeared normal otherwise, with no hyperplasia, erythema, or keratotic changes. The patient had a 14-year history of recurrent erythroleukoplakia (with microscopic dysplasia) on the left tongue that had been managed by surgical removal (scalpel and carbon dioxide laser), biopsies, and close follow-up. She had no other medical conditions. She reported that she had an implant placed to replace tooth #18 4 years ago that had been removed without flap reflection, curettage, or biopsy 1 year previously as a result of peri-implantitis. Periapical radiographs showed that the peri-implant radiolucency in the region of tooth #18 was unchanged in dimensions from the time of implant removal 1 year ago. Curettage and biopsy of the area were performed and showed the presence of a well-differentiated SCC. CONCLUSIONS: This is a case of peri-implant SCC development in a patient at high risk for oral SCC. The carcinoma was present within the alveolar defect in the area of a failed implant that had been removed 1 year previously. The overlying surface mucosa did not show the clinical changes typically seen in carcinoma. This case and others demonstrate the importance of periodic oral and radiographic examination after implant placement. Although rare, neoplasia must be considered in the evaluation of peri-implant pathology.

Immunosuppressants.

This paper provides a brief introduction to some of the common immunosuppressants used in oral medicine, the prevention and treatment of oral adverse effects of immunosuppressants, and considerations for dental treatment in patients taking immunosuppressants.

Alterations of neutrophil f-actin kinetics by tobacco smoke: implications for periodontal diseases.

Tobacco smoking is a major risk factor in the incidence and severity of periodontal diseases. Alterations of neutrophil function by short-term high levels of smoke during the act of smoking (acute smoke exposure) as well as long-term exposure to lower levels of tobacco substances in the bloodstream (chronic smoke exposure) may play a role in the pathogenesis of periodontal diseases in smokers. The polymerization and depolymerization of f-actin in response to infectious agents or inflammatory mediators is a critical process in a variety of neutrophil functions. In this study, we examined the effects of in vitro smoke exposure on neutrophils from smokers and non-smokers (which may be comparable to in vivo acute smoke exposure) and neutrophils from smokers not exposed to further in vitro smoke (which may be comparable to chronic smoke exposure) on f-actin kinetics. Peripheral neutrophils were isolated from seven healthy smoking subjects and seven healthy age-matched non-smoking subjects and exposed to 1-5 min of acute smoke in a smoke box system or not exposed to further smoke (baseline controls). Selected aliquots of neutrophils from control and 5-min exposures of acute smoke were then stimulated with the chemotactic peptide F-met-leu-phe at 10(-7) M for an additional 30-360 s. Cells were fixed and permeabilized, stained for f-actin with NBD phallacidin, and analyzed by flow cytometry. From baseline to 5 min of in vitro smoke exposure, there was a 38% decline in f-actin stain in non-smokers and a 30% decline in f-actin stain in smokers (p > 0.05) with f-actin values slightly higher in smokers than-non-smokers (p > 0.05). With F-met-leu-phe stimulation, both smokers and-non-smokers demonstrated a characteristic rise in f-actin stain from 0 to 120 s with a subsequent decline to baseline at 360 s and no significant differences in f-actin levels at any time of stimulation between groups. After preincubation with 5 min of in vitro smoke, the magnitude of rise in f-actin was less in both smokers and non-smokers when compared to cells not incubated with 5 min of smoke (p < 0.05 at 120 s for both smokers and non-smokers). F-actin values in smokers were higher than-non-smokers from 30 to 360 s of F-met-leu-phe exposure (p > 0.05). These results demonstrate that in vitro smoke exposure may impair normal f-actin kinetics. These alterations in f-actin kinetics may in turn affect other neutrophil functions which may impact on the pathogenesis of periodontal diseases in smokers.