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Objectives: Breast lymphedema has supplanted upper extremity lymphedema as a common and debilitating sequela of breast cancer treatment, but has no objective measurement. We assessed the utility of ultrasound‐measured difference in dermal thickness between affected and unaffected breasts as a measure of breast lymphedema. We associated this measure with patient characteristics, treatment parameters, and patient‐reported impact on quality of life. Methods: We enrolled 30 invasive breast carcinoma patients treated with breast‐conserving surgery, sentinel lymph node biopsy, and radiotherapy, and 10 control patients evaluated for benign breast conditions without prior breast surgery or radiotherapy. Patient and treatment variables were ascertained from medical records and radiotherapy instruments. Impacts on quality of life were measured with a modified Disability of the Arm, Shoulder, and Hand questionnaire. We characterized breast lymphedema by calculating the difference in ultrasound‐measured dermal thickness between affected and unaffected breasts. Associations with patient characteristics, treatment, and quality of life were quantified with log‐binomial regression models. Results: Breast lymphedema was defined as a dermal thickness difference of >0.3 mm. Nineteen patients in the invasive group (63%) had breast lymphedema by this definition. We observed positive associations between ultrasound‐defined breast lymphedema and surgical factors (size of primary tumor, number of lymph nodes removed), radiotherapy factors (breast volume irradiated, receipt of radiation boost), and patient‐reported outcomes (sleep quality and overall confidence). Conclusions: Difference in dermal thickness is an easy and inexpensive measurement for quantifying breast lymphedema, and correlates with treatment parameters and patient‐reported impacts on quality of life. Access the CME test here and search by article title. [ABSTRACT FROM AUTHOR]

Purpose: This study tested the effects of phosphate treatment of titanium on bone volume fraction (BV/TV) at 30 to 60 µm from the implant surface using microcomputed tomography to analyze the mineralized tissue. Materials and Methods: Electrolytically phosphated (50/100 volts [T1/T2]) or nonphosphated 3.3- × 8-mm titanium implants (C) with sandblasted acid-etched surfaces were placed in 40 mandibular sites in five foxhounds 6 weeks after the extraction of the premolars. After 4 weeks, the animals were sacrificed, and BV/TV was analyzed using microcomputed tomography. Results: The mean BV/TV (± standard deviation) of the control implants was 31.4% ± 15.3% (range, 10.9% to 55.3%). For the T1 implants, a mean BV/TV of 38.4% ± 10.7% (range, 21.6% to 57.3%) was seen, and for T2 implants, the mean BV/TV was 40.3% ± 15.1% (range, 16.5% to 61.1%). Mean BV/TV values for the groups were not significantly different. For all groups (C, T1, and T2), there were no significant differences in BV/TV at the most coronal slices. For all groups, there was a positive slope showing more bone apposition as the slices moved from coronal to apical. The T2 group showed significantly increased mineralized tissue moving from the coronal to the apical section of the implant, compared to the control and T1 implants. Conclusion: Access to better blood supply and bone cells from the marrow spaces in the apical regions may lead to a better trabecular bone response. Increased mineralized tissue apposition may allow for accelerated loading and more predictable implant placement in sites with poor-quality bone or patients with compromised bone healing. [ABSTRACT FROM AUTHOR]

Purpose: This study evaluated the effects of phosphate coating of acid-etched titanium on the mineral apposition rate (MAR) and new bone-to-implant contact (BIC) in a canine model. Materials and Methods: Titanium implants (2.2 × 4 mm) with acid-etched surfaces that were electrolytically phosphated or not were placed in 48 mandibular sites in six foxhounds. Tetracycline and calcein dyes were administered 1 week after implant placement and 1 week before sacrifice. At 12 weeks after implant placement, the animals were sacrificed. MAR and BIC were evaluated using fluorescence microscopy. Light microscopic and histologic evaluations were performed on undecalcified sections. Results: Microscopic evaluation showed the presence of healthy osteoblasts lining bone surfaces near implants. Similar BIC was observed in phosphated and nonphosphated titanium implant sites. MAR was significantly higher around the nonphosphated titanium implant surfaces than around the phosphated titanium samples. No significant differences were found between dogs or implant sites. Conclusion: Acid-etched implants showed significantly higher MARs compared to acid-etched, phosphate-coated implants. [ABSTRACT FROM AUTHOR]

Purpose: The purpose of this study was to evaluate the effects of phosphated titanium and enamel matrix derivatives (EMD) on osteoblast function. Materials and Methods: Primary rat osteoblasts were cultured on disks of either phosphated or non phosphated titanium. In half of the samples 180 μg of EMD was immediately added. The medium was changed every 2 days for 28 days and then analyzed using transforming growth factor-β1 (TGF-β1) and interleukin-1β (IL-1β) enzyme-linked immunosorbent assays (ELISAs). Scanning electron microscopy and light microscopy were used to evaluate nodule formation and mineralization. Results: Microscopic evaluation revealed no differences in osteoblast attachment between the 4 groups. Osteoblast nodule formation was observed in all groups. In the absence of mineralizing media, nodules on the nonphosphated titanium samples showed no evidence of mineralization. All nodules on the phosphated titanium had evidence of mineralization. ELISA revealed no significant differences in IL-1β production between any of the groups. The EMD-treated osteoblasts produced significantly more TGF-β1 than non-EMD-treated cells for up to 8 days, and osteoblasts on phosphated titanium produced significantly more TGF-β1 at 8 days. Discussion and Conclusion: Osteoblast attachment appeared unaffected by surface treatment. EMD initiated early TGF-β1 production, but production decreased to control levels within 10 days. Phosphated titanium increased TGF-β1 production at 8 days and induced nodule mineralization even in the absence of mineralizing medium. [ABSTRACT FROM AUTHOR]