The naevoid basal cell carcinoma syndrome (NBCCS; Gorlin's Syndrome) was first fully described by Gorlin and Goltz in 1960 and consists of the classic triad of multiple basal cell carcinomas, odontogenic keratocysts and skeletal anomalies (Gorlin & Goltz, 1960; Gorlin, 1987). Osteosclerotic foci are a rare feature of this condition (Hermann & Som, 1981; Blinder et al, 1984) and we present a case in which bone scintigraphy proved helpful in excluding presumed metastatic disease as a cause of these sclerotic lesions. A 46-year-old woman on follow-up for NBCCS complained of 2 months low back pain and sciatica in February 1990. Lumbosacral and pelvic radiographs, obtained at the time, showed multiple sclerotic foci within the pelvis (Figure 1) and lumbar vertebral bodies (Figure 2). A presumptive diagnosis of multiple metastases was made and the patient referred for further assessment.

No abstract

Introduction: Angiogenesis is thought to be important for granulation tissue formation and for the delivery oxygen and other nutrients to the healing wound bed. We examined whether angiogenesis inhibitors (AI) such as endostatin decrease neovascularization in full‐thickness wounds leading to impaired granulation tissue formation and delayed wound closure. Methods: Endostatin at tumor‐inhibiting doses (20 mg/kg/BID) was injected daily starting three days prior to surgery. Two full‐thickness wounds were created on the mouse dorsum using a novel wound healing model developed in our lab. A second experimental group had topical VEGF (10 μg/QD) applied to these wounds. Both groups were compared to PBS‐treated controls. Wounds were analyzed for closure time, granulation tissue formation, and wound vascularity using CD31. Results: Endostatin‐treatment delayed wound closure compared to control mice (17.4d ± 1.51 vs. 12.8 ± 0.89, P < 0.05), resulted in decreased granulation tissue formation at all time points (P < 0.05), and significantly reduced wound vascularity as measured by CD31+ vessel counts (P < 0.05). VEGF application to the wound bed of endostatin‐treated mice normalized wound closure despite endostatin treatment (13.8d ± 1.1 vs. 17.44d ± 1.51, P < 0.05). Conclusion: Endostatin impairs wound angiogenesis, granulation tissue formation and delays full‐thickness wound closure. Topical VEGF was able to reverse this effect and may represent a novel approach to improve wound healing in patients receiving AI. These findings may have serious implications for patients undergoing AI treatment that require surgery or who have wound healing complications. Acknowledgements: This project received no outside funding.

Intro: Pathophysiology of hypertrophic scar formation remains unclear, potentially involving mechanical strain, burns, or infection. We sought to specifically examine the role of mechanical strain in hypertrophic scars. To do so, we developed and characterized a novel murine model which uses mechanical strain to produce hypertrophic scars in mice. Methods: Paired incisions were created on C57BL6 mice (n = 20). After closure, mechanical strain was applied across one wound using a novel device; the other wound was a control. Starting at day 3, mechanical strain was increased every other day over 4 wks. Wounds were harvested each week, and examined histologically using Sirius red, DAPI, BrdU for proliferation, and caspase 3 for apoptosis. Results: Strained wounds showed features of hypertrophic scars: raised borders, loss of rete pegs and adnexal structures in the epidermis overlying scars, blood vessels that were perpendicular and fibrillary collagen that was parallel to skin surface. Features persisted beyond 6 months. Wound collagen deposition in strained wounds increased 6‐fold at 1 wk and over 12‐fold at 2–4 wks, in parallel to an increase in number of stromal cells within scar (28‐fold). This resulted in an increase in number of cells per unit area of collagen (over 42%). In all wounds, there was no significant difference in proliferation. There was a significant reduction in blood vessel (4‐fold) and fibroblast (3‐fold) apoptosis at 1–4 wks in strained wounds. Conc: Mechanical strain alone is sufficient to produce hypertrophic scars in this model that are indistinguishable from human scars. Notably, hypertrophic scars appear to result from a marked reduction in apoptosis, rather than from a significant proliferation and upregulation of cellular collagen deposition, validating previous in vitro studies.