Intracranial Penetration During Temporal Soft Tissue Filler Injection-Is It Possible?

BACKGROUND Treating temporal volume loss for aesthetic and reconstructive purposes can be achieved by superficial or deep injections of soft tissue fillers into the temples. The latter is performed with bone contact that can lead to intracranial penetration when the bone is accidentally penetrated. OBJECTIVE Based on a clinical case, the potential risk of accidental intracranial penetration was investigated. MATERIALS AND METHODS Twenty fresh-frozen hemi-faces (all Caucasian ethnicity, 10 women, 10 men, mean age 72.8 +/- 11.2 years) were investigated. Shape of pterion and bone-stability parameters of the temporal fossa were investigated. Bone stability was tested using uniaxial mechanical indentation (18-G, 1.25-mm diameter, 15-mm length blunt-tip device) until intracranial perforation occurred. RESULTS Variations in the shape of the pterion, bone thickness, and density correlates were detected, however, without statistical significant differences in side symmetry. Minimum force necessary to penetrate intracranially was 40.4 N. Maximum force generated by an 18-g, 70-mm length blunt-tip cannula was 32.1 +/- 4.2 N in 70 mm length and 75.3 +/- 10.2 N in 15 mm length. CONCLUSION Based on the results of this investigation, it can be concluded that there is a risk for intracranial penetration performing the deep temple injection technique with direct pressure on the bone

Bonding of articular cartilage using a combination of biochemical degradation and surface cross-linking

After trauma, articular cartilage often does not heal due to incomplete bonding of the fractured surfaces. In this study we investigated the ability of chemical cross-linkers to facilitate bonding of articular cartilage, either alone or in combination with a pre-treatment with surface-degrading agents. Articular cartilage blocks were harvested from the femoropatellar groove of bovine calves. Two cartilage blocks, either after pre-treatment or without, were assembled in a custom-designed chamber in partial apposition and subjected to cross-linking treatment. Subsequently, bonding of cartilage was measured as adhesive strength, that is, the maximum force at rupture of bonded cartilage blocks divided by the overlap area. In a first approach, bonding was investigated after treatment with cross-linking reagents only, employing glutaraldehyde, 1-ethyl-3-diaminopropyl-carbodiimide (EDC)/N-hydroxysuccinimide (NHS), genipin, or transglutaminase. Experiments were conducted with or without compression of the opposing surfaces. Compression during cross-linking strongly enhanced bonding, especially when applying EDC/NHS and glutaraldehyde. Therefore, all further experiments were performed under compressive conditions. Combinations of each of the four cross-linking agents with the degrading pre-treatments, pepsin, trypsin, and guanidine, led to distinct improvements in bonding compared to the use of cross-linkers alone. The highest values of adhesive strength were achieved employing combinations of pepsin or guanidine with EDC/NHS, and guanidine with glutaraldehyde. The release of extracellular matrix components, that is, glycosaminoglycans and total collagen, from cartilage blocks after pre-treatment was measured, but could not be directly correlated to the determined adhesive strength. Cytotoxicity was determined for all substances employed, that is, surface degrading agents and cross-linkers, using the resazurin assay. Taking the favourable cell vitality after treatment with pepsin and EDC/NHS and the cytotoxic effects of guanidine and glutaraldehyde into account, the combination of pepsin and EDC/NHS appeared to be the most advantageous treatment in this study. In conclusion, bonding of articular cartilage blocks was achieved by chemical fixation of their surface components using cross-linking reagents. Application of compressive forces and prior modulation of surface structures enhanced cartilage bonding significantly. Enzymatic treatment in combination with cross-linkers may represent a promising addition to current techniques for articular cartilage repair

VEGF-D-mediated signaling in tendon cells is involved in degenerative processes

Vascular endothelial growth factor (VEGF) signaling is crucial for a large variety of cellular processes, not only related to angiogenesis but also in nonvascular cell types. We have previously shown that controlling angiogenesis by reducing VEGF-A signaling positively affects tendon healing. We now hypothesize that VEGF signaling in non-endothelial cells may contribute to tendon pathologies. By immunohistochemistry we show that VEGFR1, VEGFR2, and VEGFR3 are expressed in murine and human tendon cells in vivo. In a rat Achilles tendon defect model we show that VEGFR1, VEGFR3, and VEGF-D expression are increased after injury. On cultured rat tendon cells we show that VEGF-D stimulates cell proliferation in a dose-dependent manner; the specific VEGFR3 inhibitor SAR131675 reduces cell proliferation and cell migration. Furthermore, activation of VEGFR2 and -3 in tendon-derived cells affects the expression of mRNAs encoding extracellular matrix and matrix remodeling proteins. Using explant model systems, we provide evidence, that VEGFR3 inhibition prevents biomechanical deterioration in rat tail tendon fascicles cultured without load and attenuates matrix damage if exposed to dynamic overload in a bioreactor system. Together, these results suggest a strong role of tendon cell VEGF signaling in mediation of degenerative processes. These findings give novel insight into tendon cell biology and may pave the way for novel treatment options for degenerative tendon diseases

Stress-relaxation curves for the two sample geometries and bonding dependence on compression

<p><b>Copyright information:</b></p><p>Taken from "Bonding of articular cartilage using a combination of biochemical degradation and surface cross-linking"</p><p>http://arthritis-research.com/content/9/3/R47</p><p>Arthritis Research & Therapy 2007;9(3):R47-R47.</p><p>Published online 15 May 2007</p><p>PMCID:PMC2206351.</p><p></p> Stress-relaxation curves for the sample geometries G1 and G2 (see Figure 1e) were determined in a standardised creep modulus set-up. Samples were compressed by a stamp and the resulting force relaxation behaviour was analysed by recording the load over time. G1 (almost no compression) or G2 (compression) cartilage blocks were subjected to different cross-linkers (without degrading pre-treatment). Adhesive strength as a measure of bonding was determined immediately after cross-linking. Bars represent the mean with standard error of the mean of at least 16 samples derived from 4 independent experiments, each with at least 4 replicates per group. values in the graph are from pairwise comparisons using the Mann Whitney-U test. EDC, 1-ethyl-3-diaminopropyl-carbodiimide; NHS, N-hydroxysuccinimide

Glycosaminoglycan (GAG) release from cartilage blocks determined after treatment with surface-degrading agents

<p><b>Copyright information:</b></p><p>Taken from "Bonding of articular cartilage using a combination of biochemical degradation and surface cross-linking"</p><p>http://arthritis-research.com/content/9/3/R47</p><p>Arthritis Research & Therapy 2007;9(3):R47-R47.</p><p>Published online 15 May 2007</p><p>PMCID:PMC2206351.</p><p></p> Cartilage blocks were subjected to pre-treatment with trypsin, pepsin, or guanidine, as indicated for the bonding experiments; the samples in the control group were incubated in PBS buffer. Subsequently, the GAG content within the cartilage blocks was determined. Additionally, the amount of GAG released into the medium (per cartilage block) was measured. Nine samples were measured per group. Bars represent the mean with standard error of the mean. values are from Tukey test for pairwise comparisons. Additionally, histological cross-sections of cartilage blocks were stained for GAGs