PubMed · 14123729
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S FOMON, J W BELL, J LUBART, A SCHATTNER, V R SYRACUSE. 1964. VENTRAL NASAL OBSTRUCTION.. https://pubmed.ncbi.nlm.nih.gov/14123729/
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Traumatic events are a primary cause of local lesions of articular cartilage. Tissue engineered, cartilage-like structures represent an alternative to current treatment methods. The time necessary for tissue maturation and the mechanical quality of the regenerate at implantation are both critical factors for clinical success. Low-intensity pulsed ultrasound has proven to accelerate chondrogenesis in vitro. The goal of this study was to evaluate whether low-intensity pulsed ultrasound is capable of accelerating the process of cartilage maturation and increasing regenerate stability. Hyaline-like cartilage specimens were generated in vitro and subcutaneously implanted in the backs of nude mice. Twenty-eight animals received 20 min of low-intensity pulsed ultrasound treatment daily, and 28 animals received a sham treatment. Specimens were explanted after 1, 3, 6, and 12 weeks, mechanically tested with the use of an indentation test, histologically examined, and processed for RT-PCR. The Young's moduli significantly increased from 3 to 12 weeks, and at 6 weeks were comparable to those of native articular cartilage. In histological examination, specimens showed neocartilage formation. There was no significant difference between ultrasound-treated and sham-treated groups. The mechanical stability of the neocartilage specimens increased with treatment time and reached values of native cartilage after 6 weeks in vivo. Low-intensity pulsed-ultrasound stimulation showed no stimulatory effect on tissue maturation. In contrast, ultrasound-treated specimens showed a reduced Col 2 expression at 1 week and were significantly less stiff compared to native cartilage at 6 and 12 weeks. An acceleration of the maturation of tissue-engineered neocartilage in a clinical setting by means of low-intensity pulsed ultrasound therefore appears rather unrealistic.
This research demonstrates that controlled material degradation and transforming growth factor-beta1 (TGF-beta1) release can be achieved by encapsulation of TGF-beta1-loaded gelatin microparticles within the biodegradable polymer oligo(poly(ethylene glycol) fumarate) (OPF), so that these microparticles function as both a digestible porogen and a delivery vehicle. Release studies performed with non-encapsulated microparticles confirmed that at normal physiological pH, TGF-beta1 complexes with acidic gelatin, resulting in slow release rates. At pH 4.0, this complexation no longer persists, and TGF-beta1 release is enhanced. However, by encapsulating TGF-beta1-loaded microparticles in a network of OPF, release at either pH can be diffusionally controlled. For instance, after 28 days of incubation at pH 4.0, final cumulative release from non-encapsulated microparticles crosslinked in 10 and 40 mM glutaraldehyde (GA) was 75.4+/-1.6% and 76.6+/-1.1%, respectively. However, when either microparticle formulation was encapsulated in an OPF hydrogel (noted as OPF-10 mM and OPF-40 mM, respectively), these values were reduced to 44.7+/-14.6% and 47.4+/-4.7%. More interestingly, release studies, in conditions that model the expected collagenase concentration of injured cartilage, demonstrated that by altering the microparticle crosslinking extent and loading within OPF hydrogels, TGF-beta1 release, composite swelling, and polymer loss could be systematically altered. Composites encapsulating less crosslinked microparticles (OPF-10 mM) exhibited 100% release after only 18 days and were completely degraded by day 24 in collagenase-containing phosphate-buffered saline (PBS). Hydrogels encapsulating 40 mM GA microparticles did not exhibit 100% release or polymer loss until day 28. Hydrogels with no microparticle component demonstrated only 79.3+/-9.2% release and 89.2+/-3.4% polymer loss after 28 days in enzyme-containing PBS. Accordingly, these studies confirm that the rate of TGF-beta1 release and material degradation can be controlled by altering key parameters of these novel, in situ crosslinkable biomaterials, so that TGF-beta1 release and scaffold degradation may be tailored to optimize cartilage repair.