Biomedical subjects

T M Simon

Publications and source records attributed to T M Simon.

41 records · Page 3Linked to original sources

PubMedDate not supplied

Biologic remodeling after anterior cruciate ligament reconstruction using a collagen matrix derived from demineralized bone. An experimental study in the goat model.

A matrix of demineralized cortical bone was used to reconstruct the anterior cruciate ligament in the goat model. This graft underwent considerable site-specific remodeling and transformation from a Haversian system at time zero into a ligament-like structure at 1 year. This transformation included new bone formation filling the osseous tunnels and replacing the demineralized matrix, development of a ligament-like transition zone within the graft, and ligamentous collagen orientation with crimp in the intraarticular portion of the graft. One year after surgery, the mean anterior-posterior translation in the reconstructed stifle joints at 30 N of tibial loading was 2.1 +/- 0.4 (+/- SEM). The mean ultimate force to failure for the reconstructed ligament at 1 year was 474 +/- 146 N compared with the time-zero (initial) strength of the matrix of 73 +/- 9 N. The cellular repopulation of the graft had no associated inflammatory cells. The potential clinical significance of these findings includes 1) replacement of a collagen matrix with bone within the osseous tunnels, 2) establishment of a more physiologic fibrocartilage transition at the graft insertion site, 3) the time-zero structural properties of a collagen matrix increasing to more desired values with biologic remodeling, and 4) a sterile biologic allograft with essentially no long-term inflammatory response.

Animals↗

PubMedDate not supplied

Meniscal repair supplemented with exogenous fibrin clot and autogenous cultured marrow cells in the goat model.

This study was undertaken to evaluate the placement of fibrin clot and cultured autologous marrow cells in surgically created, full-thickness, meniscal lesions in the avascular zone in 32 female Spanish goats. The menisci were repaired with two vertically oriented sutures (N = 8), exogenous fibrin clot was placed into the meniscal defect before placement of the two sutures (N = 8), fibrin clot plus cultured adherent bone marrow cells were placed in the defect (N = 8), or the meniscal lesions were left unrepaired (N = 8). On gross and manual inspection, meniscal lesions showed some degree of healing in all animals except for the eight unrepaired lesions. All the experimental specimens had decreased tensile strength compared with the contralateral control medial menisci. Ultimate load to failure, energy absorbed to failure, and stiffness were less than 40% of the controls for all groups. Histologic sections demonstrated focal cellular areas consisting of giant cells and macrophages in the repair sites. Our observations failed to demonstrate a statistically significant enhancement of healing with the use of exogenous fibrin clot compared with vertically oriented sutures alone. The addition of cultured adherent autologous bone marrow-derived cells in conjunction with the fibrin clot did not enhance the meniscal healing.

Animals↗

PubMedDate not supplied

Cartilage substitutes: overview of basic science and treatment options.

Articular cartilage defects that are symptomatic and refractory to nonoperative treatment represent a clinical management challenge. Although there have been important advances in stimulating intrinsic repair mechanisms, cartilage regeneration, and other substitution techniques, to date none has unlocked the understanding necessary to duplicate normal articular cartilage. The objectives of treatment of cartilage lesions are to obtain pain relief, reduce effusions and inflammation, restore function, reduce disability, and postpone or alleviate the need for prosthetic replacement. As the field of articular cartilage repair continues to evolve rapidly, the most appropriate treatment option for an individual patient should be based on the pathologic characteristics of the lesion and the patient's symptoms and expectations. The orthopaedic surgeon needs to be familiar with both the existing and the newly emerging cartilage treatment techniques in order to best educate patients and meet their expectations for long-term benefits.

Animals↗

PubMedDate not supplied

IV N-acetylcysteine treatment of hematologic reactions to chrysotherapy.

Twelve patients with adverse hematologic reactions to chrysotherapy received intravenous N-acetylcysteine (IV NAC) to achieve removal and/or redistribution of gold. Urine gold excretion while on IV NAC doubled that predicted from control measurements. Treatment within 20 days of the last gold injection was associated with better recovery of hematologic parameters. No untoward reactions from IV NAC were encountered. The pathogenesis of gold induced hematologic reactions is examined from both toxic as well as immunological perspectives.

Acetylcysteine↗

PubMedDate not supplied

Effects of chrysotherapy on cell mediated immune response.

Auranofin (AF) differs significantly from gold sodium thiomalate (GSTM) in formulation, i.e., aurous gold is stabilized by dual sulfur and phosphorus ligands, hydrophobic rather than hydrophilic characteristics, and lack of ionic charge. These attributes facilitate: oral absorption of AF, plasma membrane penetration, increase in intracellular lymphocyte gold concentration; and perhaps thereby influence lymphocyte function. AF treated subjects recorded prompt and sharp declines in mitogen-induced lymphoproliferative response (LMR) greater than 80%; suppressed response to skin testing with dinitrochlorobenezene (DNCB) in 11 of 14 subjects; and blebbing of lymphocyte membranes by scanning electron microscopy. In contrast, lymphocytes from a matched group of GSTM treated subjects recorded later onset and less suppression of LMR; normal response to DNCB skin testing; and did not manifest membrane blebbing. Accordingly, the therapeutic action of AF on immune response was observed in the 16 subjects receiving 6 mg/d of an average of 45 weeks to effect primarily cell mediated rather than humoral immune response when compared with a matched group of GSTM treated patients.

Arthritis, Rheumatoid↗