On fragmenting, densely mineralised acellular protrusions into articular cartilage and their possible role in osteoarthritis.

High density mineralised protrusions (HDMP) from the tidemark mineralising front into hyaline articular cartilage (HAC) were first described in Thoroughbred racehorse fetlock joints and later in Icelandic horse hock joints. We now report them in human material. Whole femoral heads removed at operation for joint replacement or from dissection room cadavers were imaged using magnetic resonance imaging (MRI) dual echo steady state at 0.23 mm resolution, then 26-µm resolution high contrast X-ray microtomography, sectioned and embedded in polymethylmethacrylate, blocks cut and polished and re-imaged with 6-µm resolution X-ray microtomography. Tissue mineralisation density was imaged using backscattered electron SEM (BSE SEM) at 20 kV with uncoated samples. HAC histology was studied by BSE SEM after staining block faces with ammonium triiodide solution. HDMP arise via the extrusion of an unknown mineralisable matrix into clefts in HAC, a process of acellular dystrophic calcification. Their formation may be an extension of a crack self-healing mechanism found in bone and articular calcified cartilage. Mineral concentration exceeds that of articular calcified cartilage and is not uniform. It is probable that they have not been reported previously because they are removed by decalcification with standard protocols. Mineral phase morphology frequently shows the agglomeration of many fine particles into larger concretions. HDMP are surrounded by HAC, are brittle, and show fault lines within them. Dense fragments found within damaged HAC could make a significant contribution to joint destruction. At least larger HDMP can be detected with the best MRI imaging ex vivo.

Conjugated linoleic acid depresses the delta9 desaturase index and stearoyl coenzyme A desaturase enzyme activity in porcine subcutaneous adipose tissue.

Conjugated linoleic acid (CLA) has been shown to have an effect on subcutaneous fatty acid composition and has been reported to decrease stearoyl coenzyme A desaturase (SCD) activity by decreasing mRNA expression and(or) catalytic activity in rodents and rodent cell lines. This investigation was designed to study the effects of CLA, corn oil, or beef tallow supplementation on s.c. adipose tissue fatty acid composition, adiposity, SCD enzyme activity, and the delta9 desaturase index in piglets. Eighteen crossbred barrows 16 to 18 d of age were adapted to diet for 1 wk and then assigned randomly to one of three treatments: 1.5% added CLA, 1.5% added corn oil, or 1.5% added beef tallow. Barrows were penned individually and fed the supplemental oils for 35 d (to 25.6 +/- 0.6 kg BW). Subcutaneous adipose tissue samples were obtained after slaughter. Fatty acid composition of the s.c. adipose tissue differed for each fatty acid measured due to diet with the exception of 18:3. The concentrations of CLA trans-10, cis-12 and cis-9, trans-11 were elevated from nondetectable to 1.62 and 2.52 g/100 g lipid, respectively (P < 0.001 for both isomers). Conjugated linoleic acid decreased the delta9 desaturase index (P < 0.01) and SCD enzyme activity, expressed as nanomoles of palmitate converted to palmitoleate/(7 min x g of tissue) (P = 0.075) and nanomoles of palmitate converted to palmitoleate/(7 min 105 cells) (P= 0.056). Tallow-fed pigs had a greater proportion of large adipocytes (> 700 pL) and the greatest SCD activity. These data provide the first direct evidence that dietary CLA depresses SCD enzyme activity in porcine adipose tissue, which may in part be responsible for the depression of adiposity by CLA observed by others in market weight pigs.

Direct bone resorbing activity of murine myeloma cells.

The cellular mechanism(s) responsible for tumor-associated bone resorption in multiple myeloma remain uncertain. Both in vivo and in vitro evidence is presented for the direct resorption of bone by mouse plasmacytomas. Morphological examination of autopsy specimens from tumor-bearing mice revealed in vivo erosion of bony surfaces at sites of tumor cell-bone matrix apposition. No osteoclastic bone resorptive activity was evident. Using a 45Ca-labelled, devitalized bone explant assay system, mouse myeloma cells caused the release of isotope at levels from 200-300% above control values. Control cells such as normal spleen lymphocytes and liver cells did not resorb bone. Demonstration of the ability of myeloma cells to independently destroy bone is important to the understanding of the causes of and development of chemotherapeutic approaches to myelomatous bone resorption.