Object. Ossification of the posterior longitudinal ligament (OPLL) often progresses after surgery, and this may cause late-onset neurological deterioration. There have been few studies, however, to clarify any correlation between progression and clinical outcome, partly because of the lack of studies involving reliable and reproducible methods by which detection of progression is made possible. The authors conducted a multicenter study to investigate the occurrence of postoperative progression and to elucidate the possible risk factors in a large-scale patient population, and a novel computer-assisted measurement method was used to provide the basis for future clinical studies. Methods. The authors analyzed lateral plain radiographs obtained immediately and at 1 and 2 years after surgery in 131 patients who underwent posterior decompression at 13 institutions. The x-ray films were transformed via scanner into digital images; the length and thickness of ossifications were measured using a new computer-assisted measurement system, and the incidence of progression was determined. Odds ratios for progression according to age group and types of OPLL were determined and compared to elucidate significant risk factors of progression. Conclusions. This is the first multicenter study to investigate the incidence of OPLL progression after posterior decompression by using a standardized measurement method. The rate of postoperative progression at 2 years was 56.5%, which was comparable with results reported in other studies. Progression occurred more frequently in younger-age rather than in older-age patient populations at both 1 and 2 years postoperatively. Mixed-type and continuous-type OPLL progressed more frequently than the segmental-type lesion at 2 years. The results of the present study could serve as basis for future studies to assess the efficacy of drug therapy to prevent OPLL progression.

Structural analysis of bones is now actively studied by many researchers using the finite-element method (FEM) to better understand the mechanism of bone fractures. Most previous studies, however, only obtained distribution patterns of stress or strain, and did not show how a fracture initiates and proceeds or how a fracture line grows. The purpose of this study was to simulate a fracture procedure using FEM and to assess its usefulness. Correlation of the strain value of the simulation and of the experiment was satisfactory (r = .81). The simulated fracture process and the consequent fracture lines were quite compatible with the experimental fracture. Quantitatively, however, there was a difference of yield load between the simulation and the experiment, i.e., 2000N and 8400N, respectively, likely caused by inaccuracies of material properties of the elements of the finite-element model.

To evaluate the temporal features of physiological fluctuation in serum PTH concentration, we sampled peripheral blood at 4-min intervals for 24 h from five normal men (32.8 yr; range, 26-40 yr) and measured serum PTH levels using a two-site immunoradiometric assay with the exquisite sensitivity and specificity for human PTH-(1-84) (intact PTH). The resultant 24-h time series of serum intact PTH levels were assessed by contemporary techniques in chronophysiology for rhythmic and episodic peak detection. Cosinor analysis disclosed a significant circadian rhythm in serum intact PTH concentrations in all five men, with the mean circadian amplitude and acrophase of 7.2 +/- 4.4 ng/L and 2305 +/- 401 h, respectively (mean +/- SD; n = 5). No apparent fixed ultradian periodicity was found by autocorrelation and spectral analyses. Evaluation of episodic intact PTH pulsatility by Cluster analysis revealed 23.0 +/- 4.4 discrete PTH pulses/24 h (P less than 0.01 vs. signal-free noise), which occurred at an interpulse interval of 61.6 +/- 11.1 min. The average duration of a serum intact PTH peak was 42.8 +/- 7.3 min, and its mean incremental amplitude was 12.6 +/- 1.3 ng/L, which corresponded to a 31.8 +/- 5.2% increase above the preceding nadir. Discrete PTH peaks were separated by nonpulsatile valleys which lasted for 17.9 +/- 4.4 min. Cross-correlation between the time series of serum intact PTH and whole blood ionized calcium (Ca2+) was at its maximum (-0.5) at concurrent time points in three subjects, while significant positive correlation between serum intact PTH and simultaneous serum inorganic phosphorus concentrations was observed in four of five subjects. There was no apparent correlation between the levels of serum intact PTH and serum magnesium. Our data show that serum levels of intact PTH, the only biologically active form of PTH in the blood, is characterized by a significant circadian periodicity, spontaneous episodic pulsatility with distinct peak properties, and a significant temporal coupling with Ca2+ and inorganic phosphorus concentrations. We conclude that PTH secretion, as judged by the temporal pattern of serum intact PTH levels, is pulsatile in normal men.

Human myeloma cells were purified from bone marrow aspirates from four patients having advanced myeloma, including one with common acute lymphoblastic leukemia antigen-positive myeloma. All of these myelomas had marked bone lytic lesions. From the culture supernatants of these purified myeloma cells, bone-resorbing activities were significantly revealed by 45Ca-release bone resorption assay, and IL-1 activities were also detected by IL-1 bioassay (mouse thymocyte comitogenic assay). Sandwich enzyme immunoassay for IL-1 alpha or IL-1 beta revealed that IL-1 beta was responsible for IL-1 activity of these culture supernatants. Furthermore, the bone resorbing activities of these culture supernatants were completely neutralized by pretreatment of anti-IL-1 beta, but not anti-IL-1 alpha antibody. By Northern blot analysis, IL-1 beta mRNA was identified from these myeloma cells. Therefore, it is concluded that myeloma cells produce IL-1 beta, which acts as bone-resorbing activity in multiple myeloma.