With the aging of the population in developed countries, spine surgeons have recently been more likely to encounter elderly patients in need of treatment. This study investigated whether decompression surgery for cervical spondylotic myelopathy (CSM) in elderly patients aged 80 years or older would likely be a reasonable treatment. We retrospectively reviewed 605 consecutive patients with cervical myelopathy who underwent decompression surgery between 2004 and 2008. Patients with other conditions that could affect functional status or compression factors other than spondylosis were excluded from this study. Of the remaining 189 patients, 161 with CSM whose condition could be evaluated 6 months after surgery were analyzed. The patients were divided into two age groups: 80 years or older (Group A, 37 patients) and younger than 80 years of age (Group B, 124 patients). We evaluated the differences in symptom duration, clinical data, involved levels, surgical outcome, comorbidities, and postoperative complications between the two groups. The symptom duration was significantly shorter in Group A. The average JOA scores preoperatively and 6 months postoperatively were significantly lower in Group A; however, there was no significant difference in the recovery ratio. There were no significant differences in the percentages of patients with comorbidities or those with postoperative complications. Elderly patients aged 80 years or older regained approximately 40% of their function postoperatively, and the incidence of postoperative complication was similar to that in younger patients. Since this age group shows a rapid deterioration after onset, prompt decompression surgery is required.

No abstract

Our findings indicate that, in an animal model of arthritis, intermittent PTH administration activates bone formation, resulting in increased BMD and preventing deterioration of mechanical properties. However, PTH has no effect on the arthritis itself.

To elucidate the effects of inflammation on the response of bone to mechanical stress, we performed experiments using a rat with collagen-induced arthritis (CIA) model. Six-month-old female Wistar rats were used in the experiment. Bovine type II collagen sensitization and additional sensitization after 1 week were preformed in all CIA groups. Loads were applied using a four-point bending device. The right tibia was loaded in both CIA and control (CONT) groups at 35 N (low groups), 40 N (medium groups), or 47 N (high groups) for 36 cycles at 2 Hz three times per week for 3 weeks. Histomorphometrical data were collected from the periosteal and endosteal surfaces of the tibia in all rats. The tibia periosteal surface was subdivided into lateral and medial surfaces. Formation surface (FS), mineral apposition rate (MAR) and bone formation rate (BFR) were calculated. At lateral surface of periosteal surface, all three parameters showed significant differences between the loaded and nonloaded tibiae. All these parameters were significantly lower in CIA groups than in CONT groups, and interaction was seen between applied loading and CIA. There was a significant correlation between peak strain and the right-left difference of FS in the CONT groups. At medial surface of periosteal surface, there were force-related increase in FS, MAR, and BFR on the loaded side in both CIA and CONT groups, except MAR in the CONT group. All three parameters showed significant differences between the loaded and nonloaded tibiae. At endocortical surface, force-related increase was observed only in FS on the loaded side in CONT groups, and FS was significantly higher on the loaded side than the nonloaded side. CIA lowered all three parameters significantly. We examined the response to mechanical loading on the tibia in untreated CONT rats and rats with CIA by bone histomorphometry, and found that arthritis suppressed bone formation induced by mechanical loading.

The effects of BPs on bone formation during mechanical loading are still unknown. In this study, we evaluated the effect of minodronate on the cortical bone response to mechanical loading applied using a 4-point bending device. We used six-month old female Wistar rats and randomized into five groups (N=10/group): Vehicle administration (VEH), low dose minodronate administration (MIN-L, 0.01 mg/kg BW), middle dose minodronate administration (MIN-M, 0.1mg/kg BW), high-dose minodronate administration (MIN-H 1mg/kg BW), and very high-dose minodronate administration (MIN-VH, 10mg/kg BW). Minodronate or vehicle was administered orally using the feeding needle at a dosage 3 times/week for 3 weeks. Loads on the right tibia at 38 N for 36 cycles at 2 Hz were applied in vivo by 4-point bending on the same day for 3 weeks. After calcein double labeling the rats were sacrificed and tibial cross sections were prepared from the region with maximal bending at the central diaphysis. Histomorphometry was performed at the entire periosteal and endocortical surface of the tibiae, dividing the periosteum into lateral and medial surfaces. The formation surface was reduced significantly in MIN-H and MIN-VH groups at the medial surface, and in MIN-VH group at the endocortical surface of the loaded tibia (p<0.01 vs. VEH). The mineral appositional rate was reduced significantly in MIN-H and MIN-VH groups at the endocortical surface of the loaded tibia (p<0.01 vs. VEH). The bone formation rate was significantly reduced in MIN-H group at the medial surface, and in MIN-H and MIN-VH groups at the endocortical surface of the loaded tibia (p<0.01 vs. VEH). However, no significant differences were observed in any parameters between the VEH group and either the MIN-L or MIN-M groups for both the loaded and non-loaded tibiae. Based on previous preventive studies in OVX rats, the optimal dose of minodronate for the treatment of osteoporosis would be 0.03 mg/kg (0.21 mg/kg/week). Therefore, we used 0.1mg/kg of minodronate 3 times/week (0.30 mg/kg/week) that was close to 0.21 mg/kg/week. In conclusion, minodronate does not reduce the cortical bone response to mechanical loading at the optimal dose for the treatment of osteoporosis in rat model.