Based on the above findings, the analgesic effects of LLLT were found to be valid. The serum PGE(2) levels are therefore considered to directly reflect nociceptive pain.

The distribution of neural elements in the triangular fibrocartilage complex (TFCC) of the human wrists was studied via immunohistochemical staining of protein gene product (PGP) 9.5 and calcitonin gene-related peptide (CGRP). Articular branches projecting to the TFCC arose from the dorsal branch of the ulnar nerve in all wrists examined. The TFCC is subdivided into the following six regions: the articular disc proper (ADP), meniscus homolog (MH), radio-ulnar ligament (RUL), loose part of ulnar collateral ligament (lUCL), dense part of ulnar collateral ligament (dUCL), and internal portion (IP). The IP consists of a mixture of dense and loose connective tissues enclosed by the ADP, MH, RUL, and UCL, and resides deep in the prestyloid recess, which is a pit in the MH. The densities of PGP 9.5-positive neural elements, including free nerve endings, single nerve fibers, nerve fascicles, and perivascular neural nets, were significantly higher in the IP than in other regions. Some of the neural elements except for the perivascular neural nets were positive for CGRP. The high density of neural elements in the IP suggests that sensory nerves projecting to the TFCC enter into the IP and from there distribute to adjacent regions such as the MH and RUL. Free nerve endings are responsible for pain transmission. The high density of free nerve endings in the IP suggests that the IP is a source of ulnar side wrist pain.

In the presence of congenital hypoplasia of the posterior arch of the atlas, the spinal cord is highly susceptible to injury because congenital spinal canal stenosis is present. Therefore, the presence of even a mild mechanical compressive lesion leads to myelopathy. Acquired mild atlantoaxial subluxation was associated with this hypoplasia, and the association was considered to be the mechanism underlying the occurrence of myelopathy in adulthood.

In recent years, calcium phosphate cements (CPCs) have frequently been used as bone substitutes in the field of orthopedic surgery. When CPC is used as a bone substitute in vivo, blood contamination is unavoidable. To date, however, no detailed study has been conducted focusing on how the physical properties of CPCs would change under the influence of blood. In this study, the effects of blood contamination on Biopex-R (BPR, PENTAX, Tokyo) are examined in vitro and in vivo. The compressive strength of BPR after setting decreased depending on the amount of contaminating blood. The BPR, which has set in vivo, not only has a fragile surface due to the contamination by blood, but also has a propensity to shorten and be destroyed during the early postoperative stage, especially in the bone exposed to loads. On the other hand, radiographic and histological features in vivo indicated that the absorption and the bone replacement of BPR were stimulated by blood contamination. In the clinical evaluation, the patient's own peripheral venous blood was added to the BPR. One year after the surgery, the absorption was noted around the hardened BPR. To advance CPCs (including BPR) as bioabsorbable bone replaceable materials, it is essential to utilize the patient's own blood in combination with the CPC.