Rice bodies in a shoulder bursa: a cadaveric and histologic case report.

INTRODUCTION: The subacromial/subdeltoid bursa can develop inflammation and effusion related to autoimmune, infectious, and musculoskeletal disorders. Rice bodies, or loose bodies within bursa, have been described as an uncommon complication of bursitis and have been the subject of case studies over a number of years. However, they have not been described in anatomical or physical therapy-related literature. METHODS: A donor body dissected for a physical therapy anatomy course was found to have an enlarged subacromial/subdeltoid bursa. This bursa, along with the biceps brachii tendon sheath, and the subscapularis muscle bursa, were filled with numerous rice-like bodies. The bursal wall was well developed and thickened. Tissue specimens were obtained of the suspected rice bodies, the subacromial/subdeltoid bursal wall, and the biceps brachii tendon sheath. The tissue was embedded, sectioned, and processed with hematoxylin and eosin or Masson's Trichrome staining for blinded histologic assessment. RESULTS: The tissue samples from within the bursa were identified as tissue similar to that in prior descriptions of rice bodies. Tissue samples from the bursal wall and tendon sheath were identified as similar to synovial membranes. CONCLUSIONS: Rice bodies found within the cadaveric body were similar histologically to those described in rheumatology, radiology, and orthopedic literature. Anatomists teaching future health-care providers and practicing physical therapists should be familiar with rice bodies as a potential finding in cadavers, and patients.

Relaxin and fibrosis: Emerging targets, challenges, and future directions.

The peptide hormone relaxin is well-known for its anti-fibrotic actions in several organs, particularly from numerous studies conducted in animals. Acting through its cognate G protein-coupled receptor, relaxin family peptide receptor 1 (RXFP1), serelaxin (recombinant human relaxin) has been shown to consistently inhibit the excessive extracellular matrix production (fibrosis) that results from the aberrant wound-healing response to tissue injury and/or chronic inflammation, and at multiple levels. Furthermore, it can reduce established scarring by promoting the degradation of aberrant extracellular matrix components. Following on from the review that describes the mechanisms and signaling pathways associated with the extracellular matrix remodeling effects of serelaxin (Ng et al., 2019), this review focuses on newly identified tissue targets of serelaxin therapy in fibrosis, and the limitations associated with (se)relaxin research.

Relaxin's involvement in extracellular matrix homeostasis.

Burgeoning evidence suggests that the hormone relaxin modulates collagen in the extracellular matrix of diverse tissues. In separate lines of study, we provide further substantiation of this hypothesis. Immunofluorescence was used to probe isolated fibroblasts derived from volar oblique ligament explant culture for vimentin, actin, RXFP1, and estrogen receptor beta. Ligaments were obtained as surgical waste from thumb reconstruction patients. Four specimens have been examined to date. Cells derived from these patients expressed vimentin and actin, consistent with fibroblast morphology. Putative fibroblasts derived from two of three female patients expressed RXFP1 receptors; the solitary male was negative. Given the small sample, however, the data are considered preliminary. Immunohistochemistry was used on frozen sections from 26 skin biopsies obtained from children undergoing genitoplasty. A subset of samples was also probed for transforming growth factor (TGF-beta1) and TGF-beta3. Appropriate controls were used. Finally, a subset of patient blood was assayed for relaxin by using an enzyme-linked immunosorbent assay-based method. The results showed RXFP1 receptor expression in the cells that populate the basement membrane in 96% of patients, regardless of gender. Most tissue expressed TGF-beta. Finally, serology suggested that relaxin was detectable in these children. Our two lines of research provide additional evidence for the diverse tissue tropism of relaxin. In particular, connective tissues as diverse as ligaments and basal lamina keratinocytes express RXFP1. These data lend support to our contention that relaxin affects ligament integrity and wound healing.

Fate of mu receptors during rat skeletogenesis.

Studies have intimated a role for endogenous opioids in skeletal ontogeny. We hypothesized that this role may be confined to the perinatal period. We, therefore, examined both fetal and postnatal rat long bones to determine the pattern, if any, of mu receptor expression. Perfused long bones and brains were harvested from 3 to 4 each of near-term fetuses, 3- to 4-week-old neonates, and 6-week-old juveniles. Tissues were decalcified, embedded, sectioned, quenched of peroxidase, and then blocked. Sections were incubated overnight with either rabbit antirat mu receptor IgG or naïve rabbit IgG (control) at 4 degrees C. The next day, sections were washed, blocked again, and incubated with biotin-labeled secondary antibody, streptavidin-peroxidase conjugate, and a chromogen substrate with intervening wash steps. Slides were counterstained with hematoxylin and coverslipped. Digital photomicrographs were then imported into an image analysis program and the percent area of stained cortical and trabecular bone quantified. Mu receptor expression decreased significantly with age. Approximately 25% of the area of fetal long bones stained positively, including the endosteum, periosteum, and the growth plate. Little or no nonspecific staining occurred. Staining in neonatal tissue was diminished to <11% of the area and involved areas of apparent remodeling; chondrocytes in the growth plates failed to stain. Finally, juvenile bone evidenced staining approaching background levels produced by control slides (approximately 2%). Mu receptors are abundant in developing rat long bones during fetal development but become progressively less abundant postnatally. This infers a role for endogenous opioids during skeletal ontogeny.

Immunohistological detection of relaxin binding to anterior cruciate ligaments.

Relaxin, a member of the insulin-like growth factor family, alters collagen metabolism in fibroblasts. It was hypothesized that relaxin interacts with the anterior cruciate ligament (ACL), contributing to its elasticity. Twelve ACL specimens were collected from reconstruction surgeries, sectioned, rinsed, and exposed to rh-relaxin overnight. Polyclonal antirelaxin antibodies, in conjunction with HRP-AEC, localized areas of tissue binding. Controls were used to infer binding specificity. Staining was present in the positive control and all 12 ACL specimens; little or no staining occurred in the negative controls. These data suggest that relaxin binding to the ACL is specific, indicative of a receptor-mediated event.