Conducted by a team of researchers in Denmark, the study focused on ovariectomized rats, a model that closely resembles the changes in the human skeletal system during menopause. Key among them is loss of estrogen, which has been associated with accelerated cartilage degradation.
In the study, 50 female Sprague-Dawley rats were divided, randomly and equally, into five study groups: ovariectomy; ovariectomy, plus 60-day release estrogen pellet inserted; ovariectomy, plus 2.0 mg/kg of salmon calcitonin and 50 mg/kg of 5CNAC, a carrier; ovariectomy, plus 50 mg/kg of 5CNAC; and sham operation.
Blood samples were collected from every rat at baseline, on day three, and after one, two, four, six, and nine weeks. Each rat’s body weight was recorded at regular intervals. After nine weeks, the rats were euthanized. Then, researchers assessed each blood sample for increases in C-telopeptide type II collagen (CTX-II), shown to correlate with degradation of articular cartilage in rats; microscopically examined and blindly scored a section of every rat’s knee joint for surface erosions of cartilage; and performed statistical analyses of the data.
Compared with the sham-operated group, all the ovariectomized rats experienced a marked increase in levels of CTX-II for the first six weeks, indicating accelerated articular cartilage degradation. During the nine-week trial, estrogen therapy effectively worked to counteract this increase to levels lower than the carrier and non-treated groups, whose levels were not significantly different. However, calcitonin worked better, bringing levels to below those even in the sham-operated group.
Similarly, estrogen and calcitonin both provided significant protection against surface erosions of knee joint cartilage. Again, calcitonin worked better, preventing erosions completely. Of note, the rats that had estrogen therapy gained the least weight of all the ovariectomized rats, effectively easing the erosive toll on the weight-bearing knee joints. Interestingly, calcitonin had no positive impact on body weight, yet protected against the erosions linked to joint destruction in OA.
“Calcitonin treatment may counter the acceleration of cartilage degradation and the related rise of surface erosions,” concludes the study’s lead author, Bodil-Cecilie Sondergaard, “indicating important chondroprotective properties of this drug which need to be explored in upcoming clinical trials.”