Procedure—Blood samples for measurement of
serum thyroxine (T4), 3,5,3'-triiodothyronine (T3), free
T4 (fT4), and endogenous canine thyroid stimulating
hormone (cTSH) were measured twice before as well
as on days 14 and 28 of etodolac administration
(mean dosage, 13.7 mg/kg, PO, q 24 h). Plasma total
protein, albumin, and globulin concentrations and
serum osmolality were measured once before as well
as on days 14 and 28 of etodolac administration.
Results—Etodolac administration did not significantly
affect serum T4, T3, fT4, or cTSH concentrations or
serum osmolality. Significant decreases in plasma
total protein, albumin, and globulin concentrations
were detected on days 14 and 28 of administration.
Conclusions and Clinical Relevance—Results of
thyroid function tests are not altered when etodolac is
administered for up to 4 weeks. Therefore, interpretation
of results of these tests should accurately reflect
thyroid function during etodolac treatment. Plasma
total protein, albumin, or globulin concentrations that
are less than the respective reference range in a dog
administered etodolac for ≥ 2 weeks may be an effect
of treatment rather than an unrelated disease
process. A decrease in plasma protein concentrations
may reflect subclinical injury of the gastrointestinal
tract. (Am J Vet Res 2002;63:1492–1495)
Objective—To evaluate a method for experimental
induction of osteoarthritis in the hip joints of dogs.
Animals—12 mixed-breed dogs.
Procedure—A unilateral triple pelvic osteotomy was
performed. In 6 dogs, the iliac osteotomy was
repaired with 45° of internal rotation, reducing coverage
of the femoral head by the acetabulum. In the
other 6 dogs, the fragments were repaired in anatomic
alignment. Radiography, force plate evaluations, and
subjective lameness evaluations were performed
before and after surgery. Dogs were euthanatized 7
months after surgery, and samples of cartilage and
joint capsule were examined histologically.
Results—Subjective lameness scores, radiographic
appearance of the hip joints, and Norberg angles
were not significantly different between groups; however,
force plate evaluations did reveal significant differences
in vertical ground reaction forces. Femoral
head coverage was significantly decreased with rotation
of the acetabulum. Mild inflammatory changes
were discernible in the joint capsule and articular cartilage
of some dogs in both groups.
Conclusions and Clinical Relevance—Results suggest
that 45° internal rotation of the acetabulum does
not consistently induce biologically important
osteoarthritic changes in the hip joints of dogs.
(Am J Vet Res 2000;61:484–491)
Objective—To investigate the ability of ABT-116 (a proprietary antagonist of transient receptor potential vanilloid type 1) administered at 2 doses to attenuate lameness in dogs with experimentally induced urate synovitis.
Animals—8 purpose-bred mixed-breed dogs.
Procedures—In a 4-way crossover study, dogs orally received each of low-dose ABT-116 treatment (LDA; 10 mg/kg), high-dose ABT-116 treatment (HDA; 30 mg/kg), firocoxib (5 mg/kg), and no treatment (nontreatment) once a day for 2 days, in a randomly assigned order. Synovitis was induced on the second day of each treatment period by intra-articular injection of either stifle joint with sodium urate, alternating between joints for each treatment period, beginning with the left stifle joint. Ground reaction forces, clinical lameness scores, and rectal temperature were assessed before the injection (baseline) and at various points afterward.
Results—Lameness scores at the 2-, 6-, and 12-hour assessment points were higher than baseline scores for HDA and nontreatment, whereas scores at the 2- and 6-hour points were higher than baseline scores for LDA. For firocoxib, there was no difference from baseline scores in lameness scores at any point. Compared with baseline values, peak vertical force and vertical impulse were lower at 2 and 6 hours for HDA and nontreatment and at 2 hours for LDA. No changes in these values were evident for firocoxib. The HDA or LDA resulted in higher rectal temperatures than did treatment with firocoxib or nothing, but those temperatures did not differ among treatments.
Conclusions and Clinical Relevance—HDA had no apparent effect on sodium urate–induced lameness; LDA did attenuate the lameness but not as completely as firocoxib treatment. High rectal temperature is an adverse effect of oral ABT-116 administration that may be of clinical concern.
Objective—To assess effects of in vitro meloxicam exposure on metabolism in articular chondrocytes from dogs with naturally occurring osteoarthritis
Sample—Femoral head cartilage from 16 dogs undergoing total hip replacement
Procedures—Articular cartilage samples were obtained. Tissue sulfated glycosaminoglycan (SGAG), collagen, and DNA concentrations were measured. Collagen, SGAG, chondroitin sulfate 846, NO, prostaglandin E2 (PGE2), and matrix metalloproteinase (MMP)-2, MMP-3, MMP-9, and MMP-13 concentrations in culture medium were analyzed. Aggrecan, collagen II, MMP-2, MMP-3, MMP-9, MMP-13, ADAM metallopeptidase with thrombospondin type 1 motif (ADAMTS)-4, ADAMTS-5, tissue inhibitor of metalloproteinase (TIMP)-1, TIMP-2, TIMP-3, interleukin-1β, tumor necrosis factor-α, cyclooxygenase-1, cyclooxygenase-2, and nducible nitric oxide synthase gene expression were evaluated. Comparisons between tissues cultured without (control) and with meloxicam at concentrations of 0.3, 3.0, and 30.0 μg/mL for up to 30 days were performed by means of repeated-measures analysis.
Results—Meloxicam had no effect on chondrocyte SGAG, collagen, or DNA concentrations. Expression of ADAMTS-5 was significantly decreased in all groups on all days, compared with the day 0 value. On day 3, culture medium PGE2 concentrations were significantly lower in all meloxicam-treated groups, compared with values for controls, and values remained low. Culture medium MMP-3 concentrations were significantly lower on day 30 than on day 3 in all meloxicam-treated groups.
Conclusions and Clinical Relevance—Results suggested that in vitro meloxicam treatment of osteoarthritic canine cartilage for up to 30 days did not induce matrix degradation or stimulate MMP production. Meloxicam lowered PGE2 release from this tissue, and effects on tissue chondrocyte content and matrix composition were neutral.
Objective—To evaluate the quality of information
regarding osteoarthritis (OA) in dogs currently available
on the World Wide Web.
Procedure—5 search engines were searched with
the keywords "dog," "degenerative joint disease,"
"canine," and "osteoarthritis," and the first 50 sites
listed by each search engine were analyzed. Unique
Web site addresses were distributed to 3 diplomates
of the American College of Veterinary Surgeons, who
provided a standardized evaluation of each site.
Results—30 unique Web sites were evaluated.
Twenty (66%) provided information consistent with
conventional knowledge as outlined in textbooks and
peer-reviewed literature, 8 (27%) provided experimental
or anecdotal information in addition to conventional
knowledge, and 2 (7%) provided misleading information.
Mean scores for overall usefulness of the information
provided in regard to clinical features of and
treatment for OA were 1.3 and 1.5, respectively (1 =
information of minimal use; 5 = very useful information).
Twenty-three (77%) sites encouraged pet owners
to seek the advice of a veterinarian. Twenty-three
(77%) sites were given overall quality scores < 2, and
7 (23%) were given scores between 2 and 3 (1 = site
was counterproductive; 5 = site was very valuable).
Conclusions and Clinical Relevance—Results suggest
that the quality of information currently available
on the Web that addresses OA in dogs is questionable.
Although most of the sites conveyed some conventional
information with reasonable accuracy, the
information was incomplete, of minimal use, and
often considered counterproductive. (J Am Vet Med