Objective—To examine effects of an autologous platelet-rich fibrin (PRF) membrane for enhancing healing of a defect of the patellar tendon (PT) in dogs.
Animals—8 adult dogs.
Procedures—Defects were created in the central third of the PT in both hind limbs of each dog. An autologous PRF membrane was implanted in 1 defect/dog, and the contralateral defect was left empty. Dogs (n = 4/time period) were euthanized at 4 and 8 weeks after surgery, and tendon healing was assessed grossly and histologically via a semiquantitative scoring system. Cross-sectional area of the PTs was also compared.
Results—Both treated and control defects were filled with repair tissue by 4 weeks. There was no significant difference in the histologic quality of the repair tissue between control and PRF membrane—treated defects at either time point. At both time points, the cross-sectional area of PRF membrane—treated tendons was significantly greater (at least 2.5-fold as great), compared with that of sham-treated tendons. At 4 weeks, the repair tissue consisted of disorganized proliferative fibrovascular tissue originating predominantly from the fat pad. By 8 weeks, the tissue was less cellular and slightly more organized in both groups.
Conclusions and Clinical Relevance—A PRF membrane did not enhance the rate or quality of tendon healing in PT defects. However, it did increase the amount of repair tissue within and surrounding the defect. These results suggested that a PRF membrane may not be indicated for augmenting the repair of acutely injured tendons that are otherwise healthy.
Objective—To describe the effect of systemically administered oxytetracycline on the viscoelastic properties of rat tail tendon fascicles (TTfs) to provide a mechanistic rationale for pharmacological treatment of flexural limb deformities in foals.
Sample—TTfs from ten 1-month-old and ten 6-month-old male Sprague-Dawley rats.
Procedures—5 rats in each age group were administered oxytetracycline (50 mg/kg, IP, q 24 h) for 4 days. The remaining 5 rats in each age group served as untreated controls. Five days after initiation of oxytetracycline treatment, TTfs were collected and their viscoelastic properties were evaluated via a stress-relaxation protocol. Maximum modulus and equilibrium modulus were compared via a 2-way ANOVA. Collagen fibril size, density, and orientation in TTfs were compared between treated and control rats.
Results—Viscoelastic properties were significantly decreased in TTfs from 1-month-old oxytetracycline-treated rats, compared with those in TTfs from 1-month-old control rats. Oxytetracycline had no effect on the viscoelastic properties of TTfs from 6-month-old rats. Collagen fibril size, density, and orientation in TTfs from 1-month-old rats did not differ between oxytetracycline-treated and control rats.
Conclusions and Clinical Relevance—Results confirmed that systemically administered oxytetracycline decreased the viscoelastic properties of TTfs from 1-month-old rats but not those of TTfs from 6-month-old rats. The decrease in viscoelastic properties associated with oxytetracycline treatment does not appear to be caused by altered collagen fibril diameter or organization. The age-dependent effect of oxytetracycline on the viscoelastic properties of tendons may be related to its effect on the maturation of the extracellular matrix of developing tendons.
Objective—To determine the effects of oxytetracycline
on matrix metalloproteinase-1 (MMP-1) mRNA
expression and collagen gel contraction by equine
myofibroblasts in an effort to explain the mechanistic
basis for the pharmacologic treatment of flexural
deformities in foals.
Sample Population—Cultured myofibroblasts from
the accessory ligament (distal check ligament) of 6
Procedure—Collagen gel scaffolds seeded with
equine myofibroblasts were cultured in individual culture
dishes containing complete media (Dulbecco's
modified Eagle medium with 10% fetal bovine serum)
and oxytetracycline (0, 12.5, 25, or 75 µg/mL) for 48
hours. After 24 hours, the gels were released from
the bottom of the culture plate and allowed to contract.
Photographs were taken at 0, 1, 2, 4, 6, 8, and
24 hours after release to assess the degree of collagen
gel contraction. Additional gels were harvested at
2 hours after release for RNA isolation and reverse
transcriptase-polymerase chain reaction assessment
of the degree of MMP-1 mRNA expression.
Results—Oxytetracycline induced a dose-dependent
inhibition of collagen gel contraction by equine myofibroblasts.
Oxytetracycline also induced a dose-dependent
decrease in MMP-1 mRNA expression by equine
Conclusions and Clinical Relevance—Results of
this study indicate that oxytetracycline inhibits tractional
structuring of collagen fibrils by equine myofibroblasts
through an MMP-1 mediated mechanism. In
young foals, oxytetracycline administration may make
the developing ligaments and tendons more susceptible
to elongation during normal weight-bearing.
Inhibition of normal collagen organization may provide
the mechanistic explanation for the results seen following
the pharmacologic treatment of flexural deformities
in foals by oxytetracycline administration. (Am
J Vet Res 2004;65:491–496)