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. Author manuscript; available in PMC: 2016 Jul 21.
Published in final edited form as: Arthroscopy. 2013 Jul 26;29(10):1722–1731. doi: 10.1016/j.arthro.2013.05.028

Table 3.

Biochemical Outcomes for CPM

Study Biochemical Outcomes
Ferretti et al.53 COX-2 (mean No. of positive cells):
  • IMM at 24 h: 83 ± 11

  • CPM at 24 h: 22 ± 6 (P < .05)

  • IMM at 48 h: 86 ± 19

  • CPM at 48 h: 21 ± 9 (P < .05)

MMP-1 (mean No. of positive cells):
  • IMM at 24 h: 79 ± 17

  • CPM at 24 h: 26 ± 11 (P < .05)

  • IMM at 48 h: 84 ± 22

  • CPM at 48 h: 24 ± 16 (P < .05)

IL-1β (mean No. of positive cells):
  • IMM at 24 h: 103 ± 23

  • CPM at 24 h: 18 ± 9 (P < .05)

  • IMM at 48 h: 121 ± 31

  • CPM at 48 h: 13 ± 6 (P < .05)

IL-10 (mean No. of positive cells):
  • IMM at 24 h: 39 ± 18

  • CPM at 24 h: 111 ± 24 (P < .05)

  • IMM at 48 h: 51 ± 22

  • CPM at 48 h: 122 ± 27 (P < .05)

Loss of glycosaminoglycans (mean No. of positive cells):
  • IMM at 24 h: 48% in zone A, 26% in zone B

  • CPM at 24 h: 12% in zone A, 6% in zone B

  • IMM at 48 h: +37% in zone A, +26% in zone B

  • CPM at 48 h: +8% in zone A, +3% in zone B

Gassner et al.54 Nitric oxide production:
  • Resting culture (control): 1.24 ± 0.38 μm

  • Resting + CTS: 1.05 ± 0.31 μm

  • Resting + IL-1 (inflamed): 35.3 ± 7.75 μm

  • Resting + IL-1 + LMA: 4.26 ± 1.18 μm

  • CTS + IL-1: 21.8 ± 3.78 μm

  • CTS + IL-1 + LMA: 3.5 ± 1.01 μm

Proteoglycan synthesis:
  • Resting culture (control): 100%

  • CTS: 102.3% ± 13.5%

  • Resting + IL-1 (inflamed): 62.4% ± 11%

  • Resting + IL-1 + LMA: 70.3% ± 11.35%

  • CTS + IL-1: 75.43% ± 13% (P = .001)

  • CTS + IL-1 + LMA: 85.7% ± 12.3% (P = .047)

TGF-β:
  • Resting culture (control): 9 pmol/L

  • CTS: 36 pmol/L

  • Resting + IL-1 (inflamed): 16 pmol/L

  • CTS + IL-1: 40 pmol/L

Xu et al.55
  • Induction of iNOS: IL-1β increased expression of iNOS mRNA; presence of CTS suppressed iNOS mRNA expression (P ≤ .05)

  • COX-2: CTS consistently suppressed COX-2 mRNA expression at 4 and 24 h by 86% and 92%, respectively (P < .01)

  • PGE2: CTS inhibited PGE2 formation at 4 h, 24 h (82%), and 48 h (81%) (P < .05)

  • MMP-1: CTS suppressed MMP-1 mRNA expression at 4 and 24 h by 98% and 83%, respectively; CTS inhibited MMP-1 synthesis at 8 and 24 h by 92% and 87%, respectively (P < .05)

  • TIMP: consistent inhibition of TIMP-II mRNA expression with IL-1β alone; addition of CTS resulted in hyperinduction of TIMP-II mRNA at 4 h (4 ± 0.62–fold) and 24 h (7.4 ± 1.1–fold) (P < .05)

  • Collagen type II: CTS suppressed IL-1β– mediated induction of collagen type II mRNA at 24 h, 48 h, and 72 h (P ≤ .05); no induction of collagen type II mRNA with CTS alone

  • Proteoglycan mRNA expression: IL-1β consistently inhibited aggrecan mRNA expression at 4 and 24 h (12%–14% reduction); CTS + IL-1β caused hyperinduction of aggrecan mRNA expression (increase by 2.6-, 4.1-, and 5.8-fold at 4, 24, and 48 h, respectively)

  • Proteoglycan synthesis (at 24, 48, and 72 h): IL-1β alone—decreased synthesis by 62% ± 5%, 67% ± 4%, and 61%; CTS alone—decreased synthesis by 15% ± 3%, 18% ± 3%, and 14% ± 3%; CTS + IL-1β—no significant difference compared with control at any time period (i.e., 100% synthesis)

  • Timing of CTS and IL-1β: inhibition of iNOS mRNA expression greatest when CTS was initiated simultaneously with IL-1β application (82% ± 3.5%); only 40% of inhibition noted when CTS was begun 1 hour after IL-1β application; CTS was ineffective when begun 2 h after IL-1β application

COX, cyclooxygenase; CTS, cyclic tensile strain; IL, interleukin; iNOS, inducible nitric oxide synthase; LMA, L-N-monomethyl arginine; MMP, matrix metalloproteinase; mRNA, messenger ribonucleic acid; PGE2, prostaglandin E2; TGF, transforming growth factor; TIMP, tissue inhibitor of metalloproteinase.

Significant decrease in proteoglycan synthesis in alone versus CTS + IL-1β (P ≤ .05).