While its use is in decline, many chiropractic practices still commonly use Therapeutic Ultrasound in the treatment of patients. The latest Practice Analysis of Chiropractic (2010) suggests that 63% of chiropractors now use the modality. This is a decline in utilization from the high of 70.3% in 1998. This decline is driven by reduced reimbursement and that decline was in turn due to the lack of evidence to support the efficacy of ultrasound therapy.
However this picture is changing. Recently, there has been an increase in interest by the research community in evaluating ultrasound. This has produced some important basic science and human studies that lend strong support for its use. During the last year several studies support the benefits of therapeutic ultrasound for several purposes including the treatment of tendon injuries.
The first four abstracts below provide “strong supporting evidence from animal studies about the positive effects of ultrasound on tendon healing”. Three previous articles provide evidence supporting the efficacy of therapeutic ultrasound in clinical practice. These were published on ChiroACCESS:
Note: These mini-reviews are designed as updates and direct the reader to the full text of current research. The abstracts presented here are no substitute for reading and critically reviewing the full text of the original research. Where permitted we will direct the reader to that full text.
- Evidence Supports the Use of Therapeutic Ultrasound for Joint Osteoarthritis
- Ultrasound Therapy 2010 Research Support
- Therapeutic Ultrasound A Review of the Literature
Effect of therapeutic ultrasound on tendons.
] Am J Phys Med Rehabil.
Tsai WC, Tang ST, Liang FC. Department of Physical Medicine and Rehabilitation, Chang Gung Memorial Hospital at Linkou, College of Medicine, Chang Gung University, Taoyuan, Taiwan.
Ultrasound is a therapeutic agent commonly used to treat sports-related musculoskeletal conditions, including tendon injuries or tendinopathy. Despite the widespread popularity of therapeutic ultrasound, few clinical studies have proved its efficacy. Several animal studies have been conducted to explore its effectiveness. In addition, a number of in vitro studies investigating the mechanisms underlying the ability of this physical modality to enhance tendon healing or to treat tendinopathy are in progress. There is strong supporting evidence from animal studies about the positive effects of ultrasound on tendon healing. In vitro studies have also demonstrated that ultrasound can stimulate cell migration, proliferation, and collagen synthesis of tendon cells that may benefit tendon healing. These positive effects of therapeutic ultrasound on tendon healing revealed by in vivo and in vitro studies help explain the physiologic responses to this physical modality and could serve as the foundation for clinical practice.
Comparing therapeutic ultrasound with microamperage stimulation therapy for improving the strength of Achilles tendon repair.
] Connect Tissue Res.
2011 Jun;52(3):178-82. doi: 10.3109/03008207.2010.500752. Epub 2010 Jul 30.
Ng GY. Department of Rehabilitation Sciences, The Hong Kong Polytechnic University , Hong Kong, SAR , China. email@example.com
In exploring the effects of therapeutic ultrasound (US) and microamperage stimulation (MAS) on the biomechanical performance of repairing Achilles tendon in rats, 35 Sprague-Dawley rats receiving surgically induced injury to their right medial Achilles tendon were studied. The rats were divided into four groups of low-dose US (group 1, n = 10), high-dose US (group 2, n = 11), MAS (group 3, n = 7), and control (group 4, n = 7). The treatment started on day 6 after injury. Groups 1 and 2 received 4 min of daily US treatment at 1.0 and 2.0 W/cm(2), respectively. Group 3 received 30 min of daily transcutaneous MAS treatment. Group 4 received 30 min of daily sham MAS treatment. On day 31, the Achilles tendons were mechanically tested. Data on the right side were normalized to the left side and analyzed with MANOVA with a = 0.05. Results of MANOVA was significant and post hoc tests revealed that the normalized strength of groups 1, 2, and 3 were higher than that of group 4 (p = 0.003) but no significant difference was found among the treatment groups. The ANOVA result of the normalized load relaxation and stiffness was p = 0.06 and p = 0.07, respectively. These findings suggested that both low/high doses of US and MAS therapies could improve the strength of Achilles tendon but in view of its short treatment time, US is considered to be more efficient than MAS for improving the strength of the repairing tendons.
Low-intensity pulsed ultrasound accelerates healing in rat calcaneus tendon injuries.
] J Orthop Sports Phys Ther.
2011 Jul;41(7):526-31. Epub 2011 Feb 18.
Jeremias Júnior SL, Camanho GL, Bassit AC, Forgas A, Ingham SJ, Abdalla RJ. University of Sao Paulo, School of Medicine, Department of Orthopaedic Surgery, Sao Paulo, SP, Brazil.STUDY DESIGN:
Controlled laboratory study. OBJECTIVE:
To evaluate the effect of low-intensity therapeutic ultrasound on the murine calcaneus tendon healing process. BACKGROUND:
Therapeutic ultrasound promotes formation and maturation of scar tissue. METHODS:
Calcaneus tendon tenotomy and tenorrhaphy was performed on 28 Wistar rats. After the procedure, the animals were randomly divided into 2 groups. The animals in the experimental group received a 5-minute ultrasound application, once a day, at a frequency of 1 MHz, a spatial average temporal average intensity of 0.1 W/cm2, and a spatial average intensity of 0.52 W/cm2 at a 16-Hz frequency pulse mode (duty cycle, 20%). Data for the injured side were normalized in relation to the data from the contralateral healthy calcaneus tendon (relative values). The animals in the control group received sham treatment. After a 28-day treatment period, the animals were sacrificed and their tendons surgically removed and subjected to mechanical stress testing. The parameters analyzed were cross-sectional area (mm2), ultimate load (N), tensile strength (MPa), and energy absorption (mJ). RESULTS:
A significant difference between groups was found for the relative values of ultimate load and tensile strength. The mean ± SD ultimate load of the control group was -3.5% ± 32.2% compared to 33.3% ± 26.8% for the experimental group (P = .005). The mean tensile strength of the control group was -47.7% ± 19.5% compared to -28.1% ± 24.1% for the experimental group (P = .019). No significant difference was found in cross-sectional area and energy absorption. CONCLUSION:
Low-intensity pulsed ultrasound produced by a conventional therapeutic ultrasound unit can positively influence the calcaneus tendon healing process in rats.
The cross-talk between transforming growth factor-beta1 and ultrasound stimulation during mechanotransduction of rat tenocytes.
] Connect Tissue Res.
2011;52(4):313-21. Epub 2010 Nov 30.
Chao YH, Tsuang YH, Sun JS, Cheng CK, Chen MH. Institute of Biomedical Engineering, National Yang-Ming University, Taipei, Taiwan.
Ultrasound is an effective noninvasive treatment for various tendinopathies. However, how tenocytes convert ultrasound stimulation into cascades of cellular and molecular events is not well understood. The purpose of this study is to elucidate the signaling pathways of tenocytes during ultrasound stimulation. Primary cultures of tenocytes were harvested from Achilles tendons of Sprague-Dawley rats. The viability and proliferation of tenocytes, their genes expression, and the signaling pathways after ultrasound treatment with or without specific inhibitors were evaluated and analyzed. The results showed that ultrasound treatment (100 mW/cm(2) for 20 min) significantly enhanced matrix metalloproteinase 13 (MMP-13), c-Fos, and c-Jun gene expression, increased JNK and p38, but not extracellular signal-regulated kinase-1/2 (ERK1/2), phosphorylation at 5 min, and sustained up to 60 min. JNK inhibitor and p38 inhibitor, but not ERK1/2 inhibitor, attenuated ultrasound-dependent induction of MMP-13 expression, indicating that the JNK and p38 pathways are required for ultrasound-induced MMP-13 expression in tenocytes. We also found that SB431542 (transforming growth factor-beta (TGF-ß) receptor kinases inhibitor) suppressed ultrasound-induced MMP?13 and c-Fos gene expression, and p38 phosphorylation. This study revealed that ultrasound treatment stimulates tenocytes proliferation and regulates their matrix metabolism through the cross-talk between TGF-ß and ultrasound-induced mitogen-activated protein kinases (MAPKs) signaling pathways.
Therapeutic ultrasound stimulation of tendon cell migration.
] Connect Tissue Res.
Tsai WC, Chen JY, Pang JH, Hsu CC, Lin MS, Chieh LW. Department of Physical Medicine and Rehabilitation, Chang Gung Memorial Hospital, and College of Medicine, Chang Gung University, Taoyuan, Taiwan. firstname.lastname@example.org
Ultrasound is a therapeutic agent commonly used to treat sports-related tendinopathy. Tendon healing requires tendon cells migration to the repair site, followed by the proliferation and synthesis of extracellular matrix. This study was designed to determine the effect of ultrasound on migration of tendon cells intrinsic to rat Achilles tendon. Furthermore, the existence of a correlation between this effect and the expression of the contractile actin isoform, alpha-smooth muscle (SM) actin, which is associated with cell mobility, was also examined. Cell migration was evaluated by transwell filter migration assay. The mRNA expressions of alpha-SM actin were determined by reverse transcription-polymerase chain reaction. Dose-dependent ultrasound enhancement of tendon cells migration through the transwell filter was demonstrated. Using immunofluorescence stain for alpha-SM actin, the percentages of alpha-SM actin-positive cells of total cells, nonmigrated cells, and migrated cells on the filter were calculated. Ultrasound-treated cells which had migrated to the bottom side of the filter were more likely to express alpha-SM actin than migrated control cells and nonmigrated cells. However, there was no change of mRNA and protein expression of alpha-SM actin as well as expression of FAK and p-FAK. In conclusion, ultrasound stimulates tendon cell migration in association with increased expression of alpha-SM actin of tendon cells.
Ultrasound stimulation of types I and III collagen expression of tendon cell and upregulation of transforming growth factor beta.
] J Orthop Res.
Tsai WC, Pang JH, Hsu CC, Chu NK, Lin MS, Hu CF. Department of Physical Medicine and Rehabilitation, Chang Gung Memorial Hospital, 5, Fu-Shin Street, Kweishan, Taoyuan 333, Taiwan. email@example.com
Traumatic tendon injuries are commonly treated with ultrasound. However, previous research has not examined the molecular mechanism of this therapeutic effect on collagen synthesis of tendon cells. This study was designed to determine the effect of ultrasound on the expression of type I and type III collagen of tendon cells intrinsic to rat Achilles tendon. Whether a correlation exits between this effect and the expression of transforming growth factor beta (TGF-beta), which enhances collagen synthesis, was also investigated. Tendon cells after ultrasound treatment and protein expression of types I and III collagen were determined by immunocytochemistry. The mRNA expressions of alpha1(I) procollagen, alpha1(III) procollagen, and TGF-beta were determined by reverse transcription-polymerase chain reaction (RT-PCR). Furthermore, the concentration of TGF-beta in conditioned medium was evaluated by enzyme-linked immunosorbent assay (ELISA). Immunocytochemical staining revealed that ultrasound-treated tendon cells were stained more strongly for types I and III collagen than were control cells. Upregulation of procollagen alpha1(I) gene, procollagen alpha1(III) gene, and TGF-beta at the mRNA level was confirmed by RT-PCR. A dose-dependent increase in the concentration of TGF-beta in conditioned medium obtained from cells treated with ultrasound was demonstrated by ELISA assay (p = 0.043). In conclusion, ultrasound stimulates the expression of type I and type III collagen in a process that is likely mediated by the upregulation of TGF-beta.