Ultrasound (US) is a form of MECHANICAL energy, not electrical energy and therefore strictly speaking, not really electrotherapy at all.  Mechanical vibration at increasing frequencies us known as sound energy.  The normal human sound range is from 16Hz to something approaching 15-20,000 Hz (in children and young adults).  Beyond this upper limit, the mechanical vibration is known as ULTRASOUND.  The frequencies used in therapy are typically are typically between 1.0 and 3.0 MHz (1MHz = 1 million cycles per second).

Sound waves are LONGITUDINAL waves consisting of areas of COMPRESSION and REFRACTION.  Particles of a material, when exposed to a sound wave will oscillate about a fixed point rather than move with the wave itself.  As the energy within the sound wave is passed to the material, it will cause oscillation of the particles of that material.   Clearly any increase in the molecular vibration in the tissue can result in heat generation, and ultrasound can be used to produce thermal changes in the tissues, though current usage in therapy does not focus on this phenomenon (Williams 1987, Baker et al 2001 er Haar 1999, Nussbaum 1997, Watson 2000).  In addition to thermal changes, the vibration of the tissues appears to have effects, which are generally considered to be non-thermal in nature, though, as with other modalities (e.g. Pulsed Short-wave) there must be a thermal component however small.  As the US wave passes through a material (the tissues), the energy levels within the wave will diminish as energy is transferred to the material.

As the penetration (or transmission) of US is not the same in each tissue type it is clear that some tissues are capable of greater absorption of US than others.  Generally, the tissues with the higher protein content will absorb US to a greater extent, thus tissues with high water content and low protein content absorb little the US energy (e.g. blood and fat) whilst those with a lower water content and a higher protein content will absorb US far more efficiently.  It has been suggested that tissues can therefore be ranked according to their tissue absorption.

Although cartilage and bone are at the upper end of this scale, the problems associated with wave reflection mean the majority of US energy striking the surface of either of these tissues is likely to be reflected.  The best absorbing tissues in terms of clinical practice are those with high collagen content – LIGAMENT, TENDON, FASCIA, JOINT CAPSULE, SCAR TISSUE (Watson 2000, er Haar 99, Nussbaum 1998, Frizzel & Dunn 1982).

The application of therapeutic US to tissues with a low energy absorption capacity is less likely to be effective than the application of the energy into a more highly absorbing material.  Recent evidence of the ineffectiveness of such an intervention can be found in Wilkin et al (2004) whilst application in tissue that is a better absorber will, as expected, result in a more effective intervention (e.g. Sparrow et al 2005, Leung et al 2004).

Ultrasound Application in Relation to Tissue Repair

The process of tissue repair is a complex series of cascaded, chemically mediated events that lead to the production of scar tissue that constitutes an effective material to restore the continuity of the damaged tissue. The process is more complex than be described here, but there are several interesting recent papers and reviews including (Wener & Grose 2003, Toumi & Best 2003, Watson 2003, 2006, Hill et al 2003, Neidlinger-Wilke et al 2002, Lorena et al 2002, Latey 2001).


During the inflammatory phase, US has a stimulating effect on the mast cells, plate4lets, white cells with phagocytic roles and the macrophages (Nussbaum 1997, ter Haar 1999, Fyfe & Cahal 1982, Maxwell 1992). For example, the application of the ultrasound induces the degranulation of mast cells, causing the release of arachidonic acid which itself is a precursor for the synthesis of prostaglandins and leukotreine – which act as inflammatory mediators (Mortimer & Dyson 1988, Nussbaum 1997, Leung et al 2004). By increasing the activity of these cells, the overall influence of therapeutic US is certainly pro-inflammatory rather than anti-inflammatory. The benefit of this mode of action is not to ‘increase’ the inflammatory response as such (though if applied with too greater intensity at this stage, it is a possible outcome (Ciccone et al 1991), but rather to act as an ‘inflammatory optimizer’. The inflammatory response is essential to the effective repair of tissue, and the more efficiently the process can complete, the more effectively the tissue can progress to the next phase (proliferation).  

Studies which have tried to demonstrate the anti inflammatory effect of ultrasound have failed to do so (e.g. El Hag et al 1985 Hashish 1986, 1988) and have suggested that US is ineffective. It is effective at promoting the normality of the inflammatory events, and as such has a therapeutic value in promoting the overall repair events (ter Haar 99). A further benefit is that the inflammatory chemically mediated events are associated with stimulation of the next (proliferative) phase, and hence the promotion of the inflammatory phase also act is as a promoter of the proliferative phase. Employed at an appropriate treatment dose, with optimal treatment parameters (intensity, pulsing and time), the benefit of US is to make as efficient as possible to earliest repair phase, and thus have a promotional effect on the whole healing cascade. For tissues in which there is an inflammatory reaction, but in which there is no ‘repair’ to be achieved, the benefit of ultrasound is to promote the normal resolution of the inflammatory events, and hence resolve the ‘problem’. This will of course be most effectively achieved in the tissues that preferentially absorb ultrasound – i.e. the dense collagenous tissues.


During the proliferative phase (scar production) US also has a stimulative effect (cellular up regulation), though the primary  active targets are now the fibroblasts, endothelial cells and myofibroblasts (Ramirez et al 1997, Mortimer and Dyson 1988, Young & Dyson 1990, Young & Dyson 1990b, Nussbaum 1997, 1998, Dyson & Smalley 1983, Maxwell 1992).  These are all cells that are normally active during scar production and US is therefore pro-proliferative in the same way that it; is pro-inflammatory – it does not change the normal proliferative phase, but maximizes it efficiency – producing the required scar tissue in an optimal fashion.  

Harvey et al (1975) demonstrated that low dose pulsed ultrasound increases protein synthesis and several research groups have demonstrated enhanced fibroplasias and collagen synthesis (Enwemeka et al 1989, 1990, Turner et al 1989, Huys et al 1993, Ramirez et al 1997). 


During the remodeling phase of repair, the somewhat generic scar that is produced in the initial stages is refined such that it adopts functional characteristics of the tissue that it is repairing.  A scar in ligament will not ‘become’ ligament, but will behave more like a ligamantous tissue.  This is achieved by a number of processes, but mainly related to the orientation of the collagen fibres in the developing scar (Culav et al 1999, Gomez et al 1991) and also to the predominantly Type III collagen to a more dominant type I collagen.  (Vanables 1989, Forrest 1983).  The remodeling process is certainly not a short duration phase – research has shown that it can last for a year or more – yet it is an essential component of quality repair.  (El Batouty et al 1986, ter Haar 1987)

The application of therapeutic ultrasound can influence the remodeling of the scar tissue in that it appears to be capable of enhancing the appropriate orientation of the newly formed collagen fibres and also to the collagen profile change from mainly Type III to a more dominant Type I construction, thus increasing tensile strength and enhancing scar mobility (Nussbaum 1998, Wang 1998).  Ultrasound applied to tissues enhances the functional capacity of the scar tissues (Nussbaum 1998, Huys et al 1993).