104 include their relative simplicity, lower cost, quicker recovery time, and fewer long-term side effects when compared with traditional surgery, many question their efﬁcacy. The goal of this article is to discuss the rationale for using intradiscal steroids and to review the literature regarding the efﬁcacy of intradiscal steroids to treat low back pain of discogenic origin. Rationale for the use of intradiscal steroids The intervertebral disc, which is composed of a central nucleus pulposus and surrounding annulus ﬁbrosis, permits mobility between opposing surfaces of the vertebral body. It is ideally suited for the distribution and dissipation of tremendous longitudinal forces. The nucleus pulposus, can tolerate a static load indeﬁ- nitely and adjust to ﬂuctuations through a physiologic response in which there is a compensatory change in ﬂuid retention. Since the nucleus acts as a conﬁned ﬂuid, it dis- tributes vertical forces equally in all directions. The annulus ﬁbrosus is a highly elastic tissue that sur- rounds the nucleus pulposus and absorbs tangential forces. With its low matrix content and high concentration of ﬁbrous and elastic tissue, it thrives under tension but deteriorates rapidly when subjected to direct pressure [9]. When degenerative changes exist in the nucleus pulpo- sus, some of the force between the vertebral end plates is exerted directly on the annulus ﬁbrosus. Degeneration of some central ﬁbers appears ﬁrst, subsequently leading to tears and ﬁssures. Although in the early phases these changes are microscopic in appearance, they cause an inﬂammatory reaction in the surrounding, sensitive, longi- tudinal ligaments of the spine. This creates a clinical picture of acute low back pain. Inﬂammation, either from direct chemical irritation or secondary to an autoimmune response to the nucleus pul- posus has been implicated as the primary pain source [10]. Both steroids and non-steroidal anti-inﬂammatory drugs have partial effectiveness in treating pain associated with inﬂammation [11]. When the symptom of pain is thought to result from inﬂammation, it is natural to think that an anti-inﬂammatory agent can be useful for treatment. Therefore, the rationale for using intradiscal steroids is to suppress the inﬂammation within the disc, thereby alleviating the patient’s symptoms [12]. Structurally, intradiscal steroids are thought to promote spinal segment stabilization via further disc degeneration. Yong-Hing and Kirkaldy-Willis described the ‘‘degenera- tive cascade’’ of disc disease [13]. The cascade is divided into three stages based on the amount of damage to the disc and facet joints at a given point in time. This cascade of Curr Rev Musculoskelet Med (2008) 1:103–107 individual motion segment degeneration is thought of as a continuum rather than as three clearly deﬁnable and sepa- rate stages. The ﬁrst and second stages, dysfunctional and instability stages, respectively, are ongoing ﬁssuring or tearing of the outer annulus ﬁbrosus, decline in the amount of nuclear proteoglycan composition, and patients presenting with intense low back pain [14]. The third stage, stabilization, is characterized by endstage tissue damage and attempts at repair. Nucleus pulposus resorption occurs in this stage resulting in worsening intervertebral disc space narrowing, ﬁbrosis, endplate irregularities, and the formation of osteophytes. The body restabilizes the segment and the patient experiences fewer episodes of back pain [13]. Early studies have shown that after intradiscal injection, radial bulges of the disc are decreased and its height is increased, both are signs of spinal stabilization [15]. Additionally, Kato et al. [16] in 1993 concluded that disc- ograms with intradiscal steroid injections bring about a progressive degeneration of the intervertebral disc. Rather than being a deleterious action, the degeneration of the disc results in clinical improvement (i.e., pain reduction). This occurs because the steroids cause a contraction of the tissue and stabilization of the surrounding spinal segment. Aoki et al. [17] followed these studies in 1997 and evaluated histologic changes in intervertebral discs of rabbits after intradiscal injection of corticosteroids. They found that after 24 h, rabbits receiving methylprednisolone acetate injection had degenerated tissue in the nucleus pulposus and inner layer of the annulus ﬁbrosus. They also observed matrix vehicles, an indication of primary tissue calciﬁcation. They concluded that methylprednisolone causes degeneration and primary calciﬁcation in discs. This was proposed as the basis for the clinical improvement in patients where steroids were used within the disc space for the treatment of low back pain and sciatica. Another practical reason for using intradiscal steroids is that the administration of steroids can be performed at the same time as a diagnostic discogram,without added mor- bidity, time, or signiﬁcant expense. Whether or not intradiscal steroids present a signiﬁcant risk to patients remains an area of controversy. The risks of spinal canal ossiﬁcation and calciﬁcation are low as con- cluded by Ito et al. in patients who were followed for 5 years after undergoing discography and betamethasone injection [18]. There have been, however, a few reported cases of necrotic granulomatous lesions associated with intradiscal steroids [19]. While the earlier trials of intradiscal steroids have shown promising potential, more recent trials have been less encouraging. We will review the earlier as well as more recent studies on the use of intradiscal steroid for the treatment of discogenic low back pain.