Chronic low back pain (CLBP) is a pervasive condition that significantly impairs the quality of life of patients by limiting daily activities and overall well-being (1,2). Additionally, anterior column pain, the cause of CLBP, has been theorized to stem from the pain receptors of intervertebral discs. However, recent histological data suggest that the vertebral endplates may play a predominant role, as they manifest up to four times the number of nerve receptors compared with intervertebral discs (3-5).

Overall, vertebrogenic low back pain and discogenic low back pain are considered two entirely dissimilar entities. Discogenic pain arises from the degeneration of the intervertebral disc, particularly the annulus fibrosus, and is transmitted via the sinuvertebral nerve. Discogenic pain accounts for a substantial portion of cases of CLBP, with estimates ranging from 26 to 42% (2-5). It is caused by structural defects, such as annular tears, disc dehydration and the loss of disc height, leading to inflammation, nerve ingrowth and altered biomechanics. Clinically, it presents as axial low back pain worsened by sitting and flexion, with referred pain above the knees in a non-dermatomal pattern and no neurological deficits. Magnetic resonance imaging (MRI) may depict disc desiccation and high-intensity zones, whilst a discography can confirm diagnosis, although this is considered invasive (3-7). On the contrary, vertebrogenic pain is a newer concept linked to the damage and inflammation of the vertebral endplates, innervated by the basivertebral nerve. It is noteworthy that vertebrogenic pain is estimated to affect ~1 in 6 individuals with CLBP in the USA (3-6). It is associated with Modic type 1 or 2 alterations observed on an MRI and results from endplate microtrauma, allowing inflammatory disc material to infiltrate the bone marrow. Symptoms typically involve midline low back pain, which deteriorates in the morning or with activity, with possible referral to paraspinal or gluteal regions. Unlike discogenic pain, it is not aggravated by extension and may present without significant disc abnormalities on imaging (5-7). First-line management for CLBP, including vertebrogenic CLBP, involves nonpharmacologic therapy such as exercise, physical therapy, spinal manipulation and acupuncture, while non-steroidal anti-inflammatory drugs, muscle relaxants etc. are used as second-line therapy (7); however, in a significant portion of individuals, those treatments do not exhibit the desired outcomes (5-7). The main limitations of the conservative management of vertebrogenic CLBP are considered limited long-term effectiveness, the inability to address the source of pain, the risk of dependence on pain medication and the lack of improvement with certain therapies such as traction or transcutaneous electrical nerve stimulation (4-8).

In light of this evidence, interventions have been employed to manage CLBP by specifically targeting the intradiscal space and vertebral endplates, including intradiscal steroid injections (IDSIs) and intraosseous basivertebral nerve radiofrequency ablations (BVAs) (8,9). IDSI involves injecting corticosteroids in the center of intervertebral discs (10), whereas BVA cauterizes the basivertebral nerve within the vertebral body (11,12). There is clinical ambiguity as regards which of these two interventions is superior concerning the treatment of vertebrogenic CLBP. Targeting the basivertebral nerve may be more effective than targeting the disc itself for vertebrogenic pain, as the basivertebral nerve is the primary nerve responsible for transmitting pain signals from the vertebral endplates, which are frequently damaged in cases of vertebrogenic pain, and nerve density is higher in endplates (7-12). To the best of our knowledge, no study in the existing literature to date has performed a direct comparison of IDSI and BVA for the treatment of vertebrogenic CLBP. Thus, the present study aimed to fill this gap in the literature. The present study aimed to compare the efficacy of these two interventions in reducing disability and pain levels in patients with vertebrogenic CLBP, while utilizing the Oswestry Disability Index (ODI) (13), as it is specific for CLBP and easy to use. The present study aimed to provide clinicians with insight into the most effective treatment options for this challenging condition.

Both treatments revealed very promising results in reducing CLBP to levels practically considered complete resolution. In the present study sample, there were only two outliers, one for each method, which reported no difference in symptoms. These patients were excluded from the analysis due to the possible misdiagnosis of discogenic pain as the origin of their symptoms. At this point, it is imperative to underline that excluding 2 patients who were non-responsive may have led to bias in the outcomes and may overstate the effectiveness of the treatments. Notwithstanding, even in the event that those patients were finally included, both treatments resulted in a >90% reduction in pain and disability. In the analysis in the present study, as demonstrated by the data in Tables I and II, an improvement of <50% was considered subjectively moderate. A value >50% was considered notable, and a value <30% was considered as non-notable.

For IDSI (Table I), the mean pre-treatment ODI was 29.9±16.5, which significantly decreased to 14.8±20.4 post-treatment (P=0.0001), representing an absolute reduction of 16.5 and a 66% relative improvement (Figs. 1 and 2). Of note, only 2 patients achieved moderate improvement (<50%). BVA treatment also demonstrated satisfactory results in reducing CLBP (Table II). In the BVA group (n=10), the mean ODI score significantly decreased from 30.1±13.6 before treatment to 10.1±12.6 after treatment (P=0.0023). When both groups were analyzed together, the overall baseline ODI mean was 28.5±15.2, which was reduced to 6.3±8.7 post-treatment, corresponding to a 78% mean reduction in disability. Notably, 90% of the patients experienced significant improvement (>50%) (Figs. 3 and 4).

Covariate analysis (ANCOVA) was conducted to control for potential confounding factors. The adjusted pre-treatment means were 26.7±14.8 for both groups. Covariates utilized in ANCOVA were baseline ODI scores, anxiety that was assessed using the Beck Anxiety Inventory (BAI) (mean ± SD: 12.4±3.5), fear-avoidance score using the Fear Avoidance Beliefs Questionnaire (FABQ) (18.9±5.2), age (47.2±8.1 years), sex (male:female, 9:13) and BMI (26.8±3.4 kg/m²). The adjusted post-treatment mean values were 8.7±6.1 for IDSI and 5.9±4.8 for BVA, with a statistically significant between-group difference (P=0.046). Overall, there appears to be a small improvement in BVA in the present study; however, owing to the small sample size of our patients, the statistical power of our research was 40%, which is not sufficient-enough for highly credible outcomes.

Both interventions in the present study resulted in a notable improvement for >80% of the patients treated and at least a moderate reduction in disability (between 30 and 50%) for >90% of them (Figs. 2 and 3). Furthermore, a minimal, yet considerable advantage was demonstrated in the analysis for BVA vs. IDSI, with the obvious caveat of the low statistical power of the research. Notably, both treatments resulted in post-treatment ODI scores of <10, 75% for IDSI and 80% for BVA, which translates to the almost complete resolution of symptoms (Figs. 1 and 2). Another noteworthy element is that 2 patients (1 patient from each group) exhibited no difference pre- and post-intervention, which may be attributed to unknown factors or that the treatments themselves could be ineffective in a percentage of patients (Fig. 1, Fig. 2, Fig. 3 and Fig. 4); it would be of interest to evaluate this finding in a larger patient sample.

Consequently, both IDSI and BVA could be considered viable and highly recommended options for immediate pain reduction in patients with CLBP; however, due to the methodological weaknesses of the present study, the findings can be considered as hypothesis-generating.

The comparative analysis of IDSI and BVA for the treatment of vertebrogenic CLBP can provide several critical insights. Both treatments have demonstrated efficacy in reducing pain and disability; however, their mechanisms and clinical outcomes vary, highlighting the need for a personalized approach in managing CLBP. The mechanisms of action for IDSI and BVA are distinct and crucial; although they are used for the same pathologic entity (CLBP), both demonstrate similar and high efficacy. IDPI utilizes the anti-inflammatory properties of locally infused corticosteroids in the body of the intervertebral disc (9,10).

Contrariwise, BVA targets the nerve pathways responsible for pain transmission on the vertebral endplates themselves, providing a more direct approach to pain relief. This method has exhibited consistent results across a broader range of patients, making it a reliable option for many patients (21-25). The direct disruption of pain signals can provide long-lasting relief, which is crucial for managing chronic conditions (4,5).

The difference in both the area and mechanism of treatment, compared with the similar effectiveness of IDSI and BVA, raises the question of which pain receptors are involved and what exactly the pathologoanatomical substrate of vertebrogenic CLBP is. If either disc or vertebral pain receptors are prevalent in CLBP, then the expected result of one of the treatments used herein would clearly be highly superior to that of the other, which was not the case reported in the present study or in the existing literature. As a result, further large-scale studies are warranted to investigate and differentiate the factors associated with CLBP.

Both treatments may trigger potential side-effects that need to be carefully managed. The side-effects of IDSIs, such as transient pain and increased blood sugar levels, require monitoring, particularly in patients with diabetes (9,10). BVAs, while generally well-tolerated, carry risks of nerve damage and infection, necessitating precise techniques and patient education about potential risks (23-25). Clinicians should weigh the benefits and risks of each treatment option, considering patient preferences and the likelihood of response. The selection between IDSI and BVA should be made by a comprehensive clinical assessment, ensuring that the selected treatment aligns with the specific condition and goals of the patient. The presence of outliers in both treatment groups suggests that neither IDSI nor BVA is universally effective for all patients. It should be emphasized that the exclusion of these patients represents a methodological flaw that can distort the reported outcomes. The variability in responses highlights the requirement for careful patient selection on the basis of specific clinical criteria. Factors, such as the nature of the pain, previous treatment responses and patient comorbidities should guide treatment decisions. Personalized treatment plans can optimize outcomes by matching patients with the most appropriate intervention. Given the various notable limitations of the present study, it is not facile to propose a standard treatment algorithm for vertebrogenic CLBP. Nonetheless, it can be denoted that these two interventions can be utilized in patients aged 18-70 years with no considerable comorbidities and persistent LBP for a period of >3 months where conservative treatment has failed, whist the selection of employing either IDSI or BVA as treatment of choice lies in the attending physician as they both seem as viable fruitful treatment options. In the case of the failure of one method, the attending physician may consider utilizing the other treatment method as an alternative; however, this practice can be the objective of further research.

Further research is essential to refine these treatments and identify predictors of response. Perusing the existing literature, no other study could be retrieved comparing these two treatment methods for CLBP, whilst only a limited number of review articles could be found presenting the various minimally invasive treatments for CLBP that already exist. Hence, prospective studies with larger sample sizes and randomized controlled trials are vital and could provide more definitive evidence on the comparative effectiveness of IDSI and BVA. Additionally, exploring combination therapies and adjunctive treatments may offer new avenues for patients who do not respond to either intervention alone.

For a more balanced interpretation of the outcomes, it is vitally important to acknowledge the copious major limitations of the present study which include the following: The retrospective design of the study, the small sample size, the exclusion of outliers, the absence of a placebo or sham control group, methodological flaws, reliance on subjective data (ODI scores), limited follow-up duration and low statistical power. At this point, the necessity for further larger-scale studies in this field is accentuated, as the present study can be considered as thought-provoking material.

In conclusion, both IDSI and intra-osseous BVA appeared to effectively reduce disability. The IDSIs demonstrated a higher percentage of complete symptom resolution, whereas BVAs provided more consistent significant improvements across patients. Despite potential side-effects, both treatments can provide substantial pain relief, potentially underscoring the significance of personalized treatment plans. Notwithstanding, in spite of both treatments exhibiting potential, taking into account the various considerable limitations of the present small-scale study, the findings should be regarded as hypothesis-generating, highlighting the requirement for further pertinent research in this area.