Comments on the Evidentiary Framework of the EFCD‐ESE‐ORCA Guideline on Deep Caries Management

Dear Editor,

I read with great interest the recently published article “Deep Caries Management: EFCD‐ESE‐ORCA S3‐Level Clinical Practice Guideline” by Schwendicke et al. While the effort to standardise clinical decision‐making through a structured evidence‐based process is commendable, I wish to express methodological and scientific concerns regarding the evidentiary framework underlying several of the guideline's central recommendations.

Although each of the four clinical questions addressed by the working groups raises important issues worthy of discussion, for reasons of brevity I will focus specifically on the question concerning caries removal strategies in deep carious lesions.

The guideline states in the Introduction: “Importantly, dental caries is not an infectious disease that requires eradication of bacteria, but a behaviourally‐modifiable condition…”.

This assertion is not merely therapeutic guidance; it is fundamentally a biological claim. However, such claims cannot be adequately established through randomised clinical trials or survival‐based outcome studies alone. Whether residual bacteria within the remaining “firm dentine” remain viable and pathogenic, whether pulpal inflammation persists despite the absence of symptoms, and whether bacterial invasion of pulpal tissues may still occur after selective excavation are fundamentally histopathological and microbiological questions.

Nevertheless, the evidentiary framework of the guideline is constructed almost entirely around PICOTS‐based clinical outcome studies emphasising tooth survival, loss of vitality, and patient‐reported outcomes, whereas histopathological evidence appears largely absent despite its direct relevance to the biological mechanisms under discussion.

This creates an important methodological problem: clinical survival does not necessarily equate to biological health. Teeth may remain asymptomatic and functional for years while harbouring persistent infection or chronic inflammatory pulpal changes.

When describing the four available caries removal techniques, the guideline states that “non‐selective removal to hard dentine (NSE)… eliminates all demineralised dentine, even if bacteria‐free.”

This concept derives largely from the influential propositions of Massler, who suggested that bacterial invasion is confined mainly to superficial softened dentine, whereas deeper caries‐affected dentine remains structurally intact, bacteria‐free, and potentially remineralisable. He further proposed that residual bacteria left beneath restorations become inactive if an adequate coronal seal is achieved (Massler 1967, 1969).

These concepts strongly influenced modern operative dentistry and underpin the distinction between “infected” and “affected” dentine. However, direct histopathological evidence supporting these assumptions was not provided.

In contrast, extensive histological and microbiological investigations by Langeland and colleagues demonstrated the consistent presence of bacteria in deeper layers of carious dentine and suggested that even well‐sealed restorations do not necessarily eliminate the biological risks associated with residual infection (Langeland 1967, 1981, 1987; Langeland et al. 1975). More recently, an in vivo human study further indicated that subclinical pulpal inflammation may persist after selective excavation, and that sealing over infected dentine does not necessarily arrest residual bacterial activity (Ricucci et al. 2020).

The guideline appears to acknowledge the necessity of bacterial elimination in the section on vital pulp therapy, stating that: “The pulp possesses an intrinsic capacity for healing if the bacterial challenge is eliminated and the tooth is properly restored with a biocompatible material.” However, this statement is difficult to reconcile with the simultaneous endorsement of intentionally leaving carious dentine adjacent to the pulp.

If bacterial elimination is indeed necessary for healing, the biological rationale for selective excavation would require substantially stronger histopathological substantiation than clinical follow‐up studies alone can provide.

The guideline states: “Evidence supports selective (SE) or stepwise caries removal (SW) over non‐selective removal (NSE) to reduce the risk of pulp exposure in deep caries.”

Throughout the document, pulp exposure is repeatedly framed as a procedural complication attributable to the clinician and associated with a poorer prognosis. However, this interpretation may oversimplify the underlying pathology.

In deep carious lesions, cautious excavation with hand instruments may simply reveal an already existing communication produced by the carious process itself rather than create an iatrogenic exposure. From a biological perspective, the operative procedure may disclose the true extent of pulpal involvement rather than induce it.

In this context, it is difficult to understand why endodontists should regard pulp exposure primarily as a complication to be avoided, especially when contemporary evidence indicates that direct pulp capping and other vital pulp therapy procedures can achieve favourable long‐term outcomes when appropriately performed (Bogen et al. 2008; Ricucci et al. 2023).

The guideline itself acknowledges substantial uncertainty, repeatedly citing “very low” or “low” certainty evidence, heterogeneity among studies, and limited long‐term data.

The six randomised clinical trials (RCTs) and the single cohort study forming the basis of the recommendations raise concerns regarding their relevance and methodological robustness. Included studies involved predominantly deciduous teeth (Orhan et al. 2010) despite the guideline's focus on permanent dentition, immature permanent teeth treated with minimally invasive techniques emphasising treatment time and patient acceptability rather than pulpal biology, and studies with extremely small sample sizes (Orhan et al. 2010; Duman 2021; Rando‐Meirelles et al. 2013).

Most importantly, the observation periods appear manifestly insufficient for evaluating a chronic and slowly evolving pathological process such as carious disease. Follow‐up periods ranged only from 12 to 24 months, yet pulpal degeneration may progress silently for many years before producing overt symptoms. Consequently, the absence of symptoms after such short observation periods cannot reasonably be considered evidence of pulpal healing or long‐term biological stability.

More broadly, the guideline illustrates a growing problem in evidence‐based medicine and dentistry: the conflation of clinical effectiveness with biological validity. GRADE‐based hierarchies inherently privilege randomised clinical trials while assigning limited weight to mechanistic, microbiological, and histopathological evidence. However, in endodontics and cariology, many fundamental biological questions cannot ethically or practically be resolved through RCTs alone.

Histopathological examination frequently represents the closest attainable reference standard for assessing pulpal inflammation, whereas symptoms, sensibility testing, and radiographic findings remain imperfect surrogate markers of tissue status. Clinical guidelines on pulpal management should therefore integrate histopathological, microbiological, mechanistic, imaging, and translational evidence alongside clinical outcome studies.

Without such integration, there is a substantial risk that recommendations become driven primarily by short‐term clinical survival while the underlying biological processes remain insufficiently understood. Given the increasing international influence of these guidelines on clinical education, standards of care, and medico‐legal expectations, these issues deserve open scientific discussion.

Conflicts of Interest

The author declares no conflicts of interest.

Data Availability Statement

The author has nothing to report.