Secondary vs Tertiary Dentine: Classification and Clinical Significance
Core Distinction
Secondary dentine forms continuously throughout life after tooth eruption and root completion as a physiological process, while tertiary dentine forms only in response to pathological stimuli such as caries, trauma, or restorative procedures. 1, 2
Secondary Dentine
- Physiological formation: Begins after root formation is complete and continues at low mineralization levels throughout the tooth's lifetime 1
- Structural similarity: Has essentially the same tissue structure as primary dentine, just formed at a different developmental stage 1
- Continuous deposition: Produced by the original odontoblast layer in the absence of pathology 1
- Not sclerotic: Secondary dentine maintains normal tubular architecture and is not associated with tubular occlusion 3
Tertiary Dentine: Two Distinct Subtypes
Reactionary Dentine
- Formed by surviving odontoblasts: Secreted by existing primary odontoblasts that remain viable after mild injury 4, 2
- Maintains tubular continuity: Tubules are continuous with secondary dentine, though may be irregularly arranged and sparsely distributed 2
- Mechanism: Does not require release of TGF-β or BMPs from dentine matrix for mineral deposition, though these factors influence organization 4
- Clinical context: Occurs with unexposed medium/deep caries and heavily restored teeth where the odontoblast layer survives 2
Reparative Dentine
- Formed after odontoblast death: Produced by newly differentiated odontoblast-like cells derived from pulpal progenitor cells 1, 2
- Atubular or poorly tubular: Lacks the characteristic tubular features of genuine dentine; more closely resembles dystrophic calcified tissue or pulp stones 2
- Not true regeneration: Represents a repair response producing calcified scar tissue by pulpal fibroblasts, not physiological dentine regeneration 2
- Clinical appearance: Often amorphous, may entrap pulpal remnants, and is lined by fibroblasts and collagen fibrils rather than organized odontoblasts 2
Sclerotic Dentine: A Functional Subtype
Sclerotic dentine is not a separate category but rather a modified form of reactionary tertiary dentine characterized by tubular occlusion. 3
- Early response mechanism: Deposited during early stages of dentinal injury before significant odontoblast death 3
- Biochemical changes: Characterized by amplified collagen synthesis and increased alkaline phosphatase activity in the odontoblastic cell layer 3
- Protective barrier: Forms under the sclerotic zone after odontoblast destruction, serving as the first line of defense 3
- Location: Positioned between the injury site and subsequently formed reparative dentine 3
Molecular Signaling Pathways
- TGF-β and BMP release: Fossilized growth factors sequestered in dentine matrix are released during carious attack, injury, or cavity preparation 4, 5
- Wnt/β-catenin pathway: Not required for reactionary dentine formation, but exogenous activation enhances tertiary dentine secretion 4
- Distance-dependent signaling: Residual dentine thickness influences the effectiveness of bio-active component diffusion and cellular signaling 5
Clinical Management Implications
- Reactionary dentine formation: Can be enhanced by cavity-conditioning agents and careful material selection that promote controlled release of matrix-bound growth factors 5
- Reparative dentine expectations: Clinicians should recognize that hard tissue formed after pulp exposure represents repair (calcified scar), not true dentine regeneration 2
- Success criteria: Clinical procedures inducing hard tissue formation may successfully reduce hypersensitivity and bacterial exposure, but do not regenerate physiological dentine 2
- Monitoring requirements: Follow-up radiographic examinations at three months, six months, one year, and annually for three years are recommended for teeth with significant wear or injury requiring treatment 6
Critical Clinical Pitfall
The most important caveat is that what clinicians often call "reparative dentine regeneration" is actually a fibrotic repair process producing atubular calcified scar tissue, not functional dentine. This distinction matters for setting realistic treatment expectations and understanding the biological limitations of current pulp-capping procedures. 2