Ellen Berggreen
Professor, ph.d. The Department of Biomedicine, University of Bergen, Norway. ORCID 0000-0001-6077-943X
Inge Fristad
Professor, ph.d. Department of Clinical Dentistry, University of Bergen, Norway. ORCID 0000-0002-3054-6501
Headlines
External irritation may cause symptomatic or asymptomatic pulp inflammation
Inflammation may be spatially limited, but if the irritation is not removed, will lead to progressing necrosis
Degenerative changes occur even in healthy dental pulp tissue with age
Pulpal complications of caries, extensive wear or other external irritation may result in symptomatic or asymptomatic inflammation, followed by partial or progressing the pulp tissue degradation and necrosis. Appropriate treatment of diseased pulp aim to preserve the vitality of the pulp, either completely or partially, and can thus be regarded as preventive endodontics. Understanding of the physiology and pathology of dentin-pulp complex is a prerequisite for proper diagnosis and treatment choice. This review describes the basic structure and physiology of the healthy dental pulp and the principles of the initiation and progression of inflammatory reactions in the low-compliance environment of pulp chamber and root canals. The mechanisms of pain and hypersensitivity, as well as the means that the dentin-pulp complex may react to a repeated or persistent pain-producing irritation of the vital pulp, are also discussed. The chosen treatment modalities may vary from caries excavation and cavity sealing, partial or complete pulpotomy to pulpectomy, and will be discussed in detail in other articles in this issue dealing with the diagnostics, vital pulp therapies and emergency treatment.
Even though dentin is mineralized and the pulp a loose connective tissue, they form a developmentally interdependent and functionally integrated continuum, often referred to as the dentin-pulp complex, where physiologic and pathologic reactions in one will also affect the other. Whereas dentin forms the main body of the tooth, providing support to enamel, resilience under occlusal loads, and physical protection of the pulp against microbes and other noxious substances, the pulp tissue readily reacts to the external irritation, initiating and orchestrating the defensive reactions that aim to keep the tooth functional and protect it from microbial invasion.
Dentin
Dentin is mineralized collagenous tissue, a nanocrystalline-reinforced collagen biocomposite, with 70 w-% (55 vol-%) biological hydroxyapatite (Ca10(PO4)6(OH)2) and 20 w-% (30 vol-%) organic components []. Major part of dentin is intertubular, formed by the dentin-forming odontoblasts at the dentin-pulp border. Tubular density in root dentin is lower than in coronal dentin, especially in the most apical part []. Peritubular (intratubular) dentin forms in a regular circular manner on the walls of the dentinal tubules.
Dentin-enamel junction (DEJ) provides the mechanical attachment of enamel to dentin. Together with the outermost mantle dentin with a gradual change of the mineralization rate towards the pulp, they create a 500 m resilience zone necessary to prevent fractures under high occlusal forces [].
Primary dentin formation (primary dentinogenesis) occurs during the formation and growth of the bulk of the crown and root, forming the main portion of dentin. Thereafter, dentin formation continues as secondary dentin at much slower rate throughout life, leading to gradual obliteration of the pulp chamber and root canals [].
Tertiary dentin is formed as a response to external irritation, including wear and erosion, trauma, caries, cavity preparation and chemical irritation. The growth factors and other bioactive molecules present in mineralized dentin, liberated during caries or wear, are believed to initiate and control the tertiary dentin formation []. Tertiary dentin increases the mineralized barrier thickness between external irritation and pulp tissue, aiming to retain the pulp tissue vital and non-infected. There are two kinds of tertiary dentin, namely reactionary dentin, formed by original odontoblasts, and reparative dentin, formed by newly differentiated replacement odontoblasts []. Reactionary dentin is tubular and relatively similar to secondary dentin in structure, while reparative dentin (also called fibrodentin or even calcified scar tissue [] is believed to be relatively impermeable, forming a barrier between tubular dentin and pulp tissue.
Pulp tissue and its homeostasis
Odontoblasts are the outermost cells of the pulp, forming a barrier between the pulp and dentin. This barrier may be disrupted as a response to trauma, dentin preparation or caries. Odontoblasts leave behind dentinal tubules, in which highly mineralized peritubular dentin is formed, leading to tubule occlusion that may be accelerated during external irritation [].
The dental pulp tissue is a loose connective tissue well supplied by blood vessels and nerves. The connective tissue comprises the interstitial fluid and collagen-dominated matri
