Caries progression and dentine changes

• Dentine is one of the calcified connective tissue within the body. The inorganic part of it is made out of calcium hydroxyapatite. The inorganic part is deposited on a type 1 collagen framework radiating from the pulp to the enamel. The collagen forms fibrils that have many cross-links to provide a stable framework that is resistant to degradation
  
  
• Dentine comes from the cells of the dental papilla
  
  
• Dentine is made up of very small (smaller than those found in enamel) 10 nm calcium hydroxyapatite crystals with a carbonate ion in 1 out of 5 the phosphates ions. The carbonate ions makes the dentine more susceptible to be dissolved by acids.
  
  
• Half of the dentine by volume is made up of hydroxyapatite and it is arranged to form tubules that radiate outwards. Within the dentinal tubules lie an odontoblast process along with dentinal fluid (consisting of albumins, transferrins, tenascins and proteoglycans)
  
  
• Dentine, unlike enamel, has the ability to react to the progression of caries due to the presence of odontoblasts. Odontoblasts can respond to irritation by depositing minerals in the dentinal tubules.

Figure 2: Carious dentine

• Caries progression is governed by the intensity of the bacterial acid challenge, the structure of the dentine and the response of dentine. Dentine caries is mainly the result of slow chronic caries
  
  Figure 3 : Location of dentine sclerosis
  
  
  
• The acids produced by carious bacteria dissolve away the inorganic calcium hydroxyapatite crystals. As a result the crystals become smaller and areas that are porous form
  
  Figure 4: Caries breaking down dentine and making it porous
  
  
  
  
• The increased porous nature of the calcium hydroxyapatite lattice and the dentine tubules allow the acids/bacteria to move further into the tooth and do extensive damage. The first group of bacteria is called pioneer bacteria
  
  Figure 5: Pioneer bacteria travelling into dentine tubules
  
  
  
• Underlying dentine is necessary to support the enamel. If the underlying dentine is degraded, it will cause the enamel to be easily broken.
  
  
• Advanced dentinal chances include the decalcification of the walls and the joining of the tubules. The tubules get filled with necrotic debris and adjacent tubules get distorted
  
  
• The exposed collagen fibres that form as a result of the acid attack converts reversibly to their precusors form. Therefore, remneralisation can occur the collagen fibres can reorganize and form a structural framework (Miyauchi et al, 1978)
  
  
• However extensive damage to the collagen fibres results in permanent loss of the collagen framework and irreversible loss of the dentine structure. This is due to the fact that as the caries continues, the exposed collagen becomes increasing less resistant to the bacterial acids

• Do the different type of dentine react differently to the carious progress? or do they as a whole react only in one main manner?
• With regards to the earlier question, do people with dentinogensis imperfecta II/III display markedly different dentine changes ?
  
• At what point does the collagen matrix stop having the abilty to repair/reform itself in order for dentine to regrow?
• Does the dentine still continue to react even when the pulp has been exposed ? or does the exposure of the pulp signal the end of dentines resistance to the caries?
• Is it possible to introduce fibroblast (that make type 1 collagen) or specific enzymes into teeth dentine and hope that they reasemble some of the collagen matrix and enable "irreversibly" damaged areas to regow?
• Most importantly, how significant is the "S" shape of the dentine tubule in determining how dentists perform restorative treatments? Do they account for the "S" shape and drill according ? Or do they merely adopt a fixed approach without consideration for the tubules ?
• More importantly, is it possible to intoduce chemicals into the pulp via the dentine? so as to intitiate the odontoblast to make more dentine, esp if the caries are rampant ?
  

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