PULPAL RESPONSE TO PULP CAPPING AGENTS
(VITAL PULP THERAPY):
Anticipating Pulpal Reaction To Dental Materials:
1] ability of the dental material to stimulate tissue repair;
2] ability of the dental material to seal the interface between the tooth preparation and the restoration;
3] role of microbes in pulpal disease (from caries, oral environment) à maintenance of asepsis;
4] role of tooth preparation procedures in pulpal disease.
Influence Of Bacteria On Pulpal Healing:
The classic study by Kakehashi et al. (1965) clearly showed the pathologic role of bacteria in pulpal diseases.
|Pulpal exposures were made in …|
|Normal rat||Germ-free rat|
|8 days later||Partial necrosis of dental pulp||—|
|14 days later||Complete necrosis & periradicular abscess||—|
|32 days later||Complete necrosis & periradicular abscess||Intact dentin bridge with normal pulp tissue beneath newly-formed dentin.|
This landmark study showed that bacterial infection of dental pulp was a critical etiologic factor for pulp necrosis. Thus, in Vital Pulp Therapy (VPT), the factors that modify healing of the exposed pulp are:
- Methods to reduce/ eliminate bacteria à pulpal healing must occur in an environment free of microbes.
- Duration of pulp exposure: Clinical studies by Cvek (1978) and Mejare (1993) showed that in younger patients, the superficial pulp is resistant to bacterial invasion (bacteria invaded only upto 2 mm at the end of 7 days. Partial Pulpotomy with Calcium hydroxide (Ca[OH]2) dressing can give radiographic success of 93% at follow-up of 4.5 yr.
- Size of pulp exposure: Cvek (1978) performed partial pulpotomies after traumatic crown fractures and pulp exposures of 0.5-4 mm. The success was 96% with an average follow-up of 31 months in both mature and immature teeth. Hence the exposure size may not be a major factor in the success of VPT.
- Hemostatic control:
Bleeding from an exposed pulp is due to –
a] Pulpal inflammation in response to bacteria and toxins from the carious dentin, and;
b] Trauma from the caries removal procedure.
Importance of hemostasis –
a] Bleeding leads to compromised seal and is not conducive to the formation of tertiary dentin bridging or maintenance of pulp vitality, and;
b] Open/ cut vessels may carry the pulp capping materials deep into the pulp, and block the blood vessels and reduce blood flow. This causes delayed healing. The caustic nature of Ca[OH]2 may cause perivascular foci of mummification and inflammation (Ca[OH]2 emboli).
- Method of placement: The pulp capping material must be placed gently over the exposure site. If placed deeply, the deeply impacted particles of the pulp capping material leads to reduced success of VPT. The material (Ca[OH]2) may be phagocytized and may be retained indefinitely by macrophages and giant cells in the area beneath the dentin bridge.
- Quality of dentin bridge (the use of appropriate dental materials):
a] Ca[OH]2 – The integrity of dentin bridge is suspect due to the porous nature (tunnel defects) at 4 weeks, that may continue to form overtime (90 days). These porous/ incomplete dentin bridges are not a favourable clinical outcome because any breach of the restoration seal leads to bacterial ingress.
b] Dentin bonding agents – It was theorized that etching and bonding will adequately seal the exposure site with a hybrid layer. But this theory is no longer accepted because dentin bonding agents do not express any proteins/ signals that are required for the induction of odontogenesis.
c] Mineral Trioxide Aggregate (MTA) – This Portland cement-based material gives a good seal and dentin bridging due to its ability to dissolve bioactive dentin matrix components, and the activation of transcription factors that act as signaling molecules for pulp repair.
|Benefits of Ca[OH]2 in VPT||Drawbacks of Ca[OH]2 in VPT|
|Antibacterial||Tunnel defects (porous dentin bridge)|
|Hard tissue barrier –
® Ca[OH]2 (high alkalinity ) extracts the fossilized (sequestered) growth factors and bioactive dentin matrix components à Induction of dentin regeneration at the site of pulp exposure.
® Ca++ ions released from Ca[OH]2 stimulate the fibronectin synthesis by pulp stem cells à induction of differentiation of pulp progenitor cells into mineralized tissue-producing cells.
|Inadequate mechanical strength|
|No adhesion to dentin
|High solubility à leads to gap formation beneath the base material.|
|Benefits of MTA in VPT|
|Hard tissue barrier –
MTA is highly alkaline à this enables the extraction of fossilized (sequestered) growth factors and bioactive dentin matrix components à Induction of dentin regeneration at the site of pulp exposure.
|Dentin bridge is dense, thicker and continues as compared to Ca[OH]2.|
|Has currently replaced Ca[OH]2 as the material of choice in VPT.|
Molecular Responses To Pulp Exposure:
In response to pulpal injury, there is the upregulation of genes/ markers.
|Gene/ Marker||Released by||Function|
Dentin Sialophosphoprotein (DSPP)
|Nestin||Odontoblasts, other pulp cells
|Transforming Growth Factor (TGF)|
|Bone Morphogenetic Protein – 2 (BMP-2)|
|Dentin Matrix Protein – 1
|Notch Signaling Proteins
|Polymorphonuclear (PMN) lymphocytes||Differentiation of pulp stem cells into odontoblast-like cells and perivascular cells.|
|Adrenomedulin||Vasodilator peptide hormone (uncertain role).|
[From: Seltzer & Bender’s Dental Pulp].
- Seltzer & Bender’s Dental Pulp. 2nd
- Ingle’s Endodontics. 6th
- Cohen’s Pathways of the Pulp. 10th
- Walton & Torabinejad. Principles & Practice of Endodontics.
- Grossman’s Endodontic Principles & Practice.
- Mount GJ, Hume WR. Preservation and restoration of tooth structure. Barcelona, Spain: MOSBY International. 1998.
- Inoki R, Kudo T, Olgart LM. Dynamic aspects of dental pulp. Cambridge, Great Britain: Chapman and Hall. 1990.
- Orban’s Oral Histology.