Dental pulp health is commonly linked with periapical pathology, as bacterial invasion of the dental pulp would commonly lead to an inflammatory lesion around the apex of the tooth.
Pulp reacts to irritation with inflammation, however the rigid dentine walls do not allow pulp to increase in volume. The pulp is protected by laying down tertiary dentine in tubules.
- When a stimuli applied to dentine it causes an increase blood flow as well as causing pain.
- The resulting nerve excitation results in release of neuropeptides such as substance P & CGRP.
- These peptides cause arteriole dilation and increased capillary permeability. This causes fluid to flow out into the tubules and protects toxins from diffusing inwards.
- Inflammatory reactions can be reduced by sympathetic nerves but are also modulated by paracrine and local hormones.
Aetiology of pulpitis
Microbial:
- Caries
- Exposed dentine (TSL – tooth surface loss)
- Periodontal Disease
Trauma
Iatrogenic Factors:
- Dehydration of dentine
- Restoration placement
- Cements and filling materials
- Marginal leakage
- Therapeutic irradiation
- Orthodontic treatment
Systemic Influences:
- Nutritional deficiencies
- Tumour spread / metastases
Operative procedures can cause a reaction in the pulp. Preparations with rotary instruments heat the pulp increasing pulpal blood flow ( natural pulp response to lower the temperature), when extensive, this can damage the pulp. The use of LA vasoconstrictors exacerbates the effect of the heat by preventing blood flow
Reactionary Dentine VS Reparative Dentine
The pulp can protect itself by the deposition of tertiary dentine. Tertiary dentine can be classes as reactionary or reparative dentine.
Mild injury results in the production of reactionary dentine, whilst more severe injury results in the production of reparative dentine.
This is because:
- Mild injury will not damage primary odontoblasts so reactionary dentine is deposited.
- More severe injury results in the damage of primary odontoblasts, the body reacts by causing an up-regulation of progenitor cells which in turn produce secondary odontoblasts. This leads to the formation of reparative dentine.
Both types of tertiary dentine are rapidly laid down, contain fewer tubules, and are less well mineralised, relative to secondary dentine.
Time frame of dentine-pulp reactions to moderate dentine loss:
TIME AFTER INJURY | RESPONSE |
---|---|
1 second | Nociceptor activation |
1 minute | Early inflammatory response: kinins, prostaglandins, peptides and vasodilation |
10 minutes | Nociceptor Sensitization: oedema, extravasation of fluid and polymorph migration |
100 minutes | Enzyme activation & monocyte presence |
1 day | Nerve sprouting |
1 week | Tissue repair – tertiary dentine |
Variable | Completion of repair and recovery |
The apical periodontium consists of cementum, PDL and alveolar bone surrounding the root apex.
Apical periodontitis = pulpal related inflammation of the attachment apparatus of the tooth. It can lead to considerable bone loss.
Aetiology:
- Pulpitis – local pulpitis may cause inflammatory changes in the apical periodontium, when increased pulpal pressure is reduced symptoms should clear.
- Pulp Necrosis – after trauma chemotactic activity and immunogenic response results, this leads to collections of neutrolphils and macrohpages which engulf everything causing pulp necrosis
- Infection of the root canal – crown is the main entry point for bacteria however can also enter via apical foramen and accessory canals through haematogenous spread of bacteria
- Infection of periapical tissues – some bacteria can infiltrate granulomas in periapical tissue and can be unaffected by host inflammation and immune response
Once a pulp is damaged beyond repair, the bodies natural defences can no longer compensate, necrosis and periapical periodontitis will inevitably occur, unless the pulp is extirpated followed by endodontic therapy
Endodontic Microbiology
- Around 700 species of bacteria found in oral cavity. Any individual can have 100-200 species
- When the root canal is infected coronally, infection spreads apically until the bacteria stimulates periapical tissues leading to apical periodontitis
- Endodontic infections have a polymicrobial nature dominated by obligate anaerobic bacteria
How do microorganisms enter root canal system?
- Caries
- Dental Trauma
- Leaky restorations
- Restorative procedures
- Cracked tooth
- Periodontally (accessory canals)
Infection and Microorganisms
- Intraradicular microorganisms are usually constrained to the root canal due to the defence barrier.
- If the defence barrier is broken then this may develop into an extraradicular infection and may cause an acute apical abscess with purulent inflammation in the periapical tissue.
- Dominant microorganisms present are anaerobic.
Intraradicular primary infections are caused by:
- Black pigmented gram negative anaerobic rods such as Prevotella & Porphyromonas
- Tanerella Forsythia
- Fusobacterium
- Gram-negative coccobacilli
- Spirochetes – Treponema
- Gram-positive anaerboc rods
- Gram-positive cocci – streptococcus & enterococcus Faecalis
Extraradicular infections are caused by:
- Actinomyces
- Treponema
- Treponema Forsythia
- Porphyromonas endodontalis
- Porphyromonas gingivalis
- Prevotella
- Fusobacterium Nucleatum
- Propionibacterium propionicum
Some bacteria may persist after intracanal disinfection during RCT causing re-infection. They are resistant to antimicrobial treatment and can survive after biomechanical preparation.
Gram negative anaerobic rods include:
- Fusobacterium Nucleatum
- Prevotella
- Campylobacter Rectus
Gram positive bacteria include:
- Streptococcus (mitis, gordonii, anginosus, oralis)
- Lactobacilli
- Staphylococci
- E-faecalis
E- Faecalis & Yeast (C-albicans)
These are normal intestinal organisms,that are also found in the oral cavity and gingival sulcus. When this bacterium is present in small numbers, it is easily eliminated; but if it is in large numbers, it is difficult to eradicate. E.faecalis have distinct features deeming it an excellent survivor in root canals. They are able to:
- Live and persist in poor nutrient environment
- Survive in presence of medications (CaOH) and irrigants (sodium hypochlorite)
- Form biofilms in medicated canals
- Invade fluids in dentinal tubules and adhere to collagen
- Convert into viable and non-cultivable state
- Acquire antibiotic resistance
- Survive in extreme environments with low pH, high salinity and high temperatures
- Endure prolonged periods of starvation and use gingival crevicular fluid
External resorption is the process which consist of removal of dental hard tissues by osteoclasts. The resorption is identical in its developmental process and is divided in categories that are clinically relevant:
External Surface Resorption:
- Surface resorption, normally self-limiting following trauma and heals fully in a couple weeks.
External Inflammatory Resorption:
- Following infection or trauma and results in long term progressive loss of tooth tissue
- Positive response to treatment
- Common in immature/young teeth, may occur is excessive pressure is applied to the tooth for a long time
External Replacement Resorption:
- Replacement of the tooth by bone
- Inflammation is absent
- Associated with ankylosis and trauma
- Treatment is difficult and directed towards the resorption
External Cervical Resorption:
- Localised in the cervical area of the root
- Tooth is still vital and rarely affects pulp
- Cervical resorption is assumed to be primarily inflammatory in aetiology, caused by the periodontal flora, though this does not explain cases where multiple lesions affect several teeth
Internal resorption must follow loss of the pre-dentine layer separating pulp from dentine, but the causes of this loss are unknown. A degree of inflammation or increased pulpal pressure are likely to be factors.
Internal Surface Resorption
- Comparable to external surface
- Osteoclastic activity and self-limiting
Internal Inflammatory Resorption
- Ovoid or fusiform of pulp chamber
- Enlargement expands in an apical and lateral direction
- May be associated with chronic pulpal inflammation
Internal Replacement Resorption
- Rare, more irregular enlargement of the canal space
- May get pulp canal obliteration
Ricketts D. Management of the deep carious lesion and the vital pulp dentine complex. Br Dent J 2001;191 (11):606-610 https://www.nature.com/articles/4801246;
Sigurdsson A. Pulpal Diagnosis. Endodontic Topics 2003;5: 12-25 https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1601-1546.2003.00024.x
Lakshmi Narayanan L, Vaishnavi C. Endodontic microbiology J Conserv Dent. 2010 Oct-Dec; 13(4): 233–239. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3010028/
Haapasalo M, Endal U, Zandi H, Coil J. Eradication of endodontic infection by instrumentation and irrigation solutions. Endodontic Topics 2005:10:77-102 https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1601-1546.2005.00135.x
Gulabivala K, Patel B, Evans G, Ng YL. Effects of mechanical and chemical procedures on root canal surfaces. Endodontic Topics 2005:10:103-122 http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.537.1354&rep=rep1&type=pdf
Darcey, J. and Qualtrough, A., 2013. Resorption: part 1. Pathology, classification and aetiology. British dental journal, 214(9), pp.439-451. https://www.nature.com/articles/sj.bdj.2013.431
Darcey, J. and Qualtrough, A., 2013. Resorption: part 2. Diagnosis and management. British dental journal, 214(10), pp.493-509. https://www.nature.com/articles/sj.bdj.2013.482
See also Pulp Management