Overview

Dental caries, also known as tooth decay, is the most common non-communicable disease worldwide. Dental caries is the result of microbial activities that induce the progressive localised destruction of the teeth.¹ They are the major causes of pulpal inflammation (pulpitis) and irritation. The bacteria invade deeply into the dentin (a hard layer behind enamel) and the pulp, thus irritating the pulp, causing inflammation that could be mechanical, thermal, and chemical. 

The outcome of pulpal insult is a dynamic process that depends on the invading microorganism and the host's response to it, which includes inflammation and immunity.² The inflammation, which is localised, can progress to pulpal necrosis (pulp tissue death), requiring root canal treatment and adversely affecting the health of the tooth.³ The commensal oral microbiota (community of microorganisms that live in the oral cavity), which colonise and multiply in the root canal system as a result of pulp necrosis brought on by caries, tooth trauma, or a poor restoration, has been connected to endodontic (root canal) infections.⁴

What causes dental caries?

Frequent sugar consumption causes the biofilm microbiota that typically maintains balance in the oral cavity to shift into an acid-producing, cariogenic (tooth decay-causing) population, which leads to dental caries. The cariogenic bacteria metabolise sugars to produce acid, which over time demineralises the tooth structure, and if left untreated, caries will advance through dentine, stimulating pulpitis (pulpal inflammation) and eventually causing pulp infection and necrosis of the tooth. As a result, dental caries is seen as a dietary-microbial disease that necessitates the presence of a cariogenic biofilm and consistent exposure to fermentable carbohydrates from diet, such as glucose, fructose, maltose, and sucrose.

How do dental caries form?

Dental pulp cells, especially dental pulp fibroblasts, are known to produce various inflammatory mediators, such as IL-8, IL-6, and vascular endothelial growth factor, in response to caries-related bacteria. There are over 500 distinct bacterial species in the oral microbiota. The most common bacteria responsible for oral infections, periodontal diseases, and dental caries are Streptococcus mutans, lactobacilli, and actinomycetes at the site of the disease.⁵

Dental caries, being the result of microbial invasion, can induce progressive destruction of teeth, and without treatment, it can lead to infection of the dental pulp and surrounding tissue. Streptococcus mutans is a major pathogen of dental caries as it contains collagen-binding proteins that act as cell surface antigens for the adherence of S. mutans to the collagen tissue.⁹

E. faecalis, the main human enterococcus, has also been related to oral diseases, such as caries, endodontic infections, and periodontitis.¹⁰

Distribution of caries on the tooth surface

The chewing surfaces and in between the teeth are areas the most susceptible to caries.

These areas are home to acidogenic (generating organic acids) and/or aciduric (resistant to an acidic environment) microbial populations.

Plaque community diversity is greater between teeth and the tongue surface of molar teeth, and less diverse on buccal (cheek) and anterior or front teeth.⁶ Bacterial infections of the oral cavity include:

Microbial composition of caries-causing pulpitis

They can be widely classified as primary colonisers and secondary colonisers.

 How do bacteria enter pulp tissue?

•  Bacteria can enter the pulp through tooth decay, after the demineralisation of enamel and dentin
•  It can enter the pulp while performing dental procedures like caries excavation and restoration, endodontic, and orthodontic procedures
• Through trauma to the teeth, which can be due to fracture or due to habits like bruxism (clenching or grinding of teeth)

Causes of pulpitis

•  Dental caries, which involves loss of hard tissue and microbial infection ³
•  Trauma to the tooth or invasive crown preparation
•  Contact with amalgam restoration
•  Thermal shock during cavity preparation
•  Chemical stimuli

Factors triggering an inflammatory reaction

• One common factor is caries, primarily involving gram-negative and gram-positive bacteria
• Fungi such as Candida albicans are reported to form cross-kingdom synergisms with cariogenic bacteria and possess cariogenic properties³
• Endogenous signalling molecules from damaged, necrotic, or stressed tissue, known as damage-associated molecular patterns, contribute to inflammation

Types of pulpitis

Reversible pulpitis  

• Acute (symptomatic)
• Chronic (asymptomatic)

Irreversible pulpitis

•  Acute
• Chronic

Reversible pulpitis

It is a mild to moderate condition of the pulp caused by damaging stimuli in which the pulp is capable of returning to an uninflamed state after the removal of stimuli.

Symptoms

• It is characterised by sharp shooting pain lasting for a moment
• Pain increases after the consumption of cold food

Treatment for reversible pulpitis

• Prevention is the best course of action for reversible pulpitis
• Caries periodical detection, and filling the cavity with stepwise excavation
• Selective carious tissue removal, where soft dentine is left on the pulpal aspect, whereas peripheral carious dentine is removed⁷
•  Care must be taken during cavity preparation and polishing of the tooth to prevent pulpitis

Irreversible pulpitis

It is a prolonged inflammatory condition of the pulp, which can be symptomatic or asymptomatic, produced by painful stimuli. The most prevalent cause is bacterial invasion of the pulp owing to caries.

Symptoms

• It is characterised by sharp shooting and severe pain, which continues even after the removal of the stimulus
• The patient might have referred pain in his sinuses or adjacent teeth
• The discomfort can get worse and is characterised as throbbing or gnawing, and the pain increases after the consumption of hot food

Treatment

• Vital pulp treatment including direct pulp capping: application of biomaterial directly onto the exposed pulp, before immediate placement of a permanent restoration
• In paediatric patients, coronal pulp removal or pulpectomy is recommended for posterior teeth
• In adult patients, root canal treatment should be considered as a choice
• Surgical removal of the tooth if it’s not restorable

Structural changes in pulpitis

• Stages of inflammation: The inflammatory response can be divided into two basic types: acute and chronic inflammation.  While acute inflammation constitutes the initial response to injury or infection and involves rapid and non-specific mechanisms, chronic inflammation is a prolonged and often more specific response involving both innate and adaptive immune components
• Characteristics of the pulpal inflammatory response: due to tubular permeability and cellular nociception in the dentin, the pulp tissue reacts early to pathogenic external stimuli, such as bacteria from caries, which have not yet come into direct contact with the tissue³

This includes:

• Neurovascular changes: upon stimulation, sensory nerves release several neuropeptides leading to recruitment of inflammatory cells, vasodilation (widening of blood vessels), and increased permeability of the microvascular system
• Tertiary dentin formation: wound healing involves sclerosis (hardening) of dentinal tubules and formation of tertiary dentin. It can be reparative or reactionary³

In reaction to damage or infection, the pulp-dentin complex has a considerable capacity for regeneration. 

Defensive response of the pulp to caries

Various types of pulp cells react immunologically to the microbes, initially via pathogen recognition by odontoblasts (cells that form dentin) and later fibroblasts, stem cells, and immune cells. Although the odontoblast has an immunocompetent role, its principal function is as a secretory cell, forming primary dentine during tooth development and later, the production of secondary dentine, as well as tertiary dentine production when challenged. 

Tertiary dentine forms alongside inflammation locally beneath the area of challenge.⁸ If the pulp is exposed, the reparative dentine forms a mineralised bridge, which is generally not in the form of tubular dentine but does protect the pulp tissue from further insult.⁸

Pulpal diagnosis

It is usually done by visual, tactile examination, along with the radiograph and other tools such as caries dyes and fibre optic fluorescent light. The depth of the cavity plays an important role in determining the extent of the carious lesion.

Prevention and treatment of microbial infections

• Early intervention and maintaining good oral hygiene by brushing, flossing, and regular dental check-ups are needed
• Dietary modification, which includes reduced sugar intake and a balanced diet
• In severe cases, antibiotics, antifungals, and antiviral medications should be used depending on the infection

Summary

Most of the signs and symptoms associated with progressive pulp disease occur more frequently but not exclusively with inflamed pulp. The primary cause of pulpitis is caries, trauma, or any dental procedures that can lead to the pulp becoming more exposed to bacteria. Early intervention is key to preventing permanent damage and alleviating symptoms.