Reversible Pulpitis

Reversible pulpitis is a clinical diagnosis based on a set of subjective and objective findings. It is characterized by mild inflammation of the pulp tissue. Once the cause of the inflammation has been eliminated, the pulp returns to its normal state, which is a hallmark of this condition.

Etiology

Reversible pulpitis may arise from various factors, including tooth decay (caries), recent dental procedures, or trauma.

Caries is the primary cause of pulp inflammation, affecting the tissue at every stage of the active disease. Toxins, bacterial metabolic byproducts, proteolytic enzymes, and dentin degradation products permeate through the dentin tubules, reaching the pulp. In response, the tissue becomes infiltrated by macrophages, plasma cells, and lymphocytes. This irritation triggers a cascade of nonspecific inflammatory responses, including the release of histamine, bradykinin, and arachidonic acid metabolites. Additionally, lysosomal enzymes from polymorphonuclear leukocytes and protease inhibitors are activated. The proliferation of terminal afferent nerve fibers in the pulp further leads to the release of proinflammatory neuropeptides, causing vascular reactions such as vasodilation, increased blood flow, and enhanced vascular permeability.

Moreover, the dental pulp can be irritated by mechanical, chemical, and thermal factors, such as tooth preparation, dental trauma, occlusal trauma, deep periodontal curettage, or orthodontic tooth movement.

Pulp irritation during dental procedures may occur due to vibration, damage to odontoblast processes during tooth preparation, or heat exposure, especially when air-water cooling is insufficient or not utilized at all. Dehydration can also be a trigger, potentially causing odontoblast nuclei to be aspirated into the dentin tubules. Furthermore, the toxic effects of residual monomers, certain dental materials, and aggressive cavity treatment solutions may also harm the pulp. In cases of improper application, restorative materials may shrink during polymerization, compromising the integrity of the restoration and allowing microorganisms to infiltrate the dentin tubules, which leads to inflammation.

Mechanical, thermal, and chemical irritants induce rapid fluid movement within the dentin tubules. Consequently, the myelinated A𝛅 nerve fibers in the pulp, located superficially at the pulp-dentin junction, are stimulated. These fibers have a low sensitivity threshold and transmit signals directly to the thalamus, resulting in sharp, localized pain.

The pulp, enclosed in a confined space with decreased collateral circulation, is highly sensitive to damaging stimuli and has limited regenerative capacity. However, when exposed to short-term or mild irritation, it can mobilize defense mechanisms to promote healing and minimize damage. In response to irritation, tertiary (reparative or reactionary) dentin forms at the junction between the dentin and pulp. In addition, the dentin becomes sclerotic around the carious lesion, and immune responses are simultaneously activated within the pulp.

Moreover, the toxic effect reduces the constant flow of dentinal fluid and its buffering capacity. All the mechanisms mentioned above aim to decrease permeability and limit the number of any possible irritants that may penetrate the pulp. Note that pulp inflammation may regress if the infected dentin is removed and the damaging factor is eliminated. In some cases, aspirated odontoblast nuclei may undergo autolysis. The tertiary dentin that has formed following previous inflammation does not heal completely and leaves a “scar” on the tooth surface.

Anatomic Pathology

Depending on the cause of pulp irritation, the following changes may be observed in the affected tooth:

• a carious lesion adjacent to the pulp chamber;
• a dental restoration adjacent to the pulp chamber;
• signs of compromised sealing in a restoration (e.g., defects, cracks, marginal pigmentation, or secondary caries);
• signs of trauma, such as cracks, chipping of the enamel or dentin, or partial pulp exposure.

The peripheral coronal pulp tissue is often edematous and hyperemic. At the junction between the dentin and pulp, especially within the area of the carious lesion, tertiary dentin may be deposited.

Diagnosis

Currently, there are no clinical methods available that can help adequately assess pulp tissue condition. Since the pulp cannot be accessed directly during a routine examination, a dentist is not able to identify any common signs of inflammation, such as redness, swelling, increased temperature, and dysfunction, except for pain. Furthermore, clinical symptoms of an inflamed pulp often do not align with histological findings.

To diagnose reversible pulpitis, the following methods can be used:

• Medical history: It is essential to inquire about any recent trauma or dental treatments, including tooth restorations, periodontal curettage, or orthodontic procedures.
• Tooth percussion: Usually painless or inconclusive.
• Palpation along the mucobuccal fold: Usually painless.
• Thermal sensibility test: Cold and hot stimuli often provoke sharp pain that subsides quickly (within a few seconds) once the stimulus is removed.
• Radiography (intraoral contact radiography, radiovisiography, cone-beam CT): A carious cavity, restoration, or traumatic defect adjacent to the pulp chamber may be observed; however, in some cases, there may be no changes.

Clinical Manifestations

In clinical settings, it can be rather challenging to distinguish between reversible and irreversible pulpitis. Patients may report sharp, transient pain triggered by cold or hot stimuli, or there may be no specific complaints. For instance, cold or hot air and substances may provoke sharp pain, which usually subsides quickly once the irritant is removed.

Treatment

The primary goal of treatment is to eliminate the irritant and seal the exposed dentin and/or vital pulp. Carious lesions require careful preparation of the cavity, removal of the infected dentin, and restoration of the tooth.

In cases of traumatic pulp damage, treatment options include tissue restoration, direct coverage of the exposed vital pulp with biocompatible materials, or, alternatively, performing a partial pulpotomy.

Ongoing follow-up with regular assessment of pulp vitality is essential. It is important to inform patients about the potential risk of irreversible inflammation or pulp necrosis. They should also seek immediate dental care in case of any symptoms indicative of irreversible pulpitis, such as prolonged pain due to temperature changes or spontaneous pain.

Irreversible Pulpitis

Irreversible pulpitis refers to inflammation of the dental pulp that persists even after the causative factor is eliminated.

Etiology

The primary cause of pulpitis is tooth decay that spreads to the pulp. The condition may also develop as a result of a trauma (mechanical trauma, occlusal trauma, or orthodontic tooth movement) or due to iatrogenic factors (such as tooth preparation without adequate cooling, poor isolation of the operative field, accidental pulp exposure, or toxic liners and restorative materials).

When microbes reach the pulp, inflammatory defense mechanisms are activated, leading to the accumulation of neutrophils and other immune cells. Neutrophils migrate from the pulp to the adjacent dentin tubules and release reactive oxygen species, lysosomal enzymes, and nitric oxide, which cumulatively contribute to tissue destruction.

The release of proinflammatory neuropeptides triggers vasodilation and increases vascular permeability, causing fluid to escape from the vessels into the tissues. The exudate initially appears serous but progresses to seropurulent and eventually purulent forms. This results in increased pressure within the tissues and a necrotic focus in the pulp.

The necrotic area is typically surrounded by neutrophil granulocytes that phagocytize bacteria, along with acellular tissue showing signs of partial degradation. Surrounding tissues exhibit chronic inflammation, characterized by an accumulation of macrophages, fibroblasts, mast cells, and foam cells. Even a limited area of necrosis indicates the transition from reversible to irreversible pulpitis. The initial necrotic area gradually spreads deeper in an apical direction.

As the inflammation progresses, purulent liquefaction and necrosis of the pulp may develop. However, if the exudate drains spontaneously, the acute process can shift to a chronic state. Proliferative changes prevail in chronic pulpitis: the inflammatory edema subsides, and fibrous elements proliferate significantly.

Inflammatory mediators, such as bradykinin and histamine, activate C-type nerve fibers. C-fibers are unmyelinated fibers that have slower conduction velocities, a smaller diameter, and a higher threshold of excitation compared to A𝛅 fibers. They are located deeper within the tissue and are primarily activated by heat, causing dull, aching, persistent, and sometimes diffuse pain. In patients with symptomatic irreversible pulpitis, exposure to cold may cause vasoconstriction and a drop in pulp pressure, providing temporary pain relief. One more feature that makes C- and A-fibers distinct is that the former ones are able to maintain functional integrity under hypoxic conditions.

This keeps them functional for longer periods of time as the inflammation progresses. The response of C-fibers indicates that the pulp damage is irreversible.

Anatomic Pathology

Depending on the etiological factor, the following changes may be observed in the affected tooth:

• a carious lesion penetrating into the pulp chamber;
• a dental restoration located close to the pulp chamber or directly adjacent to the pulp tissues;
• signs of compromised sealing in a restoration (e.g., defects, cracks, marginal pigmentation, or secondary caries);
• signs of trauma, such as cracks, chipping of the enamel or dentin, or pulp exposure.

In acute cases, the pulp becomes edematous, hyperemic, and bright red. Small hemorrhages may appear around the vessels. Initially, purulent exudate forms as a localized accumulation but later spreads throughout the coronal and radicular pulp, acquiring a grayish-red or gray appearance.

In chronic cases, the pulp is gradually replaced by granulation tissue, which eventually transforms into dense, coarse, whitish fibrous scar tissue.

Classification

• Acute irreversible pulpitis;
• Chronic irreversible pulpitis.

Diagnosis

• Medical history: A comprehensive assessment of patient complaints and history is crucial. Key aspects include pain, its nature, location, and duration, as well as any pain-free intervals. It is also important to identify factors that trigger or relieve pain. Recent dental treatments and any history of trauma should be noted.
• Tooth percussion: Usually painless or inconclusive.
• Palpation along the mucobuccal fold: Usually painless.
• Thermal sensibility test: Cold or hot stimuli often induce pain that persists even after the stimulus is removed. Note that there may be no response to cold, while sensitivity to heat may persist if the pulp is extensively affected.
• Pulp sensibility tests (electrical): Teeth with irreversible pulpitis show a higher threshold of electrical stimulation compared to healthy teeth or teeth affected by reversible pulpitis.
• Bite test: Negative.
• Selective anesthesia: Used to identify the causative tooth in cases of referred pain or to differentiate between odontogenic and non-odontogenic pain.
• Radiography (intraoral contact radiography, radiovisiography, orthopantomography, cone-beam CT): A carious lesion, restoration, or traumatic defect adjacent to or penetrating the pulp chamber may be observed. Generally, there are no periapical changes. However, as the condition progresses, thickening of the periodontal ligament space may become apparent.

Clinical Manifestations

In acute pulpitis, patients report spontaneous, paroxysmal pain regardless of external stimuli. The frequency and duration of pain episodes, as well as pain-free intervals, are not stable and tend to change over time. Initially, short episodes of pain (from a few minutes to a few hours) alternate with prolonged pain-free intervals (from a few hours to a few days). As the condition progresses, these features gradually escalate. Patients often experience dull, aching, persistent pain at night. It may also be sharp and throbbing and sometimes may transform into a severe, unbearable attack. This pain frequently radiates to adjacent teeth or antagonists and may migrate.

Exposure to thermal, mechanical, and chemical stimuli leads to prolonged pain episodes that persist even after the irritant is removed.

Chronic pulpitis is characterized by a discrepancy between mild pain symptoms and the extent of tooth damage. Patients may complain of prolonged pain triggered by external stimuli. Spontaneous and nocturnal pain is usually absent.

Treatment

Acute irreversible pulpitis accompanied by spontaneous pain is an emergency requiring immediate treatment.

The primary treatment for this condition is endodontic therapy. This is when the pulp tissue is completely removed, followed by mechanical and chemical debridement of the root canals. Subsequently, the root canals are hermetically sealed, and the tooth is restored.

In permanent teeth with incomplete root development, revascularization and apexogenesis techniques may be employed.

In cases where endodontic treatment may have unfavorable outcomes, tooth extraction is indicated.

Pulp Hyperplasia

Pulp hyperplasia (synonyms: hyperplastic pulpitis, pulp polyp) is a form of irreversible pulpitis that develops when chronically inflamed pulp grows through a carious cavity onto the surface of the tooth.

Etiology

This condition is most commonly found in younger patients. It typically develops when the entire roof of the pulp chamber is destroyed due to extensive carious damage. In such cases, the pulp is exposed and continuously subjected to mechanical irritation and infection. As a result, the connective tissue of the pulp proliferates, forming a highly vascularized polyp on a broad stalk. If in contact with the gingival tissue, the pulp polyp may undergo epithelialization.

Anatomic Pathology

In the affected tooth, there is extensive communication between a deep carious cavity and the pulp chamber. The proliferating pulp tissue extends out of the carious cavity, taking on the appearance of a red-pink mass resembling a cauliflower.

Histologically, two types of pulp polyps are distinguished:

• Pulp without epithelial lining;
• Pulp lined with stratified squamous epithelium that invades the connective tissue as papillae. In terms of histology and differentiation, the epithelial layer covering the hyperplastic connective tissue resembles keratinized gingival epithelium of the oral cavity.

Pulp polyps may vary in size. They may slightly protrude above the level of the pulp chamber roof or, in some cases, fill the entire carious cavity and extend above the occlusal surface of the tooth.

Diagnosis

• Visual examination, palpation, probing.
• Tooth percussion: Usually painless.
• Palpation along the mucobuccal fold: Usually painless.
• Thermal sensibility test: A cold stimulus causes mild pain that subsides quickly.
• Pulp sensibility tests (electrical): Reduced excitability of the pulp.
• Radiography (intraoral contact radiography, radiovisiography, orthopantomography, cone-beam CT): An extensive carious cavity penetrating the pulp chamber is typically seen, with no changes in the periapical area.

Clinical Manifestations

Hyperplastic pulpitis is usually asymptomatic. An interview may reveal that the affected tooth has been painful but does not cause any pain at present. The patient may experience mild discomfort and occasional bleeding from a carious cavity while eating. Sometimes, patients may also complain of prolonged pain triggered by thermal stimuli.

Upon examination of the oral cavity, a large carious cavity filled with a fleshy tumor-like growth resembling a cauliflower is identified. In some cases, the tissue appears red-pink, firm, covered with epithelium, and is relatively non-tender on palpation. In other cases, the tissue is bright red and bleeds at a touch.

Probing deeper into the cavity reveals a broad stalk connecting the growth to the underlying pulp tissue. The proliferating tissue shows minimal sensitivity to superficial probing; however, deep probing near the root canal orifices is painful.

Treatment

The primary treatment for pulp hyperplasia is endodontic therapy. This is when the pulp tissue is completely removed, followed by mechanical and chemical debridement of the root canals. Subsequently, the root canals are hermetically sealed, and the tooth is restored.

In cases where endodontic treatment may have unfavorable outcomes, tooth extraction is indicated.

Pulp Necrosis

Pulp necrosis is an irreversible condition characterized by the death of the dental pulp.

Etiology 

Pulp necrosis is one of the outcomes of irreversible pulpitis, as a bacterial infection spreads deeper into the pulp. Other contributing factors include mechanical trauma (acute or chronic), thermal factors (e.g., overheating the pulp during tooth preparation without adequate cooling), and chemical agents (such as toxic liners, restorative materials, or aggressive cavity treatment solutions). Depending on the extent of the damage, pulp necrosis can be partial or complete.

In irreversible pulpitis, microbial invasion leads to liquefactive (colliquative) necrosis. During the exudative phase, tissue edema exacerbates, while such processes as hypoxia, anaerobic glycolysis, and acidosis intensify. The purulent exudate contains enzymes released from lysosomes of degrading neutrophils. These enzymes liquefy the tissue, increase vascular permeability, and promote the formation of phagocytosis-inducing chemotactic substances. As a result, the area of tissue destruction gradually spreads deeper toward the root apex.

If the exudate drains through the carious cavity, pulp necrosis progression may slow down, allowing the root pulp to remain vital for a longer time. By contrast, within a closed pulp chamber, rapid and complete necrosis of the pulp typically occurs.

An acute or chronic trauma that impairs blood supply leads to ischemia and hypoxia. It also adversely affects oxidative phosphorylation and cellular transport. As a result, the cytoskeleton and cell membranes collapse, causing coagulative necrosis of the tissue.

In pulp necrosis, blood flow stops, and nerve endings lose their function. After total necrosis, the tooth becomes asymptomatic until the pathological process reaches the periapical tissues. However, exposure to a hot stimulus may cause dragging pain, possibly due to the expansion of residual fluids or gases within the pulp space that spread into the periodontal tissues. Additionally, in cases of partial necrosis in multi-rooted teeth, pulp testing in one root may show no response, while another root may respond positively, which makes the diagnosis even more challenging.

Anatomic Pathology

Depending on the etiological factor, the following changes may be observed in the affected tooth:

• a carious lesion penetrating into the pulp chamber;
• a dental restoration located close to the pulp chamber or directly adjacent to the pulp tissues;
• signs of compromised sealing in a restoration (e.g., defects, cracks, marginal pigmentation, or secondary caries);
• signs of trauma, such as cracks or chipping of the enamel or dentin.

Liquefactive necrosis causes the pulp to appear gray-black and give off a foul odor. By contrast, coagulative necrosis makes the pulp tissue dry, firm, and yellow-gray.

Diagnosis

• Medical history: A thorough assessment of patient complaints and history is crucial, including pain, its nature, and location of pain, recent dental treatments, or trauma.
• Visual examination: The tooth crown may develop a gray discoloration due to pulp breakdown products penetrating the dentin tubules.
• Tooth percussion: Usually painless.
• Palpation along the mucobuccal fold: Usually painless.
• Thermal sensibility test: There is typically no response to cold stimuli, although in cases of partial necrosis in multi-rooted teeth, a response may be noted. Exposure to heat may elicit dragging pain.
• Pulp sensibility tests (electrical): The pulp shows no response to electrical stimulation. Threshold sensitivity at 100 µA or higher is associated with the periodontal tissue reaction.
• Bite test: Typically negative; however, in case of a fractured tooth, a positive response on one cusp may be seen.
• Radiography (intraoral contact radiography, radiovisiography, orthopantomography, cone-beam CT): A carious lesion, restoration, or traumatic defect adjacent to or penetrating the pulp chamber may be observed. There are usually no periapical changes, but the periodontal ligament space may be widened due to toxin penetration into the periapical tissues.
• Diagnostic cavity preparation: Applied only when other methods are not feasible or if the findings obtained are inconclusive. The tooth is prepared without anesthesia using a small bur to make sure whether it is painful or not.

Clinical Manifestations

Pulp necrosis is generally asymptomatic. However, medical history may reveal previous episodes of tooth pain that have eventually subsided.

Some patients may report changes in tooth color, a foul odor from the tooth, or prolonged pain triggered by hot stimuli. In cases of tooth fracture or when inflammation extends to the periapical tissues, patients may also complain of pain during chewing.

Treatment

The primary treatment for pulp necrosis is endodontic therapy. This involves the complete removal of necrotic pulp tissue, followed by mechanical and chemical debridement of the root canals. Subsequently, the canals are hermetically sealed, and the tooth is restored.

In cases where endodontic treatment may have unfavorable outcomes, tooth extraction is indicated.

Antibiotic prophylaxis during nonsurgical and surgical endodontic treatment is recommended for the following patient groups:

• patients receiving intravenous bisphosphonate therapy (in cases of periapical surgery);
• patients at risk of infective endocarditis (e.g., complex congenital heart defects, prosthetic heart valves, history of infective endocarditis);
• patients with immunodeficiency conditions (e.g., leukemia, HIV/AIDS, end-stage renal disease, dialysis, inherited immune defects, uncontrolled diabetes, chemotherapy, or use of immunosuppressive or steroid medications following transplantation);
• patients who have undergone joint replacement within the first three months after surgery;
• patients undergoing cranial radiotherapy.

Pulp Calcification

Pulp calcification refers to abnormal hard tissues, known as pulp stones or denticles, that tend to form within the dental pulp.

Etiology

The exact etiology of pulp calcification remains unknown. However, several factors are believed to contribute to the condition:

• Traumatic factors: reduced blood flow and nutrient supply due to tooth injuries (e.g., contusions, luxations, fractures), occlusal trauma, excessive forces during orthodontic treatment, or surgical interventions.
• Chemical and physical irritants: amalgam restorations or overheating of the tooth during preparation without cooling.
• Dental and periodontal diseases: caries, severe abrasions, erosions, abfraction defects, and periodontal diseases.
• Hereditary disorders of tooth formation: amelogenesis imperfecta, dentinogenesis imperfecta, osteogenesis imperfecta, dentin dysplasia, and osteopetrosis (marble bone disease).

Calcifications can develop around necrotic cells, blood clots within vessels, collagen fiber bundles, or epithelial cells. Note that tissue or vascular necrosis, which results in denticle formation, may be caused by various external factors, such as microbial invasion during caries, temperature fluctuations, mechanical trauma, or exposure to toxins. Furthermore, calcium phosphate crystals can sometimes be deposited directly within cells and promote calcification. The connective tissue in the pulp serves as a protector. It encapsulates necrotic areas with fibro-dentin and effectively isolates them from vital tissues. In the root canals, diffuse calcifications along collagen fibers or blood vessels are usually observed.

True denticles, which have a structure similar to dentin with tubules, are rare. They form as a result of breaks in the remnants of the Hertwig's epithelial root sheath, with odontoblasts arranged concentrically around them.

When there is no visible tissue damage, the reason for pulp calcification remains unclear. Calcifications tend to appear in seemingly healthy pulp, indicating that functional stress is not a necessary condition for denticle formation.

Teeth affected by caries are much more mineralized compared to intact teeth. As the tooth decay progresses, the number and extent of pulp stones increase. In response to chronic irritation by bacterial toxins, the pulp may deposit reparative dentin, creating a barrier against carious invasion. The reduction of the pulp chamber due to hard tissues formed by vital pulp cells can eventually lead to complete obliteration of the chamber.

Mechanical or occlusal trauma can cause calcifying metamorphosis, a condition characterized by partial or complete radiological obliteration of the pulp chamber and root canals. The mechanisms of this reaction have not been fully explored, but it is believed that odontoblasts, and possibly other mesenchymal cell populations within the pulp, may lose regulatory control during neurovascular injury and regeneration, leading to disorganized deposition of hard tissue.

Trauma to teeth with incomplete root formation may rupture the blood vessels that enter the tooth and consequently lead to pulp infarction. The wide apical foramen allows periodontal connective tissue to proliferate and replace infarcted areas, bringing cells that can differentiate into cementoblasts or osteoblasts.

Pulp calcifications can occur in multiple teeth. A genetic origin may be suspected if all teeth are affected by calcification.

As calcifications form, the number of cells in the pulp decreases and reduces its regenerative capacity. Furthermore, extensive mineralization within the pulp chamber and root canals can hinder access and treatment during endodontic procedures. 

Anatomic Pathology

Teeth with pulp calcification may be intact or show signs of carious lesions, pathological wear, trauma, erosion, abfraction defects, or restorations.

Denticles may be located in the coronal and/or radicular pulp or at the root canal orifices. They are classified as true or false. True denticles have the structure of normal dentin with tubules, while false denticles (more common) consist of concentric layers of calcified tissue without dentin-like structures.

Depending on their relation to the pulp chamber wall, calcifications can be:

• Free (located within the pulp),
• Attached (fixed to the wall), or
• Interstitial (surrounded by the root canal walls).

In the coronal pulp, isolated concentric pulp stones are usually observed, while calcification in the radicular pulp tends to spread diffusely. Denticle size ranges from microscopic particles, often associated with arteriole walls, to growths occupying the entire pulp chamber.

Diagnosis

• Tooth percussion: Usually painless.
• Palpation along the mucobuccal fold: Usually painless.
• Thermal sensibility test and pulp sensibility tests (electrical): The threshold sensitivity to thermal and electrical stimuli may increase. In cases of significant obliteration, these tests may be inconclusive.
• Radiography (intraoral contact radiography, radiovisiography, orthopantomography, cone-beam CT): Single or multiple radiopaque areas may be observed within the pulp chamber. In cases of complete obliteration, the pulp chamber and root canals may not be visible. Complete obliteration cannot be diagnosed by radiographic means alone; clinical confirmation is necessary, as the canal may still be accessible with endodontic instruments despite not being radiographically visible.

Clinical Manifestations

Pulp calcification is typically asymptomatic and is often detected incidentally upon radiography. In cases of significant pulp chamber obliteration, the crown of the affected tooth may appear yellowish compared to that of the adjacent teeth.

Treatment

Pulp calcification does not require any treatment. The condition may be managed by eliminating potential contributing factors (e.g., treating caries and non-carious lesions, selective grinding for occlusal trauma, replacing compromised restorations, adjusting orthodontic forces).

If symptoms of irreversible pulpitis or apical periodontitis arise, endodontic treatment may be necessary.