Background
The pulp polyp, also known as chronic hyperplastic pulpitis or proliferative pulpitis, is an uncommon and specific type of inflammatory hyperplasia that is associated with a nonvital tooth.
Pulpal diseases are broadly divided into reversible and irreversible pulpitis and are based on the ability of the inflamed dental pulp to return to a healthy state once the noxious stimulus has been removed. In the case of the pulp polyp, the disease process is irreversible. In contrast to most cases of irreversible pulpitis, the pulp polyp is usually an incidental finding that occasionally mimics reactive and neoplastic diseases of the gingiva and adjacent periodontium.
View Image | Pulp polyps involving the primary, first, and second mandibular molars in a young child with extensive dental caries. |
Pathophysiology
The pulp polyp is the result of both mechanical irritation and bacterial invasion into the pulp of a tooth that exhibits significant crown destruction due to trauma or caries. The mechanical causes that may stimulate this response include a tooth fracture with pulpal exposure or loss of a dental restoration. Usually, the entire dentinal roof is exposed with the crown of a carious tooth. The large exposure of pulpal tissue to the oral environment and bacterial invasion results in a chronic inflammatory response that stimulates an exuberant granulation tissue reaction.
The hyperplastic tissue reaction occurs because the young dental pulp has a rich blood supply and favorable immune response that is more resistant to bacterial infection. Furthermore, because the tooth is open to the oral cavity, transudates and exudates from the inflamed pulpal tissue drain freely and do not accumulate within the restricted and rigid confines of the tooth. Tissue necrosis with destruction of the microcirculation that usually accompanies irreversible pulpitis does not occur in part because of this lack of significant intrapulpal pressure. In young teeth in which the apex of the root is open, the risk of pulpal necrosis secondary to venous congestion is decreased. The presence of a rich vascular network in the young pulpal tissue is an important protective mechanism against the inflammatory response that significantly decreases with age.
The possible role of a type 1 hypersensitivity reaction has been hypothesized because of an increased presence and concentration of immunoglobulin E (IgE), histamine, and interleukin-4 (IL-4) within the pulp polyps when compared with healthy pulpal tissues.[1]
Epidemiology
Frequency
United States
Pulp polyps are reportedly uncommon in the United States, and no epidemiologic studies specifically document the frequency of this entity. Although this lesion is reported to be uncommon with only isolated references in the literature, the true prevalence of this reactive pulpal disease is likely to be underestimated because it is a well-recognized sequela of extensive dental caries in children.
International
Pulp polyps are uncommon in countries with routine access to dental care, but they are encountered more frequently in developing countries. In a study of Vietnamese refugees who sought dental care, the prevalence of pulp polyps was 6%. This high number of cases is an indication of the severity of dental disease in this impoverished population. In a Brazilian clinical study of traumatized primary teeth, the occurrence of pulp polyps was 2.3% in young children.[2]
Mortality/Morbidity
Pulp polyps tend to be asymptomatic and are not associated with any significant morbidity or mortality except for gross caries destruction with premature tooth loss in many cases.
Race
No racial predilection is recognized for this sequela of dental caries; however, it is more common in individuals of lower socioeconomic background who have limited access to dental care than in other people.
Sex
No sexual predilection has been documented for this oral lesion.
Age
This pulpal disease occurs almost exclusively in children and young adults, and it can occur in both the primary dentition and the permanent dentition. When trauma is the causative factor in primary anterior teeth, most examples are observed in children aged 2 years or younger.
Causes
Causes of a pulp polyp include the following:
Carious tooth with significant loss of tooth structure
Loss of a dental restoration that results in pulpal exposure
Fractured tooth due to trauma with a pulpal exposure
Pulpal tissue with access to a good blood supply
Possible hormonal (estrogen and progesterone) influence
Possible hypersensitivity reaction
Other Tests
Diagnosis and determination of the most appropriate treatment options are based on adjunctive tests, including response to percussion, thermal stimuli, and electric pulp testing. In most cases, the results of these adjunctive tests are similar to those obtained for healthy teeth, which is in contrast to most teeth that exhibit irreversible pulpitis. The normal responses should not confuse the practitioner that the pulpal tissue is healthy and therefore requires only conservative treatment. In addition, these tests help to differentiate a true pulp polyp from hyperplastic gingivitis that is overlying a cavitation from a nonvital tooth.
Procedures
Affected teeth and pulpal tissue are occasionally submitted for gross and histopathologic examination. This examination is most important when the pulp polyp is diagnosed in multiple teeth and when the cause for this uncommon pulpal response is not obvious at clinical examination.
Histologic Findings
Microscopic findings reveal a mass of granulation tissue protruding from the crown of a fractured or carious tooth that resembles a pyogenic granuloma. The fibrovascular stroma contains numerous small, delicate vascular channels and a prominent inflammatory infiltrate composed of primarily lymphocytes, plasma cells, and neutrophils. Although the surface may be ulcerated, it is covered by stratified squamous epithelium that resembles oral mucosa in approximately 50% of these inflammatory hyperplastic lesions. The source of this epithelium appears to be from the engraftment of desquamated oral epithelial cells or the migration of the epithelium from the adjacent gingival tissues. In more mature lesions that are covered with squamous epithelium, the granulation tissue is replaced by fibrous connective tissue with minimal inflammation and foci of dystrophic calcification.
Bacteria (primarily gram positive) are found on the surface of the polyp and within the carious lesion. In many cases, the histopathologic changes are limited to the coronal pulp tissue with the apical tissue exhibiting only mild vasodilation and minimal chronic inflammation.
Ultrastructural examination of nerve fibers associated with the pulp polyp exhibits variable findings within the same tooth, ranging from normal to moderate or severe degeneration of both myelinated nerve fibers and unmyelinated nerve fibers.
Medication Summary
Systemic medications are not recommended for the management of this lesion. Antibiotics are not prescribed for the treatment of the pulp polyp, despite a bacterial component. However, an antibiotic paste mixture is used within the canals of the infected tooth when the revascularization process is performed for the treatment of the nonvital tooth.
Author
Catherine M Flaitz, DDS, MS, Professor, Division of Pediatric Dentistry, Ohio State University College of Dentistry
Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: American Academy of Pediatric Dentistry Board of Trustees; Commissioner of Dental Accreditation; Director, American Board of Ora and Maxillofacial Pathology; Associate Chief of Dentistry at Nationwide Children's Hospital<br/>Serve(d) as a speaker or a member of a speakers bureau for: American Academy of Pediatric Dentistry Speakers Bureau<br/>Travel Grant from GC America; American Academy of Pediatric Dentistry for Continuing Education Presenter for: Multiple speaking engagements for dental meetings.
Coauthor(s)
M John Hicks, DDS, MD, PhD, MS, Professor with Tenure, Department of Pathology and Immunology, Baylor College of Medicine; Medical Director of Ultrastructural Pathology, Department of Pathology, Texas Children's Hospital; Professor of Pediatrics, Baylor College of Medicine; Adjunct Professor, Department of Pediatric Dentistry, School of Dentistry, University of Texs Health Science Center at Houston
Disclosure: Nothing to disclose.
Specialty Editors
Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Drore Eisen, MD, DDS, Consulting Staff, Dermatology of Southwest Ohio
Disclosure: Nothing to disclose.
Chief Editor
Arlen D Meyers, MD, MBA, Professor of Otolaryngology, Dentistry, and Engineering, University of Colorado School of Medicine
Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Cerescan;RxRevu;Cliexa;The Physicians Edge;Sync-n-Scale;mCharts<br/>Received income in an amount equal to or greater than $250 from: The Physicians Edge, Cliexa<br/> Received stock from RxRevu; Received ownership interest from Cerescan for consulting; .
Additional Contributors
Gregory J Raugi, MD, PhD, Professor, Department of Internal Medicine, Division of Dermatology, University of Washington at Seattle School of Medicine; Chief, Dermatology Section, Primary and Specialty Care Service, Veterans Administration Medical Center of Seattle
Disclosure: Nothing to disclose.
){kind=link}