PERIAPICAL GRANULOMA: EIGHTEEN MONTHS FOLLOW UP -A CASE REPORT

FIRST AUTHOR: DR. ANAMIKA SHARMA (MDS)
PROFESSOR & HEAD
DEPARTMENT OF PERIODONTICS
SUBHARTI DENTAL COLLEGE, MEERUT
email: This e-mail address is being protected from spambots. You need JavaScript enabled to view it
Phone No.: 9358400994

Second Author: DR. VISHAL SHARMA (BDS)
Phone No : 9719015001

ABSTRACT

Periapical granuloma is a relatively common lesion or growth consisting of a proliferating mass of granulation tissue and bacteria that form in response to dead tissue in the pulp chamber of the tooth. The death of the pulp may be due to extensive decay, deep restorations or trauma to the tooth. Its formation represents the body's attempt to heal and wall off an infection. Periapical granulomas enlarge slowly and can grow to reach several centimeters in diameter.

Periapical granuloma is usually regarded as a trivial lesion rather than a serious clinical complication. It is considered a reactive inflammatory process resulting from chronic irritation originating from root canal system of the affected root. Periapical granuloma mainly consists of granulation tissue with alveolar bone loss and a large number of T lymphocytes, monocytes/macrophages together with a small number of B lymphocytes and polymorpho-nuclear leukocytes.

INTRODUCTION

The term ‘periapical granuloma’ refers to a mass of chronically inflamed granulation tissue at the apex of a nonvital tooth. Although the term apical periodontitis may be more appropriate, it may be confusing to clinicians. Formation of the apical inflammation represents a defensive reaction secondary to the presence of bacteria in the root canal with the spread of related toxic products into the apical zone. Initially, the defense reaction eliminates noxious substances that exit the canals. With time, however, the host reaction becomes less effective with microbial invasion or spread of toxins into the apical area.

It has recently been shown to contain 47% macrophages, 32% lymphocytes, 13% plasma cells, and 8% neutrophils by differential analysis.While the macrophage is the predominant cell type and the ‘hallmark’ of the granulomatous inflammation, the significant numbers of lymphocytes and plasma cells are highly suggestive of the role of cell mediated immune system in the evolution of the lesion.The   presence of immunoglobulin producing cells in the periapical granuloma has also been documented, thereby implicating the humoral immune system.

Independent  of  the advances on  the microbiological  aspects,  the  pathological  changes  taking place  at  the periapex  in  the form of  tissue destruction  and  the  accumulation  of  inflammatory  cells affect the initiation and progression of disease and therefore require appropriate treatment for control of the disease process The present article documents the resolution of periapical granuloma by non-surgical therapy without the need for further periodontal treatment.

CASE REPORT :

A 18 year old boy reported to the dental clinic. His chief complaint was pain and swelling in the left mandibular posterior region (Fig 1). Pulp test indicated necrosis of the pulp of left mandibular first molar. Periapical radiograph showed a well defined radiolucent lesion extending from mesial to the distal root (Fig 2). The widest horizontal diameter of the lesion on the film was approximately 3.2 mm. With the exception of left mandibular first molar, all the other teeth in the area of the lesion responded normally to the pulp tests. Root canal therapy was begun at this time and completed 2 weeks later. Recall radiograph taken after 8 months showed partial resolution of the lesion (Fig 3) and 18 months showed complete resolution of the lesion (Fig 4). The patient is asymptomatic since then.

ETIOLOGY

Miller5 demonstrated   the presence of several distinct types of   bacteria   in  the  necrotic  dental pulp responsible for  the development of peri-apical lesions. As   bacteria  were found only in  a small fraction  of  periapical  lesions, principally  those  with  abscess  foci,  these  lesions  were  considered  to  be  caused  not  necessarily  by  microorganisms  alone but by  other primary and independent  co-factors  such  as  the  decomposition products  of  pulp  tissue,6  stagnant  tissue fluid or  root  canal  fillings7.  Further, it had been shown that stagnant tissue   fluid and sterile necrotic pulp   tissue  do not  cause  sustaining inflammation at the periapex.8 The ultrastructure of  the endodontic  flora,  the  strategic  location  of  the microbes  in  the  apical  root  canal  and  the  anatomical contiguity of  the flora with the inflammatory lesion existing beyond the apical foramen have been clearly documented  in the etiology of peri-apical lesions.

Also, the accumulation of   inflammatory   cells in the peri-apical area has been described.9 This inflammatory response may be elicited by a variety of stimuli.10 Neurogenic inflammation is considered to be based on the observation that the stimulation of modified dilation, associated with an increase in vascular permeability, leading to extravasation of leukocytes. Substance P (SP) and Calcitonin gene-related peptide (CGRP) are sensory neuropeptides released by noxious stimulus and found in nociceptive nerve endings. SP causes leukocyte infiltration in local inflammatory sites and is believed to be one of major mediators of neurogenic inflammation.11

CLINICAL FEATURES

In case of periapical lesions, the variables accounting for differences in the incidence of cysts and granulomas include chronicity of lesions, previous endodontic treatment, lesion site and  size. It has been clearly indicated that as the lesion size increases, incidence of cyst increases.9 Most periapical lesions are asymptomatic, but pain and sensitivity can occur if acute exacerbation occurs. Typically, the involved tooth does not demonstrate mobility or significant sensitivity to percussion. The soft tissues overlying the apex may or may not be tender. The tooth does not respond to thermal or electric pulp tests unless the pulp necrosis is limited to a single canal in a multirooted tooth.1

RADIOGRAPHIC FEATURES

A radiolucency of variable size is present, and the affected tooth shows loss of the apical lamina dura1 (Fig 2).  Earlier it was accepted that periapical cyst could be differentiated radiographically from granulomas on the basis of their larger size (more than 9.5 mm in diameter) and their possession of a radiopaque cortex. 12 However, Grossman13 suggested that while radiographic differentiation of cyst and granulomas was possible in most cases, small radicular cysts could not always be differentiated from granulomas.

1. DISCUSSION

DISCUSSION

The treatment of periapical granuloma mainly consists of root canal therapy with or without subsequent apicoectomy.14 If initial conventional therapy is unsuccessful, endodontic retreatment represents the best approach for total elimination of bacteria and should be considered before periapical surgery.1 If left untreated, the periapical granuloma may ultimately undergo transformation into an apical periodontal cyst through proliferation of epithelial rests in the area14
John et al15 evaluated periapically involved teeth treated endodontically to determine their rate of success. More important to the study, the rate of failure was also established, and the causes of failure were carefully examined. Nearly 95% of all endodontically treated teeth were successful.

Lalonde16 suggested that whether a periapically involved tooth is affected by a granuloma or a cyst, nonsurgical endodontic therapy may be the treatment of choice. If the periapical lesion does 'not heal properly, an apicoectomy can be performed at a later date.

Bhaskar17 in an attempt to explain nonsurgical resolution of cysts suggested that instrumentation of root canals through the apical foramen during treatment might result in a "transitory acute inflammation with epithelial destruction" or “subepithelial hemorrhage with ulceration of the epithelial lining." He postulated that these mechanisms could destroy or disrupt the cyst epithelium, thus converting the cyst to a granuloma which could resolve without surgical intervention.

Thomas et al19 described two cases of periapical lesions treated by endodontic therapy. The canals were thoroughly debrided with sodium hypochlorite and calcium hydroxide  paste  placed in the canals. The access cavities were sealed with temporary restorations and patients were prescribed antibiotics. Four weeks post-op it was observed that the lesions showed complete resolution and it was suggested that the largeness of a lesion does not mandate its surgical removal and that even cyst-like lesions heal following conservative therapy. .

Antonios et al21 described the combined nonsurgical and surgical management of a mandibular lateral incisor associated with a rare type of dens invaginatus. Pulp involvement of the malformed tooth, periapical abscess, and severe periodontal destruction were observed.. The signs and symptoms ceased after completion of endodontic treatment. Satisfactory healing of the periradicular lesion was observed at the 6-month and 2-year follow-up examinations.

CONCLUSION

Periapical granulomas mainly result from presence of bacteria or their toxic products in the root canal, the apical tissues, or both. Therefore, successful treatment depends on the elimination of the offending organisms. General acceptance of the view that many periapical granulomas are likely to heal after nonsurgical endodontic treatment has lead to the increasing use of nonsurgical procedures in the treatment of periapical lesions. Nevertheless, unless they are symptomatic, teeth treated endodontically should be evaluated at 1 and 2 year intervals (at a minimum) to rule out possible lesion enlargement and to ensure appropriate healing.

LEGENDS

EXTRA-ORAL VIEW
PRE-OPERATIVE
8 MONTHS POST-OPERATIVE
18 MONTHS POST-OPERATIVE

REFERENCES

• Neville, Damn, Allen, Bouqout. Pulp and Periapical Disease. Oral and Maxillofacial Pathology-Second ed.
• Stern MH, Drezen S, Mackler BF, Selbst AG, Levy BM. Quantative Analysis of Cellular Composition of Human Periapical Granuloma. J Endo 1981; 7: 117-122.
• Willoughby DA, Ryan GB. Evidence for a PossiblE Endogenous Antigen in Chronic Inflammation. J Path 1970; 101: 233-239.
• Kuntz DD, Genco RJ. Localization of Immunoglobulins and Complement in Persistent Periapical Lesions. IADR Progress & Abst 1974; 53: 641.
• Miller WD. The Micro-organisms   of the Human Mouth. Philadelphia: White Dental MFG Co., 1890: 96.
• Langeland K. Erkrankungen  der Pulpa und des Periapex. In: Guldener PHA, Langeland K, ed. Endodontie. 2nd edn. Stuttgart: Thieme,   1993: 59, 66, 70.
• Rickert UG, Dixon CM. The Controlling of   Root Surgery. In: Transactions of   the Eighth International Dental Congress, Paris. 1931; Section IIIa: 15.
• Dubrow H. Silver points   and   Gutta-percha  and the  Role of  Root  Canal  Fillings.  J  Am Dent Assoc   1976: 93: 976- 980.
• Bhaskar SN. Periapical   Lesion - Types,  Incidence and Clinical  Features.  Oral   Surg Oral Med Oral   Pathol  1966:  21: 657-671.
• Nair PNR.Apical periodontitis: a Dynamic Encounter Between Root Canal Infection and Host Response. Periodontol 2000 1997; 13: 121-148.
• Foramen JC, Jordan CC, Oehme P, Renner H. Structure-activity Relationships for Substance P-related Peptides that Cause Wheal and Flare Reactions in Human Skin. J Physiol 1983; 335: 449-465.
• McCall JO, Wald SS. Clinical Dental Roentgenology, ed. 3, Philadelphia, 1952, WB Saunders Company, p 192.
• Grossman LI.Root Canal Therapy, ed. 3, Philadelphia, 1950, Lea & Febiger, p. 99.
• Shafer, HINE, Levy.A Textbook of Oral Pathology. Fourth ed.
• John I, James HS, Pierre M, Patrick B. Outcome of Endodontic Treatment and Re-    Treatment. Endodontics 1956; 22: 1-22.
• Lanolde ER: A New Rationale for the Management of Periapical Granulomas and Cysts: An Evaluation of Histopathologic and Radiographic Findings. J Am Dent Assoc. 1970; 80: 1056-1059.
• Bhaskar, SN: Nonsurgical Resolution of Radicular Cysts. Oral Surg 1972; 34: 469-
• Miyashita H, Bergenholtz G, Grondahl K, Wennstrom JL. Impact of Endodontic Conditions on Marginal Bone Loss. J Periodontol 1998: 69: 158-164.
• Thomas SB, Kandari AR, Abdul AA. Healing of Large Periapical Lesions Following Calcium Hydroxide Endodontic Therapy: Two Case Reports and Review of Literature. Endodontology 2000; 12: 32-36.
• Scott A. Conventional Endodontic Therapy of Upper Central Incisor Combined with Cyst Decompression: A Case Report. J Endod 2007; 33: 753-757.
• Antonios MC, Giorgos NT, Evangelos GM, Konstantinos IT. Combined Endodontic and Surgical Management of a Mandibular Lateral Incisor with a Rare Type of Dens Invaginatus. J Endod 2008; 34: 1255-1260.