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8/6/2019 KAREN'S ENDO CR http://slidepdf.com/reader/full/karens-endo-cr 1/15 ENDODONTIC CASE REPORT NON-SURGICAL TREATMENT OF PERIAPICAL CYST KAREN PHUNG YEE SHIN F10044704 MENTOR: Dr. WAZILLAH NASSERIE, drg. MKes UNIVERSITAS PADJADJARAN FACULTY OF DENTISTRY BANDUNG 2010

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ENDODONTIC

CASE REPORT

NON-SURGICAL TREATMENT OF PERIAPICAL CYST

KAREN PHUNG YEE SHIN

F10044704

MENTOR: Dr. WAZILLAH NASSERIE, drg. MKes

UNIVERSITAS PADJADJARAN

FACULTY OF DENTISTRY

BANDUNG

2010

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1

CHAPTER I

INTRODUCTION 

Periapical cyst is an odontogenic cyst derived from the rest of Malassez that

  proliferates as an inflammation response against a long-term local aggression due to an

endodontic infection. This endodontic infection may be elicited by bacterial infection of pulp or 

in direct response to necrotic pulpal tissue.Clinically, it is usually asymptomatic but can result in

a slow-growth tumefaction in the affected area. From the radiographic view, it shows a round or 

oval with well-circumscribed, often corticated radiolucency lesion at the apex of a non-vital

tooth(Sapp, et al., 2004; Valois & Costa-Junior, 2005).

They are two types of this inflammatory apical cyst from the histological

appearance. The pocket cyst has its cavity open to the root canal while a true cyst is completely

enclosed by lining epithelium and may be attached to the root apex by a cord of epithelium (Lin

et al, 2007). According to Lin et al (2007), there is no definite preoperative method that can be

used to differentiate periapical granulomas from apical cysts unless biopsy is done. Therefore, all

inflammatory periapical lesions should be initially treated with conservative non-surgical

 procedures.

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CHAPTER II

CASE REPORT

Patient¶s name : M.U.

Medical record no. : 2009-052xx

Gender : Female

Age : 28 years old

Address : Jakarta

Medical history : Patient denied having any systemic disease and allergies.

Dental history : Patient previously had fillings done on tooth 14 and 46 few years ago.

She also had 47 extracted due to large cavity on the tooth. Tooth 24

underwent root canal treatment a month ago.

Extra-oral findings : No abnormalities found during the examination

Intra-oral findings : The findings are as below in the odontogram.

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Chief complaint : Patient complained of sudden pain and swelling on the palate area three

days before.

Anamnesis : Patient complained of sudden pain and swelling on the palate area three

days before. She went to a community health center in Jakarta and was

  prescribed with clindamycin and mefenamic acid. Other than that, the

suspected tooth pulp that causes the swelling on the palate was

intentionally perforated to allow drainage of the abscess. Before the

swelling occurred, patient has no complain on the affected tooth except

for discoloration and staining. And since the drainage of the abscess from

the tooth, she had bad taste in the mouth. The dentist in Jakarta has

suggested her to treat the tooth surgically but she has refused to do so due

to her fear of needle.

I/O examination : Tooth 12 was examined and its vitality was determined. Upon inspection,

there was a visible crack line running vertically from middle of the tooth

at the mesial to the incisal edge. The pulp chamber of the tooth was

visible from the palatal aspect. The tooth was slightly darker color than

the adjacent teeth. When the tooth was tested with ethyl chloride, the

 patient did not feel any pain or sensitivity. Percussion was positive and

 palpation on the adjacent palatal region was positive with fluctuant and

  pain. There was sinus drainage on the swollen area as well. When

mobility test was done, a part of the tooth chipped off. However, mobility

of the tooth was negative.

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Radiographic examination: Diagnostic periapical radiograph was taken.

L R 

Diagnosis : Acute periapical abscess e/c periapical cyst of necrotic pulp of tooth 12

Treatment plan : Access drainage of the abscess and root canal treatment of tooth 12 with

calcium hydroxide as intracanal medicament.

(28/08/2009)

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Armamentarium and materials:

1.  Endodontic explorer 

2.  K files (10 and 15) and ProTaper file (S1, Sx, F1, F2, F3) with stoppers

3.  Endodontic block 

4.  Irrigating syringes and needles ± each for sodium hypochlorite (NaOCl) 2.5%, saline (for 

spooling), hydrogen peroxide (H2O2), and chlorhexidine

5.  Paper points and sterile cotton pellet

6.  Gutta-percha (for obturation) and endomethasone and eugenol (for cementation of 

obturation material)

7.  Temporary filling

Procedure: 

On the first visit, initial radiograph was taken after anamnesis and examination in order to

determine the diagnosis and prognosis of the infected tooth. Once the diagnosis was determined,

 patient was given a thorough explanation on her tooth¶s condition and its prognosis along with

 possible treatments that could be done. Patient has strongly objected to apicoectomy due to her 

great phobia to needles. An informed consent of surgical refusal was signed. With the approval

and knowledge of a supervisor, the root canal treatment was carried out. Isolation of the working

area from saliva is done by using cotton rolls and saliva ejector. The root canal was explored

withNo.10 and No. 15 file. A slight over-instrumentation beyond the apex was done in order to

ease abscess drainage from the canal. Periodic irrigations were done as well in order to remove

the debris and at same time to lubricate the canal walls, aiding instrumentations. ProTaper S1

was used to clean the canal and irrigations were done. Paper points were used to dry the canal.

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The canal was closed with a cotton pellet added with a drop of tricresol formalin (TKF) and was

sealed with temporary filling. Patient was advised to finish up her previously prescribed

medications and to return after three days.

The second visit, patient came back after three days and the swelling on the palatal has

reduced and patient still felt pain and discomfort. There was a fistula on the palatal and a sterile

 probe was used to prick it. Abscess was drained as much as possible from the fistula. When there

are no more abscesses able to be drained, the canal treatment is continued. The temporary filling

and the cotton pellet was removed and reaming and filing with K-files and Protaper files was

done with periodic irrigations. Working length was determined using apex locator. Reaming and

filing was done until the working length and was stopped at ProTaper F3 file. Irrigations of the

canal was done and dried with paper points. The canal is inserted with paper point dropped with

  p.Chlorophenol camphor mentol (CHKM) and closed using temporary filling. Patient was

advised to return in another three days.

In the third visit, the palatal swelling has remarkably reduced and patient only

complained of slight pain when percussion was done and the fistula has healed. In this visit, the

canal was reamed and filed, irrigated and dried. Ultracal® (calcium hydroxide, CaOH) was filled

into the canal. Patient felt a sharp pain momentarily when a cotton pellet was pushed into the

opening of the canal. The canal was sealed with temporary filling and patient was advised to

return in 1 month time for a trial photo to check for healing.

In the subsequent visits, the previous procedures were repeated and trial photos were

taken in order to check the progress of the healing periapical region. In every visit, percussion

was done and the paper points were checked for any blood, pus and smell. Patient continually

return every month for intra-medicament dressing using only CaOH for the next 9 months. Upon

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consultations with the supervisor, obturation was done using guttapercha after the 10th

visits (11

months after initial visit). As to date, the control after the obturation is yet to be done.

During treatment :

Control 1

(05/11/2010)

Control 2

(04/01/2010)

Control 3

(23/02/2010)

Control 4

(12/05/2010)

Obturation

(23/07/2010)

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CHAPTER III

LITERATURE REVIEW

The periapical cyst is an inflammatory lesion that occurs as a response to a long

term irritation of the dental pulp.During the periapical inflammation, the host cells in the

 periapical tissues release many inflammatory mediators, pro-inflammatory cytokines, and growth

factors through innate and adaptive immune responses as in figure 1. Several growth factors such

as EGF, KGF, and insulin-like growth factor released by stromal fibroblasts and also TGF-

released by eosinophils, macrophages and lymphocytes are identified to be able to induce

epithelial cell rests to divide and proliferate and possibly develop into an apical cyst.

Figure 1 Schematic illustration of the major mechanism that activates proliferation of epithelial cell rests in

apical periodontitis. M, macrophages; TH, helper T cell; ERM, epithelial cell rests of Malassez; O,

osteoclast; EO, eosinophil; PMN, polymorphonuclear leukocyte; IL, interleukin; TNF, tumor necrosis

factor; PGs, prostaglandins; EGF, epidermal growth factor; IGF, insulin-like growth factor; TGF-,

transforming growth factor-alpha (Lin, Huang, & Rosenberg, 2007).

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There are few theories that have been proposed as to how periapical cyst could

occur. Firstly, the nutritional deficiency theory assumes that when the islands of epithelium

expand, there will be more central epithelium cells which are distanced from their nutritional

supply and undergo necrosis. A cystic cavity eventually resulted in the center of the cell mass as

liquefaction necrosis continues to occur. Secondly, the abscess theory proposed that an abscess

cavity is formed in the periapical connective tissues. Subsequently, the abscess is completely

surrounded by epithelium because of the natural inclination of stratified squamous epithelium to

line exposed connective tissues surfaces. There is also a theory which suggested the merging of 

epithelial strands as a result of its continuous growth and finally merged to form a three-

dimensional mass. When the connective tissue trapped inside the ball mass degenerates, a cyst is

finally formed (Garcia, etal., 2007; Lin, Huang, & Rosenberg, 2007).

The pathogenesis of cysts has been described in three phases. In the first phase, the

epithelial cell rests of Malassez begin to proliferate as a direct result of the inflammation, and

influenced by bacterial antigens, the epidermal growth factors, metabolic and cellular mediators.

  Next, in the second phase, a cavity is formed, lined by epithelium (based on the mentioned

theories), and lastly, during the third phase, the cyst grows, probably through osmosis

(Garcia,etal., 2007).

Most periradicular lesions except apical true cyst heal after proper non-surgical

endodontic therapy. The healing process took place has the same principles as that of connective

tissues elsewhere in the body. When all irritants in the canals are removed by chemomechanical

instrumentation and the canal is completely sealed, all cell components participating in

inflammatory response will gradually resolve. These cells which are not needed anymore will

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undergo apoptosis (programmed cell death). Figure 2 shows the mechanisms of regression of 

inflammatory apical cysts after periapical wound healing.

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Figure 2Mechanisms of regression of inflammatory apical cysts after periapical

wound healing (Lin, Huang, & Rosenberg, 2007). 

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CHAPTER IV

DISCUSSION

Calcium hydroxide use in necrotic pulps is recommended after instrumentation

due to its greater antimicrobial effect which can last for weeks. Other than that, it may increase

the effectiveness of sodium hypochlorite at the subsequent appointment, which should enhance

the effectiveness of antimicrobial agents (Walton &Torabinejad, 2002). This intracanal

medicament appears to create favorable environment in which hard tissues formation can occur.

Calcium hydroxide precipitates as calcium proteinate or calcium carbonate crystals, either which

might act as a demarcation between the necrotic and vital pulp tissue and serve as a suitable

matrix for odontoblast alignment.It has been postulated that the high pH level of this material, as

a result of free hydroxyl ions in root canal fillings promote a state of alkanity in adjacent tissues,

a condition that favors repair. Calcium hydroxide should be ideally placed deep and densely in

the canal space so that its biologic effects can be exerted in close proximity to the appropriate

tissue (Gaikwad, Banga, &Thakore, 2000).

An overextension of calcium hydroxide paste into the cystic lesions, as performed

in the case reported, has been previously described in Valois & Costa-Junior¶s (2005) case

report. The advantages of this procedure include (1) anti-inflammatory action through

hygroscopic properties forming calcium proteinate bridges and inhibiting phospholipase, (2)

neutralization of acidic products such as hydrolases, which can affect the clastic activity, (3)

activation of the alkaline phosphatase, (4) antibacterial effect and (5) the destruction of the cystic

epithelium, allowing conjunctive tissue invagination to the lesion. In the case report also stated

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that according to Bhaskar (1972), it is suggested to slightly over-instrumentation of the root

canal during the endodontic therapy beyond the apical foramen. This will produce a transient

acute inflammation and destruction of the protective epithelial layer of the cyst, converting it into

a granulated tissue, which has a better resolution. However, this procedure is not evidently

supported. In this case, over-instrumentation is done to help eliminate microorganisms from the

apical area, thus reducing the inflammatory process by creating drainage for the abscess.

Moreover, it could facilitate cyst resolution through relief of the intra-cystic pressure.

The criteria used to establish the most adequate moment forobturation of the root

canal are associated with absence of spontaneous pain, sensitivity to percussion, negative to

exudates and edema, and the beginning of radiographic regression of the lesion.

From the control periapical radiographs, it can be concluded that the endodontic

treatment of periapical cyst using calcium hydroxide as the intracanal medicament is successful.

Further control in 6 months to a year should be done so check on the healing progress.

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REFERENCES

Gracia CC, Sempere FV, Diago MP, Bowewn EM. 2007: The post-endodontic periapical lesion:

Histologic and etiopathogenic aspects. Med Oral Pathol Oral Cir Buccal; 12(8): E585-90

Ingle JI and Bakland LK, 2002: Endodontics Volume 1. 5th

Ed. Ontario: BC Decker IC. Pp 175-201

Lin LM, Huang GTJ, Rosenburg PA. 2007: Proliferation of epithelial cell rests, formation of 

apical cysts, and regression of apical cysts after periapical wound healing. J Endod; 33:908-916

Sapp JP, Eversole LR, Wysocki GP. 2004: Contemporary Oral & Maxillofacial Pathology. 2nd

 

Ed. Missouri: Mosby. Pp 47-49

Valois CRA and Costa-Junior ED. 2005: Periapical cyst repair after nonsurgical endodontictherapy ± Case report. Braz Dent J; 16 (3): 254-258

Walton and Torabinejad. 2002: Principles and Practice of Endodontics. 3rd Ed. Philadelphia:

Saunders. Pp 233-234; 291