CHRONIC HYPERPLASTIC PULPITIS

MAKALAH ORAL BIOLOGI

BAGIAN ANATOMI, FISIOLOGI, dan HISTOLOGY

PEMBIMBING: Dr.drg. Marry Siti Mariam, M.S.

drg. Nani Murniati, M.Kes.

Dr.drg. Sri Tjahajawati, M.Kes.

Mahasiswa Adaptasi 2016

Carryl F. Sepang

Febe M. K Wangania

Glory V. Pohan

UNIVERSITAS PADJADJARAN

FAKULTAS KEDOKTERAN GIGI

BANDUNG

2017

1
 TABLE OF CONTENTS

CHAPTER I INTRODUCTION ....................................................................................... 3

CHAPTER II RELATED LITERATURE ........................................................................ 4
2.1 Normal Pulp Tissue................................................................................................. 4
2.2 Classification of Pulpitis ......................................................................................... 8
2.2.1 Reversible Pulpitis ........................................................................................... 9
2.2.2 Irreversible Pulpitis ........................................................................................ 10
2.2.3 Pulpal Necrosis .............................................................................................. 12
2.3 Causes of Pulp Inflammation ................................................................................ 13
2.3.1 Bacteria .......................................................................................................... 13
2.3.2 Traumatic ....................................................................................................... 15
2.3.3 Iatrogenic ....................................................................................................... 16
CHAPTER III CHRONIC HYPERPLASTIC PULPITIS .............................................. 17
3.1 Background ........................................................................................................... 17
3.2 Case Report of Unusual Chronic Hyperplastic Pulpitis ........................................ 19
3.3 Management of Chronic Hyperplastic Pulpitis and .............................................. 23
Healing Process Post-Extraction ........................................................................... 23
3.3.1 Management of Chronic Hyperplastic Pulpitis .............................................. 23
3.3.2 Healing Process Post-Extraction .................................................................... 24
CHAPTER IV DISCUSSION......................................................................................... 26
CHAPTER V CONCLUSION ........................................................................................ 28
REFERENCES ............................................................................................................... 29

2
 CHAPTER I

INTRODUCTION

Pulpitis is inflammation of the dental pulp resulting from untreated caries,

trauma, or multiple restorations. Pulpitis refers to inflammation of dental pulp that

involves blood vessels and the nerves and is one of the most common reasons of tooth

ache. Pulpitis can occur as a result of untreated tooth decay, trauma to the tooth or can

occur because of multiple restorations (Reversible Pulpitis Vs Irreversible Pulpitis,

2010)

Pulpal diseases are based on the ability of the inflamed dental pulp to return to a

healthy state once the noxious stimulus has been removed. Condition of the pulp can be

classified into normal pulp, reversible pulpitis, irreversible pulpitis, and necrotic pulp.

(Cawson and Odell, 1998).

This paper will be talking mainly about chronic hyperplastic pulpitis which one

of the form of irreversible pulpitis, a report about unusual case report of it, and

management of the case. In the case of chronic hyperplastic pulpitis, the disease process

is irreversible.

Chronic hyperplastic pulpitis also known as pulp polyps usually occurs in molar

teeth of children and young adults and is characterized by an overgrowth of

granulomatous tissue into the carious cavity, but there is some unusual case where

chronic hyperplastic pulpitis occurred in matured pulp (Faryabi and Adhami, 2008).

3
 CHAPTER II

RELATED LITERATURE

2.1 Normal Pulp Tissue

The dental pulp is a connective tissue consisting of nerves, blood vessels,

ground substances, interstitial fluid, odontoblasts, fibroblasts, and other cellular

components (Ali and Mulay, 2015).

The dental pulp consists of vascular connective tissue contained within rigid

dentinal walls, pulp tissue similar to other connective tissue in the human body and

owing to its functions and environment.

Figure 2.1: Tooth Anatomy (Kumar, et al., 2015)

Functions of the pulp are:

Formative. Elaboration of dentin to form the tooth

Protective. Protection against and repairing of the effects of noxious stimuli

4
 Nutritive. Preserving the vitality of all the cellular elements

Sensory. Perception of stimuli

The elaboration of dentin creates a special environment for the pulp. The pulp

space becomes limited by dentin formation in permanent adult human teeth. This

volume is continuously reduced by the deposition of secondary dentin throughout the

life of the pulp, as well as by the deposition of reparative dentin in response to noxious

stimuli (Chandra and Krishna, 2011).

There are 4 Zones of pulp:

1) Odontoblastic Zone

Odontoblasts are the characteristic cells of pulp. They form a single layer at its

periphery, synthesize the matrix, and control the mineralization of dentin. The

morphology of the cell reflects its level of activity; larger cells have a well-developed

synthetic apparatus and the capacity to synthesize more matrix. Odontoblasts can

continue at varying levels of activity for a lifetime. the odontoblast consists of two

major components, the cell body and the cell proses.

The primary function if the odontoblasts throughout the life of the pulp is the

production and deposition of dentin. Because the important and close relationship

between odontoblasts and dentin (Torabinejad and Walton, 2008).

2) Cell-free Zone

Thin layer immediately subjacent to the odontoblastic zone that contains very

few cells. This zone, although called cell-free, contains some fibroblasts, mesenchymal

cells, and macrophages.

5
 3) Cell-rich Zone

The cell-rich zone is located central to the cell-free zone. Ground substance,

fibroblasts and their product like collagen fibers, undifferentiated mesenchymal cells,

macrophages are the main components of this zone. Those components will be

explained briefly (Chandra and Krishna, 2011).

Figure 2.2: Zones of pulp. A, Lower-power dentin-pulp complex. B, Higher power,

cell-free zone (of weil) and cell-rich zone (Antonio, 2012)

(1) Fibroblast

Fibroblasts are the common cell type in the pulp and are seen in greatest

numbers in the coronal pulp. They produce and maintain the collagen and ground

substance of the pulp and alter the structure of the pulp in disease. The more active the

cell, the more prominent the organelles and other components necessary for synthesis

6
and secretion. These cells also undergo apoptotic cell death and it will be replaced by

the maturation of less differentiated cells when needed.

Figure 2.3: Light Microscopic of Fibroblast in Dental Pulp (Antonio, 2012)

(2) Undifferentiated Mesenchymal Cells

The undifferentiated mesenchymal cells are derived from the mesenchymal cells

of the dental papilla. They retain pluripotential characteristic because of their function

in repair and regeneration. These cells resemble fibroblasts as they are stellate in shape,

with a large nucleus and little cytoplasm. Usually located around blood vessels in the

cell-rich zone and are difficult to recognize (Chandra and Krishna, 2011).

(3) Macrophages, Lymphocytes, and Plasma cells

Macrophages are found in the cell-rich zone, especially near the blood vessels.

These cells are blood monocytes that have migrated into the pulp tissue. Their function

7
is to phagocytize necrotic debris and foreign materials. Lymphocytes and plasma cells,

if present in the normal pulp, are found in the coronal subodontoblastic region. The

function of these cells in the normal pulp may be immune surveillance (Chandra and

Krishna, 2011).

4) Central zone

The central zone or pulp proper contains blood vessels and nerves that are

embedded in the pulp matrix together with fibroblast. From their central location, the

blood vessels and the nerves send branches to the periphery of the pulp.

Figure 2.4: Zones of Pulp (Chandra and Krishna, 2011)

2.2 Classification of Pulpitis

Pulpitis refers to inflammation of dental pulp that involves blood vessels and the

nerves and is one of the most common reasons of tooth ache. Pulpitis can occur as a

8
result of untreated tooth decay, trauma to the tooth or can occur because of multiple

restorations.

2.2.1 Reversible Pulpitis

Reversible pulpitis is a mild to moderate inflammatory condition of the pulp

caused by noxious stimuli in which the pulp is capable of returning to the uninflamed

state following removal of the stimuli.

Reversible pulpitis may range from hyperemia to mild to moderate

inflammatory changes limited to the area of the involved dentinal tubules, such as

dental caries. Dilated blood vessel, extravasation of edema fluids, disruption of the

odontoblast layer may be seen in microscopically.

Figure 2.5: Pulpitis Reversible (Mrzezo, 2015)

Symptoms for reversible pulpitis is characterized by sharp pain lasting for a

moment, that more often cause by cold food and beverages and also cold air when apply

9
to the cavity. Pain is not spontaneous usually should be trigger, and will stop as soon as

the cause is removed.

Management for reversible pulpitis are removal of the noxious stimuli and in

case of caries, restoration with appropriate restorative material is indicated (Chaudhary,

2011).

2.2.2 Irreversible Pulpitis

According to Grossman irreversible pulpitis divided by:

Acute Symptomatic Irreversible Pulpitis

Based on subjective and objective findings that the vital inflamed pulp is

incapable of healing and that root canal treatment is indicated. Characteristic may

include sharp pain upon thermal stimulus, lingering pain (often 30 seconds or longer

after stimulus removal), spontaneously (unprovoked pain) and referred pain. Typically,

there are minimal changes in the radiographic appearance of the periradicular bone, for

advance irreversible pulpitis thickening of the periodontal ligament may be seen. Dental

history and thermal test are very important and the primary tools for assessment (Ali

and Mulay, 2015).

Chronic Asymptomatic Irreversible Pulpitis

Clinical diagnose based on subjective and objective findings indicating that the

vital inflamed pulp is incapable of healing. If its left untreated the tooth may become

symptomatic or even necrotic, and endodontic treatment should be performed as soon as

possible. These cases have no clinical symptoms and usually respond normally to

10
thermal testing but may have had trauma or deep caries that would likely result in

exposure following removal (Cohen and Hargreaves, 2006).

Histopathological features of irreversible pulpitis the area of the abscess with

microorganism present if it in the late carious state, along with lymphocytes, plasma

cells and macrophages, and also reparative dentin is absent.

Figure 2.6: Irreversible Pulpitis. A, Advanced caries in the dentin has reached the pulpal
tissue under the occlusal fissure, causing circumscribed pulpal
inflammation. B, Death of odontoblasts without formation of reparative
dentin, and inflammatory cell infiltration into the adjacent pulpal tissue.
C, Penetration of bacteria within the dentinal tubules with chemotactic
attraction of neutrophilic granulocytes (Mrzezo,2015)

Management for irreversible pulpitis is complete removal of pulp and placement

of intracanal medicament like eugenol or formocresol (Ali and Mulay, 2015).

Chronic Hyperplastic Pulpitis

Chronic hyperplastic pulpitis is found rarely, despite wide exposure and heavy

infection, the pulp not merely survives but proliferates through the opening. This may

11
even happen in fully formed teeth, as there are some case report about chronic

hyperplastic pulpitis occurred in matured pulp (Cawson and Odell, 1998).

More explanation and discussion about this type of pulpitis will be in chapter 3.

2.2.3 Pulpal Necrosis

Pulpal necrosis is the term applied to pulp tissue that is no longer living. Pulpal

necrosis occurs slowly over time, as occurs during the course of an untreated

irreversible pulpitis. In this later case the patient may gradually lose the acute and

chronic symptoms, because the nerve fibers in the pulp degenerate from the

overwhelming inflammation showing the calcification of pulp.

Figure 2.7: Pulp with Partial Necrosis. Area with cell nuclei of cells inflammation (Red
arrow), and calcification (Black arrow) (H.E., original magnification 200x)
(Bruno, et al., 2015)

In pulpal necrotic the pulp tissue may be infected with bacteria. Usually it is the

result of dental decay, in which the infection can quickly extend into the apical areas

12
and surrounding bone of the tooth. Noninfected necrosis pulpal occurs usually after a

traumatic incident, that sometimes asymptomatic for months. The signs for non-infected

pulpal necrosis may be a change in the coloration of the tooth.

A diagnostic too used to determine if a tooth has undergone pulpal necrosis

consists of gently tapping on several teeth in the area with a blunt instrument. A tooth

that has undergone pulpal necrosis will be identified, because the pressure from the

tapping will produce intense pain Called percussion test (Sapp, et al., 2004).

2.3 Causes of Pulp Inflammation

Wein classified causes of pulpal inflammation into bacterial, traumatic, and

iatrogenic (Garg, 2014). There will be brief explanation about each cause, but this paper

will be explaining more about bacteria and the reaction of the pulp to bacteria.

2.3.1 Bacteria

In 1894 W.D Miller suggested that bacteria were the most common cause of

pulp inflammation. Bacteria or their products may enter the pulp through a break in

dentin, either it is from caries, accidental exposure from developmental grooves,

percolation around a restoration, from extension of infection, from the gingiva, or by

way of the blood.

Once bacteria have invaded the pulp, the damage is almost always irreparable.

The species of bacteria recovered from inflamed or infected pulps are many and varied.

Although lactobacilli are commonly found in carious dentin, they are seldom recovered

13
from the pulp because of their low degree of invasiveness. Microorganisms doesnt

need to be present in the pulp to produce an inflammation, the products of bacteria in

dentin is enough to irritate and to cause an inflammatory reaction.

Bacteria most often found from infected vital pulp are streptococci,

staphylococci, and other microorganism i.e. anaerobes. The type of organism recovered

usually depends on whether the pulp is cultured in situ or after extraction of the tooth,

whether communicates with the fluids of the mouth, and whether the disease has

progressed to necrosis.

Pulp itself react to the bacterial invasion, the reaction of the pulp is difference

not like other infection in the other part of the body. Once the pulp is exposed by caries

or trauma, it is considered infected because microorganisms gain access to it almost

immediately. At first, the infection is localized to a small area of the pulp, just an

infection following a scratch of the arm is localized. Although the coronal area of the

pulp may be involved by a mild or even severe infective process, the body and apical

portion of the pulp may remain normal. The reaction of the pulp in the involved area is

an inflammatory response.

Polymorphonuclear leukocytes reach the area, and further dissemination of

bacteria deeper into the pulp is prevented. Because some microorganisms enter the

dentinal tubules, they may gain a foothold that is difficult to dislodge. In this respect,

injury of the pulp and injury of the arm or some other part of the body differ; in the

latter, microorganisms are more readily reached by tissue defenses. The reaction in an

inflamed pulp also differs from that in an inflamed of other organ in that small limited

14
space provided during the inflammatory state for swelling of the pulp because the pulp

is entirely enclosed in a hard, unyielding dentinal wall, except at the apical foramen. If

the inflammatory process is severe, it will extend deeper into the pulp and all the

symptoms of an acute reaction will be manifested.

Considerable inflammatory exudate accumulates and causes pain from the

pressure on the nerve endings. Area of necrosis develop, owing o disturbance in

nutritional supply, many of the polymorphonuclear leukocytes die, and pus forms,

further irritating the nerve cells. If the process is less severe, lymphocytes and plasma

cells will replace the polymorphonuclear leukocytes in numbers, and the inflammatory

reaction may be confined to the surface of the pulp.

During the inflammatory reaction, tissue pressure is increased. Stasis occurs,

with resulting necrosis of the pulp. In most cases the microorganisms survive, and if

virulent, multiply rapidly and reach the periapical tissue, where they continue their

destruction and produce an acute alveolar abscess. Meanwhile, during the process of

bacteria invasion, the dentinal tubules may become infiltrated with products of blood

decomposition, bacteria, and occasionally, food debris, and the dentin becomes

discolored. Such discoloration of tooth structure is sometimes the first clinical sign that

the pulp has died (Chandra and Krishna, 2010).

2.3.2 Traumatic

Traumatic injury may or may not be accompanied by fracture of the crown or

root. Trauma is less frequently the cause of pulp injury in adults than in children.

15
Whether the injury is a result of an automobile accident, a sport mishap, the severity

and the type of injury will determine the treatment necessary. There are number of

common injuries that occur to the teeth such as, acute trauma including fracture,

luxation or avulsion of the tooth. Where chronic trauma including parafunctional habits

like bruxism.

2.3.3 Iatrogenic

During dentine preparation, numerous dentine tubules are always exposed and

the odontoblast process cut off at the level of the dentine wound. The mechanical

opening of the dentine tubules and intra-pulp pressure lead to the dentinal fluid flowing

through the dentine tubules to the open dentine surface resulting in dehydration of the

pulp.

Iatrogenic cause pulp inflammation for which the dentists own procedure.

Various iatrogenic cause of pulpal damage can be (Garg, 2014):

1) Thermal changes generated by cutting procedures, during restorative procedure,

bleaching of enamel, laser beam, etc. that can cause severe damage to the pulp

if not controlled.

2) Orthodontic movement

3) Periodontal and periapical curettage

16
 CHAPTER III

CHRONIC HYPERPLASTIC PULPITIS

3.1 Background

Chronic hyperplastic pulpitis also known as pulp polyp is an uncommon and

specific type of inflammatory hyperplasia that is associated with a non-vital tooth. The

disease process in most cases is irreversible. Often the pulp polyp is an incidental

finding and at times may mimic reactive and neoplastic disease of gingiva clinically.

Most frequently involved teeth are deciduous or permanent molars (Saraf, 2006).

Figure 3.1: Chronic Hyperplastic Pulpitis (Flaitz, 2004)

It is usually seen in teeth of children and adolescence in which pulp tissue has

high resistance and large carious lesion permit free proliferation of hyperplastic tissue.

Since it contains few nerve fibers, it is non-painful but bleeds easily due to rich network

17
of blood vessels (Garg, 2014). Rather than undergoing necrosis, the pulp tissue reacts in

a hyperplastic manner, producing a red mass of reparative granulation tissue that

extrudes through the pulp exposure. This type of reaction is believed to be related to the

open root foramen, through which a relatively rich blood supply flows (Regezi, et al.,

2011).

Clinical features of chronic hyperplastic pulpitis it is occur as a reddish

cauliflower-like outgrowth of connective tissue into caries that has resulted in a large

occlusal exposure, and It said this kind of pulpitis has no symptoms, but if one of these

polyps is found to be symptomatic most likely not of pulpal origin but is instead an

extension of the adjacent gingiva that is overlying the disintegrated tooth crown (Sapp,

et al., 2004).

Histopathologic features are surface covered by stratified squamous epithelium.

Epithelium derived from gingiva and freshly desquamated epithelial cells of oral

mucosa or tongue. Granulation tissue projects from pulp into carious lesion.

Granulation is vascular containing collagen fibers, blood vessels, inflammatory cell

infiltrate chiefly consisting of neutrophils, plasma cells and lymphocytes (Chaudhary,

2011).

Chronic hyperplastic pulpitis usually involved deciduous teeth, but there is a

case report about unusual chronic hyperplastic pulpitis in an impacted 3rd molar of a 27-

year-old woman. The case report will be explained next in this chapter, it will give more

information on how chronic hyperplastic pulpitis occurred in permanent teeth, the

histological features and its treatment.

18
Figure 3.2: Pulp Polyp. Microphotograph of a pulp polyp extending from the pulp of a
young tooth. Black arrow: Stratified squamous epithelial, Red arrow:
Chronic inflammatory granulation tissue. (Bergenholtz, et al., 2010)

3.2 Case Report of Unusual Chronic Hyperplastic Pulpitis

A 27-year-old woman referred for treatment of left side lesion of the oral cavity.

She gave history of six months for its presence that enlarged gradually and interfered

with eating and occluding the teeth, so that made patient worried about it.

Figure 3.3: Unusual Chronic Hyperplastic Pulpitis in Unique Large Size (Faryabi and
Adhami,2008)

19
 Intraoral examination showed a large polypoid lesion with 3.5 cm height, 1.5 cm

width and a 5-mm stalk diameter protruded from the carious cavity of partially exposed

crown of the tooth, the lesion overlaid on lingual side of this tooth and obviously

presented itself in left oropharyngeal area. The lesion also covering the crown of the

adjacent teeth beside the infected 3rd molar, makes it really visible clinically.

She gave history of idiopathic thrombocytopenic purpura and splenectomy of 12

years ago, and caesarian section three years ago, but both of it had no relation to the

present lesion found in her oral cavity. Laboratory examination including CBC

differential, WBC, platelet count, prothrombin time, and partial thromboplastin time

were all within normal limits.

Orthopantomogram showed left carious mesioangular semi impacted 3rd molar

with no specific lesion in bone and adjacent tissues.

Figure 3.4: Left Side Semi Impacted Carious Lower 3rd Molar was the Origin of the
Lesion (Faryabi and Adhami, 2008)

20
 Considering the radiographic and clinical data a large pulp polyp, peripheral

giant cell granuloma, and papilloma were the possible differential diagnoses.

The specimen included the carious 3rd molar with base of the lesion in the

carious cavity and the bulk of the lesion to the pathologist for histopathologic

examination. The results of the biopsy from the laboratory will help in pointing out a

diagnosis of the lesion in order for the medical team to give the patient the right

management.

Histopathological findings revealed a mass of inflamed granulation tissue

resembling pyogenic granuloma that protruding from the crown of the carious tooth.

Figure 3.5: An Exophytic Mass of Granulation like Tissue (H&E; original

magnification, x100) (Faryabi and Adhami, 2008)

The fibrovascular stroma contained numerous capillary sized blood vessels line

by plump endothelial cells.

There were also significant mixed inflammatory cells composed of lymphocytes,

plasma cells and neutrophils. The surface of the lesion was ulcerated and replaced by

fibrin purulent membrane. Diagnosis was chronic hyperplastic pulpitis

21
Figure 3.6: Specimen Showing Capillary Blood Vessels and A Mixed Inflammatory
Cell Infiltrate of, Plasma Cells and Lymphocytes (H&E; original
magnification x400) (Faryabi and Adhami,2008)

Figure 3.7: Mixed Inflammatory Cell Infiltrate of Neutrophil, Plasma Cells and
Lymphocytes (H&E; original magnification, x1000) (Faryabi and Adhami,
2008)

Management for this case were surgical procedure for excisional biopsy of the

lesion and surgical removal of badly broken 3rd molar due to the extensive caries.

Surgical procedure was performed under local anesthesia using Persocaine-e.

22
3.3 Management of Chronic Hyperplastic Pulpitis and Healing Process Post-
Extraction

3.3.1 Management of Chronic Hyperplastic Pulpitis

Complete removal of pulp followed by its restoration should be goal of the

treatment. In case of hyperplastic pulpitis, removal of polypoid tissue with periodontal

curette or spoon excavator followed by extirpation of pulp should be done (Torabinejad

and Walton, 2009). The usual treatment of a tooth with pulp polyp is extraction. If the

molar is in the deciduous dentition, sometimes it is not extracted to maintain arch space.

It should be remembered that the polyp cannot be effectively cleaned and that the

remaining tooth structure will continue to decay, producing a chronic septic condition

that can pose a health risk to the patient (Sapp, et al., 2004).

Management of the tooth with chronic hyperplastic pulpitis in permanent tooth

includes extraction when minimal amount of tooth structure remains which is

unfavorable for restoration and conservatory approach requires a multidisciplinary

approach including endodontic management, surgical crown lengthening, and

prosthodontic management. In cases of pulp polyp young adults where there is only

coronal pulp tissue involvement pulpotomy has also been suggested as a treatment of

option (Faryabi and Adhami, 2008).

This paper discusses more about the unusual case report of chronic hyperplastic

pulpitis that occurred in permanent tooth. Therefore, the discussion for the healing

process will be on post-extraction following the management that was given in the case

report.

23
3.3.2 Healing Process Post-Extraction

The extraction wound also results in disruption of normal anatomic structure and

function. The healing of extraction wound is characterized by 5 stages of healing with

an initial exudative/inflammatory phase.

In this stage the extraction defect is filled with blood and after a series of

physiological events, the clot is formed eventually. The clot is composed of fibrin,

RBCs enmeshed with WBCs. This stage is followed by granulation stage. The

granulation tissue replaces the clot over a 4-5-day period. The granulation tissue in the

3rd stage is connective tissue hat compromises of fibroblasts cells, collagen fibers,

interspersed in a ground substance. The healing extraction socket is marked by a fourth

stage which is characterized by calcification of connective tissue or osteoid deposition.

This starts at the base and periphery of the socket. Early osteoid is seen by 7-10 days.

By 6 weeks, the socket is filled with bony trabeculae. In fifth stage the defect further

covered by an epithelium. This occurs after 24-35 days. The bone deposition keep on

taking place between 5-10 weeks and till 16 weeks the filling of extraction socket defect

by bone is complete. Osteoblasts cells are seen laying down the osteoid in maximum

number between 4-6 weeks after extraction wound and 8 weeks thereafter these

osteogenic processes slow down.

As for the bone healing, can be primary or secondary. The primary bone healing

occurs after the fractured ends of bone are aligned perfectly with compression of the

fragments and there should be no gap between the separated or fractured ends.

Obviously, the bone heals without callus formation. To achieve this perfect reduction of

24
fractured ends is difficult. At microscopic level, such perfect reduction and alignment is

impossible.

The fracture may not be treated or whenever they are treated, the surgical

management involves reduction of fractured ends in form of cast immobilization, sling

immobilization. Secondary bone healing or repair of fracture therefore begins with a

deposition of fibrous connective tissue at fibrocartilage end of bone (Saraf, 2006).

A
C

Figure 3.8: Repair Response After Tooth Extraction. A, The tooth in situ. B, after
extraction the socket is filled with clot. C, the clot resolves by (1) the
polymorph response, (2) the macrophage response, and (3) the fibroblast
response. In addition, the bony defect become colonize by new osteoblast
(4) that form new bone as the collagen scar is remodeled (D) (Antonio, 2012)

25
 CHAPTER IV

DISCUSSION

Chronic hyperplastic pulpitis is a form of irreversible pulpitis it is usually

asymptomatic, patient only feel discomfort during mastication by the pressure caused

due to the food bolus. It is the opposite of acute irreversible pulpitis where it is exhibits

pain usually caused by hot or cold stimulus, or pain that occurs spontaneously

(Torabinejad and Walton, 2009).

Chronic hyperplastic pulpitis (pulp polyp) is the most visually dramatic of all

pulp response, rising out of the carious shell of the crown and is a mushroom of living

pulp tissue that is often firm and insensitive to touch. The difference in between other

pulpitis and chronic hyperplastic pulpitis is very rare in middle aged adults but it is

more common in teeth of children and adolescents, in which the pulp tissue have a high

resistance and a good blood supply (Faryabi and Adhami, 2008). Any other pulpitis

could happen in any teeth at any age. The other type of pulpitis clinically seen like

badly broken down crown of the tooth unlike chronic hyperplastic pulpitis, where you

can see cherry red of the granulation tissue to opaque whiteness of moist keratinized

epithelium depending on the degree to which the appearance of the granulation tissue is

modified by its covering (Anilkumar, et al., 2016).

Chronic hyperplastic pulpitis inflammation may be indicative of a good pulpal

response. Presumably the young pulp does not become necrotic following exposure,

26
because its natural defenses and rich supply of blood allow it to resist bacterial

infection. Transudates and exudates which are inflammatory response products in open

chronic pulpitis, drain into the oral cavity and do not accumulate (Regezi, et al., 2012).

According to chronologic time for development of the lower 3rd molar, there is

no young pulp found in the beginning of formation of this lesion and may consider rich

blood supply to resist bacterial infection and slow process of carious formation due to

partially impaction of crown of offending tooth led to developing the hyperplastic

pulpitis in this patient (Faryabi and Adhami, 2008).

There is no significant difference in between chronic hyperplastic pulpitis

occurred in impacted tooth or not. As long as the tooth can resist the bacterial infection

and have rich blood supply that brings the transudates and exudates into oral cavity and

doesnt allow them to accumulate, chronic hyperplastic pulpitis may be takes place.

27
 CHAPTER V

CONCLUSION

This paper explains general view of chronic hyperplastic pulpitis, but highlight

with the unusual case report presentation about chronic hyperplastic pulpitis which also

known as pulp polyp in a lower third molar of a 27-year-old woman, that not only grow

into carious cavity but also extruded in a very large size that interfered with occluding

of the teeth. The management which is extraction of the lower left third molar.

In treatment planning for oral and maxillofacial lesions, we must consider the

clinical finding, and dental history of the patient and finally the histopathologic report

for management of such lesions in spite of unusual size of them.

28
 REFERENCES

Ali, S. and Mulay, S. 2015. Pulpitis: a review. IOSR Journal of Dental and Medical
Sciences. Vol. 14: 94-95
Anilkumar, K., Lingeswaran, S., Ari. G., Thyagarajan, R., & Logaranjani. A. 2016. Management of
chronic hyperplastic pulpitis in mandibular molars of middle aged adults- a multidisciplinary
approach. Journal of Clinical and Diagnostic Research. Vol.10(1): 24-25
Antonio, N. 2012. Ten Cate's Oral Histology 8th Edition. Canada: Elsevier.
Bergenholtz, G., Bindslev, P., & Reit, C. 2010. Textbook of Endodontology 2nd Ed. USA:
Wiley-Blackwell
Bruno, K., Alencar, A., Estrela, C., Batista, A., & Pimenta, F. 2009. Microbiological and microscopic
analysis of the pulp of non-vital traumatized teeth with intact crowns. Journal of Applied Oral
Science. Vol.17(5): 511
Cawson, R. and Odell, W. 1998. Cawsons Essentials of Oral Pathology and Oral Medicine 6th Ed.
UK: Churchill Livingstone.
Chandra, B., & Krishna, V. 2010. Grossmans Endodontic Practice 12th Ed. India: Wolter Kluwer
Health.
Chaudhary, M., & Chaudhary, S. 2011. Essential of Pediatric Oral Pathology. India: Jaypee
Cohen, S., & Hargreaves, K. 2006. Pathways of the Pulp 9th Ed. Mosby: Elseveir
.Faryabi, J. & Adhami, S.2008. Unusual presentation of Chronic Hyperplastic Pulpitis: A Case
Report. Internation Endodontic Journal. Vol. 2: 156-158
Flaitz, C., Hicks, M., Meyers, A & Raugi, G. 2014. Pulp Polyp. Available online at:
http://emedicine.medscape.com/article/1076860-overview.html (Accessed: March, 29th 2017)
Garg, N. & Garg, A. 2014. Textbook of Endodontics 3rd Ed. India: Jaypee
Kumar, V., Abbas., AK., & Aster, JC. 2015. Robins and Cotran Pathologic Basis of Disease 9th Ed.
Phildelphia: Elsevier
Mrzezo in Endodontics. 2015. Pathobiology. Available online at: http://Mrzezo.com/2-
pathobiology.html (Accessed: March, 29th 2017)
Regezi, J., Sciubba, J., & Jordan, R. 2012. Oral Pathology Clinical Pathologic
Correlations 6th Ed. St.Louis: Elsevier
Reversible Pulpitis Vs Irreversible Pulpitis. Identalhub. 2010. Available online at:
http://www.identalhub.com/dental-reversible-pulpitis-vs-irreversible-pulpitis-
928.aspx.html (Accessed: March, 29th 2017)
Sapp, J., Eversole, L., & Wysocki, G. 2004. Contemporary Oral and Maxillofacial
Pathology 2nd Ed. St. Louis: Mosby.
Saraf, S. 2006. Textbook of Oral Pathology 1st Ed. India: Jaypee
Torabinejad, M., & Walton, R. 2009. Endodontics principle and Practice 4th Ed.
St.Louis: Elsevier

29
30