Healing of large periapical lesions following calcium
hydroxide endodontic therapy : Two case reports and
review of literature
“Thomas SB *‘Al Kandari AR and **Abdul Rahem AA
ABSTRACT
‘Two cases of large periapical lesions are presented. The lesions were treated
by conservative endodontic therapy, following which the lesions showed
complete resolution. These results suggest that the largeness of a lesion
does not mandate its surgical removal and that even cyst-like lesions heal
following conservative therapy.
Key words ~ Periapical lesions, calcium hydro:
Introduction
Trauma to a tooth can damage the pulp
when the crown and root are not fractured. Pulp
may survive depending on the severity of the
trauma and the type of inflammatory reactioin
that follows. Due to trauma, a vascular pulp
may degenerate into vascular necrosis. The
necrotic material then seeps out of the portals
of exit of the root canal system and into the
supporting vascular attachment apparatus,
generating lesions of endodontic origin.
Based on histological findings, a chronic
periapical lesion may be diagnosed as a
granuloma or cyst. In the past, large periapical
lesions were managed by endodontic
treatment followed by surgical excision. This
was particularly true for periapical cysts.
However with the advancement of endodontics
and a better understanding of the periapical
tissues, even these cyst like lesions can be
treated by conservative method.
‘Two cases of periapical lesions that were
Endodontist
‘Amiri Dental Centre
Head of Department of Endodontics and
Amiri Dental Centre,
Ministry of Public Health, Kuwait
Endodontst
Adan Dental Centre,
Ministry of Public Health, Kuwalt
32
le.
successfully treated by nonsurgical endodontic
therapy are presented. These cases
emphasize the fact that every effort should be
made to treat such lesions irrespective of size
by conservative method.
Case Reports
Case 1
‘22-year-old woman was referred to the
clinic for the treatment of a gradually increasing
swelling on the palate of 4 weeks duration
Previous history revealed an accident and
trauma to the left maxillary lateral incisor 15
years ago. It was left untreated for many years.
Examination revealed a tender, soft
fluctuant swelling that extended from the
anterior aspect of the palate to the region of
the distal aspect of the first molar. The lateral
incisor was discoloured and nonvital on thermal
and electric pulp testing. Periapical radiograph
revealed a wide-open apex and resorption in
relation to the lateral incisor (Fig. 1a.)
For immediate drainage of the swelling,
the lateral incisor was opened which led to
draining of suppurative fluid. The swelling was
compressed and more fluid flowed out. The
canal was thoroughly irrigated with sodium
hypochlorite and provisional restoration wasThomas SB et al
ial
Fig. 1: (a) Periapical lesion
associated with maxillary leftincisors,
Fig.
Fig. 1: (@) Atthe end of 12 months. Fig 1
used to seal the access cavity, Patient was
prescribed antibiotics. The patient was recalled
the next day and the same procedure was
carried out. Intracanal calcium hydroxide [Ca
(OH),] dressing was placed and a provisional
restoration was used to seal the cavity
(Fig. 1b). The patient was recalled at 2 weeks
interval for a month and the Ca (OH), dressing
was changed. After a month, the swelling had
completely subsided. The patient was reviewed
every month. At the end of 9 months,
radiograph revealed a slight decrease in the
size of radiolucency but no apical closure
(Fig. 1¢) root canal treatment was completed
(b)Placement of intracanal
‘calcium hydroxide dressing.
1c) Remarkable decrease in
size of lesion and apical closure at
the end of 2% years.
33
Calcium hydroxide therapy...
Fig. 1 :(¢) Decrease in size of
lesion at the end of 8 months.
for the central incisor which had
tested negative for vitality,
Radiograph revealed a slight
decrease in the size of the
lesion but no apical closure
(Fig. 1d). The lateral incisor was.
opened and throughly cleaned
and Ca(OH), was reintroduced
into the canal and sealed with a
temporary restoration
The patient however did
not keep her appointments
regularly and this delayed the
treatment. She returned to the
clinic after 2% years with a
complaint of pain in the lower left
third molar area. A radiograph taken at this time
tevealed a marked difference in the size of the
lesion and formation of an apical barrier
(Fig. 1€).The patient was recalled for root canal
filing but did not show up for her appointment.
Case 2
A twenty-five year old man was referred
for treatment of palatal swelling in relation to
the maxillary left central, lateral incisor and
cannie area. He had severe pain in the area
three days before he reported for treatment.
The patient give the history of a fall at the
playground five years ago.Examination revealed a soft, slightly
tender swelling in the palate just behind the
incisor and canine area. The maxillary incisors
and canine were non-vital and periapical
fadiolucency extended from the maxillary left
central incisor to the mesial aspect of the
canine (fig. 2a).
When the root canals of the non-vital
teeth were opened, straw coloured fluid flowed
out. On compression of the palatal swelling,
more fluid was expressed through the canals.
The canals were debrided with sodium
hypochlorite and calcium hydroxide paste was
placed in the canals. The access cavities were
\
Fig. 2 : (a) Periapical lesion in the
‘maxillary left incisors and canine.
—
Fig. 2 : (¢) Obturation completed
after 4 weeks.
im | if
Fig. 2 : (b) Placement of intracanal
Calcium hydroxide dressing,
(a) Complete resolution
alter 2 years.
Endodontology, Vol. 12, 2000
sealed with temporary restoration (fig. 2b)
Patient was prescribed antibiotics.
The patient was recalled weekly for a
month and similar treatment was carried out.
Four weeks later, the canals were dried and
obturated with gutta percha (fig. 2c). The palatal
swelling had completely subsided. The patient
was reviewed every three months for 24
months after completion of endodontic therapy.
All the end of 24 months, there was complete
resolution of the periapical lesion (fig. 24)
Discussion
The precise mechanism
involved in the formation of
periapical lesions is not fully
understood. It is generally
agreed that if the pulp becomes
necrotic, its environment
becomes suitable to allow
microorganisms to multiply and
release various toxins into the
periapical tissues, initiating an
inflammatory reaction and
leading to the formation of the
periapical lesion"?, Studies
were carried out to examine the
role of bacteria in the formation
of periapical lesions** and it
was found to be present in the
root canals associated with the
lesions**. The endodontic flora
consists of rods, spirochetes,
cocci and filamentous forms’.
However only a few periapical
lesions have shown the
presence of bacteria within the
body of the lesion**. One study*
even demonstrated the
absence of bacterial colonies in
eighteen periapical lesions
examined, except —_ for
occasional isolated intracellular
bacteria which was believed to
be bacteria phagocytosed by
macrophage like cells.Thomas SB et al . oe
The histogenesis of the periapical cyst is
uncertain but remnants of the epithelial cell
rests could possibly be the source of the
epithelium in cyst lining and various factors may
contribute to the growth of the cysts. The
inflammation in the periapical region may
stimulate the proliferation of the epithelium,
which by acting as a semi-permeable
membrane, could draw fluid into the cyst cavity
by osmotic pressure’. Bone resorbing factors
such as prostaglandins could contribute to
further expansion of the cyst.
Radiographic and histopathological
evaluation of periapical lesions"? showed that
cysts are the most common periapical lesions.
‘Among periapical lesions of an area greater
than 200mm?, 92% or more were cysts". Thus,
larger the periapical lesion, greater the chance
for it to be a cyst. In Case 2, the radiographic
area of the periapical lesions was more than
200mm. Based on size, presence of
cholesterol within the lesion contents and a
defined radiographic margin, the lesions was
probably a periapical cyst’®. The exact
mechanism by which the cysts heal is not fully
understood. One concept for treatment of cyst
was to treat the involved teeth endodontically
and surgically excise the lining". Others
suggest that it would heal spontaneously after
endodontic therapy. As healing takes place,
collagen deposits compress the capillaries
supplying the cyst, thereby cutting the blood
supply to the epithelial lining. The lining
degenerates and is removed by macrophages.
Another theory is that if root canal therapy is
extended beyond the apical foramen, the
inflammatory reaction develops and destroys
the cyst lining and converts the lesion into
granuloma". When the causative factors are
removed, it heals spontaneously.
In case I, we see a clinical case of
incomplete apical development. The open apex
case"* occurs when trauma or decay causes
pulp exposure and/or periapical involvement,
prior to the completion of root development
‘An open apex refers to the absence of sufficient
Calcium hydroxide therapy...
root development to provide a conical taper to
the canal and is referred to as a “blunderbuss*
canal. Calcium hydroxide has been used in
endodontic therapy since 1920 when Hermann:
first described its use in the treatment of
nonvital teeth. Since then Ca (OH), alone or in
combination with other drugs have been used
to promote apexification. The average time
required to achieve apexification is 6 to 24
months”.
it has been stated"? that Hertwig's root
sheath is not completely destroyed when the
pulp becomes nonvital in the developing tooth.
Thus apexification procedures stimulate further
function of the sheath to continue apical
development.
Calcium hydroxide kills bacteria because
of the effect of hydroxyl ions. These ions are
extremely reactive, combining repidly with
lipids, proteins and nucleic acids. They cause
lipid peroxidation, increasing the bacterial
membrane permeability, protein denaturation,
inactivating enzymes and DNA damage. These
phenonmena cause bacterial death. The
caicium ions activate the complement system
in the immunologic reaction by activating the
calcium dependent ATP-ase which has been
associated with hard tissue formation.
The calcified material that forms over the
apical foramen has been histologically
identified as an osteoid (Bonelike) or cementiod
(cementum-like) material by investigators who
have done apexitication on periapically involved
teeth'*, Normal root formation usually does not,
occur following apexification. Instead there
appears to be a differentiation of adjacent
connective tissue cells into specialized cells;
there is also deposition of calcified tissue
adjacent to the filling material. The calcified
material is continuous with the lateral root
surfaces. The apex may be partial or complete
but consistently has minute communications
with the periapical tissues. For this reason
apexitication must always be followed by a
permanent root canal filling material.One of the most perplexing cases to treat,
is the tooth with constant clear or reddish
exudate and a large periapical radiolucency"*
Calgium hydroxide has been used as an intra
canal medicament to attain a clean and dry
canal. This is probably due to the pH of the
periapical tissues which is acidic in the weeping
stage. The pH is converted to a more basic
environment by the calcium hydroxide and this
in turn activates the alkaline phosphatase
which plays an important role in hard tissue
formation.
Healing is complete when apical
periodontal ligament is restored to normat
architecture®*. A periapical scar may formas a
residual radiolucent lesion. This may be
ignored if a continuous periodontal ligament
‘of normal thickness is present around the
affected tooth’?
The periapical lesions in both the above
cases were successfully treated non-surgically
This only confirms with the study conducted
by Schwarze and Guenay where clinical study
was performed on 103 teeth with lesions to
evaluate the success rate of surgical and non
surgical endodontic therapies. From the data
collected, it was concluded that conservative
endodontic treatment of periapical lesions
revealed high success rate (75%) than surgical
treatment (69%).
The periapical lesions in both cases were
large but resolved after nonsurgical therapy.
Periapical tissues have rich blood supply,
lymphatic drainage and abundant
undifferentiated mesenchymal cells* and there
fore, good potential for healing. Thus treatment
should be directed at removing the causative
factors,
References
1, Shear M. Histogenesis of dental cyst: Dent Pract 1963;
19:298-243
2. Pulver WH, Taubman MA, Smith PH, Immune com-
ponents in the numan dental periapical lesions. Arch Oral
Biol 1978; 23:435.443,
3. Yanagiswa S. Pathologic study of periapical granulo-
Endodontology, Vol. 12, 2000
‘mas: Clinical, histopathologic and immunohistopathologic
studies. J Oral Pathol 1980, 9:288-300.
4. Andreasen JO, Rud J: A histobacteriologic study of
dental and periapical structures after endodontic surgery.
Int J Oral Surg. 1972; 1:272-281.
8, Langeland K, Block RM, Grossman. LI. A
histopathologic study of 35 periapical endodontic surgi-
cal specimens. J Endod 1977;
6. Stabholz. A, Sela MN: The role of microorganisms in
the pathogenesis of periapical issions: Effect of
streptococcus mutans and its cellular constituents on the
dental pulp and priapical tissues of cats. J. Endod 1983:
9, 171-175.
7. Nair PNR. Light and celectron microscopic studies of
root canal flora and periapical lesions: J. Endod 1987:
13:29:39.
8. Walton RE. Ardinand K. Histological evaluation of pres:
tence of bacteria in induced periapical lesions in mon-
keys. J. Endod 1992; 18:216-221
9. Weisenfed D. in, Scully C (Ed) The mouth and perioral
tissues, Oxtord : Heinamann Medical books., 1989:49.
10.Zain RB, Roswali N. Ismail K. Radiographic evalua-
tion of lesion sizes of histologically diagnosed periapical
cysts and granulomas. Ann Dent 1989: 48:3-5.
11.Grossman LI. Root canal therapy, ed 3. Philadelphia:
Lea & Febiger. 1950:99.
12, Bhasker SN: Non surgical resolution of radicular cyst
Oral Surg. 1972; 34:458-468,
13.Shafer WG. Hine MK. Levy BM: A textbook of oral
pathology, Ed. 3, Saunders 1974:451
14.Stern MH, Mackler BF, Selbst AG: Quantitative analy-
sis of cellular composition of human penapical granu-
Toma J. Endod 1981; 7:117-122
15.Frank AL. = Therapy for the divergent pulpless tooth
by continuous apical formation. J. Am. Dent Assoc. 1966:
72:87.
16.Weine FS, Endodontic Therapy 4th Edition 1989: 626-
640,
17.A bacteriological and histological evaluation of 58
periapical lasions: J. Endod 1992; 18, 182-155,
18.Ham JW. Patterson SS. Mitchel DF : Induced apical
closure of immature pulpless teeth in monkeys. Oral Surg,
1972; 33:438,
= 19.Klein DJ. Study of endodontically apexitied teeth
Endodont Dent Traumatol 1991: 7:112.
20. Torabinejad M Walton RE. Pulp and periapical patnosis.
In: Walton RE, Torabinejad M (eds). Principlas and Prac.
tice of Endodontics, Philadelphia: Sunders, 1989: 47-48
21.Harty FJ, Endodontics in Clinical Practice, ed 2. Bristol,
England, Wright, 1982:195,
22. Gordon T. Effect of Ca (OH), on bovine pulp tissue. J
Endo 1985: 11:156-60.
23, Schwarze TH. Guenay H. Endodontics or surgical
therapy of periapicat lesions. J. Endod. 1999; 25,
36