4 Pulpoperiapical Diseses

PERIAPICAL
LESION OF NON
ENDODONTIC
ORIGIN
Lect. 4
2019-2020
PERIAPICAL LESIONS OF
NONENDODONTIC ORIGIN
periapical lesions are not of endodontic origin
should be considered in the differential diagnosis of apical periodontitis .
These lesions include but are not limited to:
trauma, foreign bodies, fibro-osseous lesions, and benign and malignant tumors
Cellulitis is a symptomatic edematous inflammation associated with diffuse spreading of

invasive microorganisms through connective tissue and fascial planes. Its main clinical
feature is diffuse swelling of facial or cervical tissues. Cellulitis is usually a sequel of an
apical abscess that penetrated the bone, allowing the spread of pus along paths of least
resistance, between facial structures.
This usually implies the fascial planes between the muscles
of the face or neck. Spreading of an infection may or may
not be associated with systemic symptoms such as fever
and malaise. Since cellulitis is usually a sequel of an
uncontrolled apical abscess, other clinical features typical of
an apical abscess are also expected. Spreading of an
infection into adjacent and more remote connective tissue
compartments may, rarely, result in serious or even life-
threatening complications. Cases of Ludwig’s angina ,
orbital cellulitis , cavernous sinus thrombosis and even
death from a brain abscess originating from a spreading
dental infection have been reported.
APICAL PERIODONTITIS AND SYSTEMIC DISEASES
Clinical and radiographic studies have shown that there is a greater prevalence of periapical
lesions in diabetics than in nondiabetics
When irritants (microbial and nonmicrobial) in the canal systems or in the periapical tissues are
eliminated by nonsurgical or surgical endodontic therapy, inflammatory mediators are no longer
produced in the periapical tissues because of the reduction of inflammatory cells.
WOUND HEALING OF APICAL
PERIODONTITIS
Also nonsurgical root canal therapy is intended to remove

irritants and provide a favorable microenvironment conductive
to regeneration of periodontal tissues damaged by apical
periodontitis.
Wound healing appears to be a programmed event.

Pathologic processes such as extensive fibrosis do not occur
often, and the damaged periapical tissues can be restored
mostly to their original structure by the process of regeneration.
During periapical wound healing, the cells of viable periodontal ligament from adjacent root
surfaces proliferate to cover the root surfaces in which the periodontal ligament was damaged by
apical periodontitis and removed by macrophages. Proteins derived from the Hertwig epithelial
root sheath (i.e., enamel matrix proteins) are required for cementoblast differentiation from
ectomesenchymal stem cells in the dental follicle during tooth development

the extracellular matrix and growth factors of cementum (i.e., IGF-, FGFs, EGF, BMP, TGF- β , PDGF)
sequestered after cemental resorption in mature teeth are capable of inducing proliferation, migration,
attachment, and differentiation of multipotent stem cells in the periodontal ligament into cementoblast-
like cells and produce cementoid tissue on the root surface denuded of periodontal ligament
Root resorption that involves cementum or both cementum

and dentin can only be repaired by cementoid tissue, because
multipotent stem cells of the periodontal ligament are incapable
of differentiating into odontoblasts that produce dentin
Bone has a remarkable capacity for regeneration in response to injury. During periapical
wound healing, the osteoprogenitor cells or mesenchymal cells lining the surfaces of
endosteum—stimulated by TGF- β , BMPs, IGFs, PDGF, VEGF, and cytokines released by
stromal cells, osteoblasts, platelets, and bone matrix after bone resorption—can undergo
proliferation and differentiation into osteoblasts and produce bone matrix
When one of the cortical bone plates (buccal or lingual/palatal) is destroyed, osteoprogenitor
cells in the inner layer of periosteum beneath the oral mucosa—stimulated by TGF- β ,
BMPs, IGFs, PDGF, and VEGF—are also capable of proliferation and differentiation into
osteoblasts and can produce bone matrix
If both buccal and lingual/palatal cortical bone plates are destroyed by large apical
periodontitis lesions, it is possible that the lesion may be repaired with fibrous scar tissue
because of extensive destruction of the peri-
osteum beneath the oral mucosa
The newly regenerated periodontal ligament will finally undergo remodeling into a mature
periodontal ligament, with one group of collagen fibers (Sharpey fibers) inserted into the newly
formed cementum and another group of collagen fibers inserted into the newly formed alveolar
bone. Thereby, regeneration of damaged periapical tissues, cementum, periodontal ligament,
and alveolar bone is completed.
CAN RADICULAR CYSTS IN APICAL PERIODONTITIS
LESIONS REGRESS AFTER NONSURGICAL
ENDODONTIC THERAPY?
It was suggested that pocket cysts in apical periodontitis lesions
might regress after nonsurgical root canal therapy by
the mechanism of apoptosis or programmed cell death, based
on molecular cell biology.
In contrast, apical true cysts may be less likely to heal after
nonsurgical root canal therapy because of their self-sustaining
nature
Regression of radicular cysts and regeneration of bone may occur concurrently; or during regression of
radicular cysts, part of the cystic lining epithelium could disintegrate due to apoptosis of local epithelial
cells.
this could allow a fibrous connective tissue capsule to grow into the lumen of radicular cysts. Eventually,
the cystic lining epithelium will completely regress or become remnants of epithelial cell rests remaining in
the periodontal ligament.
FACTORS INFLUENCING PERIAPICAL WOUND
HEALING AFTER ENDODONTIC THERAPY
Local and systemic factors may affect periapical wound healing:
 Infection will complicate and prevent wound healing ,

 foreign bodies can impair wound healing
 and nutrition can also affect wound healing.
 Diabetes was reported to reduce the likelihood of healing of apical periodontitis lesions after
nonsurgical root canal therapy.
 Impaired nonspecific immune response and disorders of the vascular system.
 Patients receiving radiotherapy of jaws and bisphosphonate therapy have a risk of developing
osteonecrosis of jawbones
Causes of persistent apical periodontitis
(i) intraradicular infection persisting in the complex apical root canal system
(ii) extraradicular infection, generally in the form of periapical actinomycosis
(iii) extruded root canal filling or other exogenous materials that cause a foreign body reaction
(iv) accumulation of endogenous cholesterol crystals that irritate periapical tissues
(v) true cystic lesions
(vi) scar tissue healing of the lesion
MORPHOLOGIC CHANGES OF THE APICAL ROOT
STRUCTURE IN APICAL PERIODONTITIS LESIONS
A. Root Resorption in Apical Periodontitis
Root resorption can be defined as the process of removal of cementum and dentin by multinucleated
clastic cells as odontoclasts:
Pathologic root resorption is also caused by traumatic injuries to the teeth, neoplastic processes in the
jaws and dental treatment procedures, among which orthodontic forces and intentional replantation are
most common.
Depending on the amount of calcified tissue lost, root resorption can be detected by periapical
radiographs. However, in many cases, the condition can be disclosed only by histologic sections
Osteoclasts and odontoclasts possess similar enzymatic properties and resorb their target tissues in a
similar manner.
Both create resorption depressions termed Howship’s lacunae on the surface of the
mineralized tissues. After adhesion of the cells, the bone surface beneath the clastic
cell becomes segregated from thee environment. Consequently, acids and enzymes
released by
the clastic cell concentrate on the surface of the subjacent mineralized tissue,
leading to resorption.
Odontoclasts do not normally adhere to nonmineralized layers of the precementum
covering the apical root surface. Similar to what happens in internal root resorption,
where a breach in integrity of the predentin and odontoblast layer is necessary for
resorption to occur, the precementum and cementoblast layers need to be lost in
order to stimulate cementum resorption.
B. Hypercementosis
Less frequent than resorption, the pathologic deposition of several layers of cementum around the
apical structure can be observed in association with some periradicular lesions.

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PERIAPICAL

Cellulitis is a symptomatic edematous inflammation associated with diffuse spreading of

Also nonsurgical root canal therapy is intended to remove

Wound healing appears to be a programmed event.

ectomesenchymal stem cells in the dental follicle during tooth development

Root resorption that involves cementum or both cementum

Local and systemic factors may affect periapical wound healing:

 Infection will complicate and prevent wound healing ,

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