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PERIRADICULAR LESIONS of pulpal origin

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Primary periodontal secondary endodontic involvement-accentuated pain from lesion. Hard to separate from endo perio Endodontic / Periodontic Relationships True ... – PowerPoint PPT presentation

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Title: PERIRADICULAR LESIONS of pulpal origin


1
PERIRADICULAR LESIONS of pulpal origin
2
Definition
  • Apical periodontitis is an inflammatory disorder
    of the periradicular tissue caused by a
    persistent microbial infection of the root canal
    system of the affected tooth

3
In other words
  • Apical periodontitis (AP) is a host response to
    infections by microbes and the subsequent
    inflammatory response

4
  • Apical periodontitis includes the infection and
    inflammation of the lateral and furcal locations.

5
  • The root canal and the pulp chamber are niche
    environments for the causative organism

6
Biofilms
  • Bacteria form biofilms and these pathological
    bacteria are embedded in the biofilms
  • Biofilms protect the bacteria from antibiotic
    attack and make them a X 1000 more resistant to
    the effects.

7
Infection portals
  • Pulp becomes infected by
  • Carious exposure
  • Leaking restorations
  • Dentinal tubules
  • Fractures or cracks

8
Inflammatory response
  • The antigens and bacterial toxins percolate into
    the surrounding tissue

9
  • Most likely anaerobic bacteria invade that
    provoke an inflammatory response i.e.
  • Chemotaxis
  • Enzymatic breakdown with the subsequent release
    of antigens

10
  • The host mounts a immune response consisting of
    several classes intercellular messengers and
    antibodies.
  • This response destroys much of the peripical
    tissue
  • This results in the formation of various types of
    apical periodontal lesions.

11
  • The defence reaction minimises the spread of
    infection.
  • It cannot eliminate the microbes entrenched in a
    necrotic root canal , and biofilm.

12
  • Treatment is required via surgical or non
    surgical endodontic therapy as biofilms protect
    the bacteria from the host defenses.

13
Classification of AP
  • Apical periodontitis is an inflammatory disease
    and classification is based on symptoms ,
    aetiology or histopathology.

14
Nomenclature and Classification
  • Numerous terms are used such as
  • Apical granulomas
  • Apical cysts
  • Periapical lesions
  • Periapical osteitis

15
  • Three main clinical groups
  • symptomatic(acute) apical periodontitis
  • asymptomatic(chronic) apical periodontitis
  • apical abscess

16
Symptomatic(acute) Apical Periodontitis
  • The principal causes are irritants diffusing from
    an inflamed or necrotic pulp.
  • Negative vitality test not always accurate
  • Pain!!!(WHY?)

17
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18
Asymptomatic(chronic) Apical Periodontitis
  • Preceded by an acute episode
  • lesion frequently develops and enlarges without
    any subjective signs and symptoms
  • Causes
  • Inadequate endodontic procedure
  • Low grade pathogenicity/ irritant
  • Pathosis is a long-standing smoldering lesion

19
Asymptomatic(chronic) Apical Periodontitis(Cont)
  • Non vital respnse
  • Radiographic evidence is the key
  • Called a peri radicular granuloma or
    periradicular cyst.
  • Periradicular Granuloma. Nobuhara and del
    Rio(JOE199319315) showed that 59.3 of the
    periradicular lesions were granulomas, 22 cysts,
    12 apical scars, and 6.7 other pathoses

20
  • Histologically, the periradicular granuloma
    consists predominantly of granulation
    inflammatory tissue with many small capillaries,
    fibroblasts, numerous connective tissue fibers,
    inflammatory infiltrate, and usually a connective
    tissue capsule

21
Apical periodontitis (granuloma) with
containedepithelium. Epithelial cells of
periodontal ligament have proliferatedwithin new
inflammatory tissue. The epithelium tends to
ramify in areticular pattern (straight arrow)
toward receding bone. It also may,as in this
case, apply itself widely to the root surface
(curved arrow).Infiltration of epithelium by
round cells is everywhere apparent.Human tooth.
Reproduced with permission from Matsumiya
S.Atlasof oral pathology. Tokyo Tokyo Dental
College Press 1955.
22
Periradicular Cyst.
  • Periradicular cyst shows a central cavity lined
    by stratified squamous epithelium
  • This lining is usually incomplete and ulcerated
  • The lumen contains a pale eosinophilic fluid and
    occasionally some cellular debris

23
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24
Apical cyst with marked inflammatory overlay.
Roundcells permeate both the epithelium and the
connective tissue immediatelydeep to it. Spaces
indicate where crystalline cholesterol hasformed
within the cyst. Bone formation is evident
(arrow). Thismay reflect narrowing of the width
of the connective tissue zone, asoccurs in some
apical cysts. Human tooth. Reproduced with
permissionfrom Matsumiya S. Atlas of oral
pathology. Tokyo TokyoDental College Press
1955.
25
Condensing Osteitis
  • Inflammation of periradicular tissues of teeth
    usually stimulates concurrent osteoclastic and
    osteoblastic activities.
  • Osteoclastic (resorptive) activities are usually
    more prominent than osteoblastic (formative)
  • Condensing osteitis is associated with
    predominant osteoblastic activity

26
Condensing Osteitis (CONT)
  • attributable to a special balance between host
    tissues and the root canal irritants.
  • Condensing osteitis, or chronic focal sclerosing
    osteomyelitis, is a radiographic variation of AAP
    and is characterized as a localized
    overproduction of apical bone.
  • usually observed around the apices of mandibular
    posterior teeth with pulp necrosis or chronic
    pulpitis

27
Condensing Osteitis (CONT)
  • The tooth associated with condensing osteitis may
    be asymptomatic or sensitive to stimuli.

28
Apical condensing osteitis that developed in
response tochronic pulpitis. Additional bony
trabeculae have been formed andmarrow spaces
have been reduced to a minimum. The periodontal
ligamentspace is visible, despite increased
radiopacity of nearby bone.
29
APICAL ABSCESSES
  • An abscess is a localized collection of pus in a
    cavity formed by the disintegration of tissue
  • Apical abscesses can be divided into symptomatic
    or asymptomatic conditions

30
APICAL ABSCESSES
  • Symptomatic Apical Abscess A sudden egress of
    bacterial irritants into the periradicular
    tissues
  • severe sequelae, acute osteitis and cellulitis.
  • Accompanied by exudate formation within the
    lesion
  • May occur without any obvious radiographic signs
  • infection and rapid tissue destruction arising
    from within AAP( Phoenix abcess)

31
APICAL ABSCESSES/clinical
  • May or may not have swelling
  • Swelling may be localized or diffuse
  • Varying degrees of sensitivity to percussion and
    palpation
  • No pulp reaction to cold, heat, or electrical
    stimuli as the involved tooth has a necrotic pulp
  • Radiographic features of the SAA vary from a
    thickening of the periodontal ligament space to
    the presence of a frank periradicular lesion

32
Radiographic features of symptomatic apical
abscess.The patient developed sudden symptoms of
pain and facialswelling. Radiographically, a
lesion is apparent apically to the maxillaryleft
lateral incisor, that did not respond to vitality
tests, confirmingpulpal diagnosis of necrosis.
33
Asymptomatic Apical Abscess
  • Asymptomatic apical abscess (AAA), also referred
    to as
  • suppurative apical periodontitis, is associated
    with a
  • gradual egress of irritants from the root canal
    system
  • into the periradicular tissues and formation of
    an exudate.
  • The quantity of irritants, their potency, and
    their
  • host resistance are all important factors in
    determining
  • the quantity of exudate formation and the
    clinical signs
  • and symptoms of the lesion. Asymptomatic apical
  • abscess is associated with either a continuously
    or
  • intermittently draining sinus tract.

34
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35
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36
  • WHO uses a symptomatic classification based on
    clinical signs
  • Acute apical periodontitis
  • Chronic apical periodontitis
  • Periapical abscess with sinus
  • Periapical abscess without sinus
  • Radicular cyst

37
Histopathological classification(Nair PNR
Pathology of Apical Periodontitis)
  • In order to understand the disease process a
    histopathological classification is used
  • The distribution of pathological cells in the
    lesion
  • Presence or absence of epithelial cells
  • Transformation of a lesion into a cyst
  • The relationship of the cyst cavity to the
    affected root

38
Histopathological classification
  • Acute apical periodontitis - an acute
    inflammation of endodontic origin . A distinct
    focus of neutrophils have to be present
  • Primary or initial short lived inflammation in a
    healthy periodontium.
  • secondary or exacerbating when an acute episode
    occurs on a preexisting chronic lesion also
    called a phoenix abcess

39
Histopathological classification
  • Established chronic apical periodontitis
  • Long standing inflammation
  • presence of granulomatous tissue
  • Cells are lymphocytes , plasma cells and
    macrophages
  • Lesion may be epithelialised or
    non-epithelialised

40
Histopathological classification
  • Periapical true cyst is an apical inflammatory
    cyst with a distinct pathological cavity
    completely enclosed in an epithelial lining so
    that NO communication to the root canal exists

41
Histopathological classification
  • A periapical pocket cyst is an apical
    inflammatory cyst containing a saclike epithelium
    lined cavity that is open and continuous with the
    root canal

42
Histopathologically the lesions of AP can be
classified as acute, chronic ,or cystic .AAP may
be (A.) primary or secondary(B) and is
characterized by a focus of PMN, (C) major
component are lymphocytes plasma cells and
macrophages, (D) true cysts enclosing the lumina
and pocket cysts (E)cavity is open to the root
canal. Arrows indicate the direction of in which
the lesion can change.
43
Important points
  • Bacteria are anaerobes
  • Bacteria have to be present
  • There has to be a portal for infection to occur
    i.e.
  • Caries
  • Clinical procedures
  • Fractures
  • Dentinal tubules

44
To treat or not to treat?
  • Anatomic considerations
  • Root shapes?
  • Can you remove infected hard and soft tissue
  • Give disinfecting agents access to the apical
    canal space
  • Create space for the delivery of medicaments and
    subsequent obturation
  • Retain the integrity of the radicular structures

45
To treat or not to treat?
  • Is the tooth restorable?
  • Is there an adequate ferule, the amount of
    remaining tooth structure
  • Is root decay present
  • Vertical fractures
  • Post preparations in teeth
  • Anatomical positions of the tooth
  • Occlusal forces on the tooth

46
To treat or not to treat?
  • Restorative requirements of the tooth
  • Aesthetic requirements
  • Sclerotic canals

47
Surgical
  • Posterior part of mandible
  • Inferior dental nerve
  • Thickness of mandible
  • Mental foramen
  • Facial artery
  • PDL
  • Consider alternative

48
Surgical
  • Posterior part of Maxilla
  • Sinus perforation with infected root fragments
  • Palatal access
  • Anterior maxilla / mandible
  • Long roots
  • Inclinations (mandible) and mental protuberance

49
  • Prepared teeth are anatomically more difficult to
    treat

50
Endodontic and periodontal relationships
  • Vascular connections exist between the pulp and
    periodontal ligament.
  • Pulp and periodontal problems are responsible for
    more than 50 of tooth mortality.
  • There is no doubt that an interrelationship
    exists in diseases that affect both the pulp and
    periodontium

51
  • When the pulp necroses for whatever reason
    products from pulp degeneration reach the
    supporting periodontium. This is characterised by
    bone loss, tooth mobility , and sometimes sinus
    tract formation.
  • Apically if this occurs , a periradicular lesion
    forms which can extend crestally (Reverse pocket
    is formed)

52
  • Periodontal disease may have a gradual , atrophic
    effect on the pulp.
  • Periodontal treatments such as deep root planing
    or curettage, or localized irritants e.g. acids
    may cause pulpal irritation.is

53
  • Apical foramina have been shown to be the most
    direct root of communication to the periodontium.
  • In addition lateral or accessory canals with 28
    at the furcation.

54
Periradicular periodontitis
  • Acute, painful to biting or percussion, the
    vitality may or may not be positive. No
    periradicular radiolucency and widened PDL,
    Apical 1/3 of root
  • Chronic , no clinical symptoms, negative vitality
    test , periapical radiolucency , altered patient
    sensation

55
Periradicular abcess
  • Acute, sensitive to pressure and palpation,
    negative vitality test , increased mobility ,
    increased pdl space, associated temperature
  • Chronic, no clinical symptoms, no vitality
    response periradicular radiolucency on
    radiograph, suppurative lesion(pus drainage )

56
  • Periodontal considerations
  • Channels exist between pulp and periodontal
    tissue
  • These include neural pathways, lateral canals
    dentinal tubules, palato-gingival grooves
    periodontal ligament alveolar bone , apical
    foramina and vascular and lymphatic pathways

57
Endodontic / Periodontic Relationships
  • Primary endodontic -lesions lateral aspects of
    the root sinus tract along the root
    gutta-percha trace
  • Primary endodontic with secondary periodontal
    involvement accumulation of plaque / calculus
    apical migration of tissue

58
Endodontic / Periodontic Relationships
  • Primary periodontal lesions -deposit in sulcus
    migrates apically. Vital pulp got to distinguish
    this from previous both look the same.
  • Primary periodontal secondary endodontic
    involvement-accentuated pain from lesion. Hard to
    separate from endo perio

59
Endodontic / Periodontic Relationships
  • True combined lesion- damage to pulp and
    periodontium at the same time that may coalesce
    classic J- lesion
  • Treatment can include the resection of roots
    (multirooted) , but lesions associated with
    cracked roots , older patients and posts.
    Regeneration procedures.

60
NONENDODONTIC PERIRADICULAR LESIONS
  • Got to differentiate between pulpal pathology and
    non-endodontic origins of alterations in bone
    morphology.
  • 38 radiolucent lesions and other abnormalities
    of the jaws.Three of these lesions, dental
    granuloma, radicular cyst, and abscess, are
    categorized as being related to necrotic pulps.
    In addition,16 radiopaque lesions of the jaws, 3
    of which, condensing osteitis, sclerosing
    osteomyelitis, and Garrés osteomyelitis, are
    also related to pulpal pathosis
  • Never assume a radiolucency is pulpal pathology.

61
NONENDODONTIC PERIRADICULAR LESIONS
  • Lesions of the jaws categorized as odontogenic or
    nonodontogenic in origin
  • Odontogenic lesions arise from remnants of
    odontogenesis (or the tooth-forming organ),
    either mesenchymal or ectodermal in origin.
  • Nonodontogenic lesions trace their origins to a
    variety of precursors and therefore are not as
    easily classified.

62
  • Differentiating between lesions of endodontic and
    nonendodontic origin is usually not difficult.
    Pulp vitality testing, when done with accuracy,
    is the primary method of determination nearly
    all nonendodontic lesions are in the region of
    vital teeth, whereas endodontic lesions are
    usually associated with pulp necrosis, giving
    negative vitality responses. Except by
    coincidence, nonendodontic lesions are rarely
    associated with pulpless teeth.

63
Odontogenic Cysts
  • Dentigerous Cyst
  • Lateral Periodontal Cyst
  • Odontogenic Keratocyst
  • Residual Apical Cyst.

64
Lateral periodontal cyst.Well-circumscribed
radiolucentarea in apposition to the lateral
surfaces of the lower premolars(black arrows
demarcate the extent of lesions). No clinical
signs orsymptoms were noted. Pulps tested vital.
65
Bone Pathology Fibro-osseous Lesions
  • Periradicular Cemental Dysplasia
  • Osteoblastoma and Cementoblastoma
  • Cementifying and Ossifying Fibroma.

66
A, Periradicular cemental dysplasia
(osteofibrosis), initial stage. Pulps in both
teeth are vital. B, Transition to the second
stage is developing. C, Biopsy of periradicular
osteofibrosis, initial stage. Fibrous
connective tissue lesion has replaced cancellous
bone.
67
Cementoblastoma. The lesion is a fairly
well-definedradiopaque mass surrounded by a thin
radiolucent line. It has alsoreplaced the apical
portions of the distal root of the first molar
68
Ossifying fibroma. The patient presented with
pain.The pulp was vital, indicating that this
was not an endodonticpathosis. Root canal
treatment was followed by root end removaland
excision of the lesion. Biopsy confirmed the
diagnosis
69
Odontogenic Tumors
  • Ameloblastoma.

70
Two examples of ameloblastoma. A, Surgical
specimenof infiltrating ameloblastoma of
mandible. B, Unicystic ameloblastoma.This
solitary lesion has displaced teeth much as an
apical cystwould do. The teeth are vital.
71
Nonodontogenic Lesions
  • Central Giant Cell Granuloma.
  • Nasopalatine Duct Cyst
  • Simple Bone Cyst.
  • Globulomaxillary Cyst
  • Enostosis.

72
Malignancies
  • Carcinomas or sarcomas of various types are found
    in the jaws, rarely as primary but usually as
    metastatic lesions
  • Carcinoma. Generally found in older patients,
    involvement of the jaws (usually the mandible) is
    by metastasis from a primary lesion elsewhere
  • Carcinoma lesions of the jaw may also manifest
    pain and swelling, loosening of teeth, or
    paresthesia, similar to endodontic pathosis
  • Radiolucent jaw malignancies have been mistaken
    for periradicular lesions.

73
  • Radicular cyst 
  • Residual cyst 
  • Paradental and mandibular infected buccal cysts
  • Mandibular Infected Buccal Cyst   
  • Lateral periodontal cyst
  • Glandular odontogenic cyst
  • Odontogenic keratocyst
  • Gorlin syndrome
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