Abscess in Periodontium Definition Classification Etiology & Risk factors Pathogenesis Histopathology Microbiology Diagnosis Differential diagnosis Problems in 1999 Classification 2017 Classification Treatment Necrotizing Periodontal Diseases Definition Classification Etiology – Host Immune Response Microbiology Pathophysiology & Histological features Diagnosis Problems in 1999 Classification 2017 Classification Differential diagnosis / Other Acute Conditions in Periodontium Treatment Endo-Perio Lesions Clinical Presentation Etiology Microbiology Risk factors Pathophysiology & Histological features Classification Diagnosis Problems in 1999 Classification 2017 Classification Treatment

1. Dr. BEENA VIJAYAN PARVATHY
3rd YEAR POST GRADUATE
Dept. of Periodontology and Oral Implantology
ACUTE GINGIVAL
&
PERIODONTALINFECTIONS

2. CONTENTS - PART 1
 Abscess in Periodontium
• Definition
• Classification
• Etiology & Risk factors
• Pathogenesis
• Histopathology
• Microbiology
• Diagnosis
• Differential diagnosis
• Problems in 1999 Classification
• 2017 Classification
• Treatment

3. ABSCESS IN PERIODONTIUM
Definition
1) A localized purulent infection in the periodontal tissues.
Meng H X et al; 1999
2) A lesion with an expressed periodontal breakdown occurring during a limited
period of time, and with easily detectable clinical symptoms, including a
localised accumulation of pus located within the gingival wall of the periodontal
pocket.
Herrera et al; 2000

5.  Classification
By the Location of the Abscess Gillets et al; 1980
Gingival Abscess Periodontal Abscess
Localised painful swelling,
affecting only the marginal
and interdental
gingiva. [Due to impacted
foreign objects]
Localised painful swelling,
affecting deeper periodontal
structures, including deep
pockets, furcations and
vertical osseous defects.
Affects only marginal soft
tissues.
Located beyond mucogingival
line.
Histologically, both lesions are identical.

6. Course of Lesion: Pini Prato et al; 1988
Acute Periodontal
Abscess
Chronic Periodontal
Abscess
Symptoms; pain, tenderness,
sensitivity to
palpation, and suppuration
upon gentle pressure.
Associated with a sinus tract,
and it is usually
asymptomatic, although the
patient can
refer mild symptoms. May
have an acute exacerbation.
A localised acute abscess may become a chronic abscess
when drainage is established through a sinus or through the
sulcus.

7.  Number of Abscess: Topoll H H et al; 1990
Single Periodontal
Abscess
Multiple Periodontal
Abscess
Associated with local factors,
which contribute to the
closure of the drainage of a
periodontal pocket.
Reported in uncontrolled
diabetes mellitus, medically
compromised patients, and
in patients with untreated
periodontitis after systemic
antibiotic therapy for non‐oral
reasons.
Seen in a patient with
multiple external root
resorptions

8. According to the International Workshop for a Classification of Periodontal
Diseases and Conditions, 1999:
 Gingival Abscess
A localized, painful, rapidly expanding lesion involving the marginal gingiva or interdental
papilla sometimes in a previously disease-free area.
 Periodontal Abscess (Acute or Chronic)
A localized accumulation of pus within the gingival wall of a periodontal pocket resulting in
the destruction of the collagen fibre attachment and the loss of nearby alveolar bone.
 Pericoronal Abscess
A localized accumulation of pus within the overlying gingival flap surrounding the crown of
an incompletely erupted tooth.
 Periapical Abscess

9. Periodontal Abscess
In periodontitis patients, there are different subgroups:
• Acute exacerbation of an untreated periodontitis.
Dello Rurso N M et al, 1985
Periodontitis-affected sites (with a pre-existing
periodontal pocket)
Healthy sites (without a pre-existing pocket)

10. • After non-surgical periodontal therapy: after scaling or professional prophylaxis,
dislodged calculus fragments can be pushed into the tissues or inadequate scaling may
allow calculus to remain in deep pocket areas, while the coronal part will occlude the
normal drainage.
• After surgical periodontal therapy: associated with the presence of foreign bodies such
as membranes for regeneration or sutures.
• Acute exacerbation in refractory periodontitis Fine D H et al, 1994
• Acute exacerbation in supportive periodontal therapy.
• Systemic antimicrobial intake without subgingival debridement, in patients with
advanced periodontitis may also cause abscess formation, probably related to an
overgrowth of opportunistic bacteria.

11. In Non-Periodontitis patients:
• Different foreign bodies have been described to be associated with the development of a
periodontal abscess, an orthodontic elastic, a piece of dental floss, a dislodged cemental
tear, a piece of a toothpick or pieces of nails in subjects with nail-biting habits. Also
termed ‘oral hygiene abscesses’.
• The root surface may be altered by different factors: perforation by an endodontic
instrument, cervical cemental tears, external root resorption, an invaginated tooth or a
cracked tooth.

12. Pathogenesis
The invasion of bacteria into the soft tissues surrounding the periodontal pocket
Inflammatory process through the chemotactic factors released by bacteria that attract
inflammatory cells
The destruction of the
connective tissues, the encapsulation of the bacterial
infection and the production of pus
DeWitt G V et al, 1985
Once the abscess is formed, the rate of destruction within the abscess will depend on the
growth of bacteria inside the focus, their virulence and the local pH.

13. Histopathology
• A normal oral epithelium and lamina propria.
• An acute inflammatory infiltrate.
• An intense focus of inflammation, with presence of neutrophils and lymphocytes in an area
of destroyed and necrotic connective tissue.
• A destroyed and ulcerated pocket epithelium.
• Gram-negative bacteria.
DeWitt G V et al, 1985

14. Microbiology
The most prevalent bacterial species identified in periodontal abscesses, using culture-based
or molecular-based diagnostic techniques, is:
o Porphyromonas gingivalis
o Prevotella intermedia
o Prevotella melaninogenica
o Fusobacterium nucleatum
o Tannerella forsythia
o Treponema spp.
o Parvimonas micra
o Actinomyces spp.
o Bifidobacterium spp
o Campylobacter spp.
o Capnocytophaga spp.
o Aggregatibacter actinomycetemcomitans

15. Based on Symptoms:
• Severe pain
• Tenderness of gingiva
• Swelling
• Tooth mobility
• Tooth elevation
• Sensitivity of the tooth to palapation
Based on Oral examination,
Clinically:
• Presence of an ovoid elevation in the gingiva along the lateral part of the root.
• Found as a diffuse swelling or simply as a red area.

16. • Suppuration either through a fistula or, most commonly, through the pocket opening,
spontaneous, or occur after applying pressure on the lesion.
• Bleeding on probing.
• Increased tooth mobility.
Radiographically:
• Normal appearance
• Some degree of bone loss [In previous pockets]
General Examination:
• Body temperature
• Malaise
• Regional lymphadenopathy
• Increased blood leukocytes

17. Differential diagnosis
 Other abscesses in the mouth: periapical or dento-alveolar or endodontic abscesses, lateral
periapical cyst, vertical root fractures, endo-periodontal abscess, postoperative infection.
 Tumor lesions, including metastatic tumoral lesions, odontogenic myxoma, non-Hodgkin´s
lymphoma, squamous cell carcinoma, metastatic carcinoma.
 Other oral lesions: pyogenic granuloma, osteomyelitis, odontogenic keratocyst, eosinophilic
granuloma.
 Self-inflicted gingival injuries.
 Sickle cell anemia.
 Abscesses after surgical procedures.

18. Problems in 1999 Classification
(1) The differentiation between gingival and PA, which could be confusing, because
this differentiation was simultaneously based on location and etiology.
(2) Considering a PA as chronic or acute may not be adequate, because an abscess, by
definition, is an acute lesion.
(3) The inclusion of pericoronitis and periapical abscesses in the classification together
with PA might not be appropriate.

19. 2017 Classification

20. Treatment
Two distinct phases:
1. Control of the acute condition
2. Management of a pre‐existing and/or residual lesion
Control of the acute condition:
Four therapeutic alternatives;
1. Tooth extraction
2. Drainage and debridement
3. Systemic or local antimicrobials
4. Surgery

21. • Tooth extraction: If severely damaged, and prognosis is hopeless after the destruction
caused by the abscess.
• Drainage and debridement: Through the pocket or through an external incision, compression
and debridement of the soft tissue wall, and the application of topical antiseptics after the
drainage. If associated with a foreign body impaction, the object has to be eliminated
through careful debridement.
• Systemic or local antimicrobials:
Smith & Davies 1986 -evaluated the incision and drainage of the abscess, together with
adjunctive systemic metronidazole (200 mg, tid, 5 days), followed by a delayed periodontal
therapy
Hafström et al, 1994 -drainage through the periodontal pocket, irrigation with sterile saline,
supragingival scaling and tetracycline for 2 weeks (1 g/day).
Herrera et al, 2000 -compared azithromycin (500 mg, once per day, 3 days) versus
amoxicillin plus clavulanate (500+125 mg, tid, 8 days), with delayed scaling (after 12 days).

22. Eguchi et al, 2008 -compared irrigation with sterile physiological saline and 2% minocycline
hydrochloride ointment, versus irrigation with sterile physiological saline without the local
antibiotic.
• Surgery: Abscesses associated with deep vertical defects, or in cases occurring after
periodontal debridement in which calculus is left subgingivally after the treatment.
The drug with the most adequate profile is metronidazole (normally prescribed, for acute
conditions, at 250 mg, tid). Azithromycin (500 mg, once per day) and amoxicillin plus
clavulanate (500+125 mg, tid) have also shown good clinical results. The duration of the
therapy should be restricted to the duration of the acute lesion, which is normally 2‐3 days.

24. Management of a pre‐existing and/or residual lesion:
Since most periodontal abscesses occur in a previously existing periodontal pocket,
periodontal therapy should be evaluated.
• If not been treated previously→ appropriate periodontal treatment should be provided.
• If within the active phase of therapy → once the acute lesion is treated the periodontal
therapy should be completed.
• If patients during SPT → a careful evaluation of the recurrence of the abscesses should
be made as well as an adequate evaluation of the tissue damage and how this affects
tooth prognosis.

25. CONTENTS - PART 2
Necrotizing Periodontal Diseases
• Definition
• Classification
• Etiology – Host Immune Response
• Microbiology
• Pathophysiology & Histological features
• Diagnosis
• Problems in 1999 Classification
• 2017 Classification
• Differential diagnosis / Other Acute Conditions in Periodontium
• Treatment

26. NECROTIZING PERIODONTAL
DISEASES
NPD is a group of infectious diseases that includes:
• Necrotizing ulcerative gingivitis (NUG)
• Necrotizing ulcerative periodontitis (NUP)
• Necrotizing stomatitis (NS)

27. Older names of NUG:
• Vincent’s disease
• Trench‐mouth disease
• Necrotizing gingivo‐estomatitis
• Fusospirochaetal stomatitis
• Ulcerative membranous gingivitis
• Acute ulcerative gingivitis
• Necrotizing ulcerative gingivitis or Acute necrotizing ulcerative gingivitis
NUP was defined by:
- 1989 World Workshop
- 1993 European Workshop
- International Workshop for a Classification of Periodontal Diseases and Conditions in 1999

28. Classification
According to the location of the tissue affected by the acute disease process, NPD can
be classified as:
• Necrotizing gingivitis: when only the gingival tissues are affected.
• Necrotizing periodontitis: when the necrosis progresses into the periodontal
ligament and the alveolar bone, leading to attachment loss.
• Necrotizing stomatitis: the necrosis progresses to deeper tissues beyond the
mucogingival line, including the lip or cheek mucosa, the tongue, etc.
Horning G M et al, 1995

29. Etiology
Host Immune Response
Non HIV patients;
• Previous history of NPD
• Poor oral hygiene
• Inadequate sleep
• Unusual psychological stress
• Poor diet
• Recent systemic diseases
• Alcohol abuse
• Tobacco smoking
• Caucasian ethnicity
• Age below 21

30. HIV Patients; Winkler et al,1988
• NPD are more frequent and show a faster progression.
• The reduction in the counts of peripheral CD4 lymphocytes.
Malnutrition;
• “Protein‐energy malnutrition”, a marked reduction in key antioxidant nutrients and an
altered acute phase response against infection.
• An inversed proportion in the ratio of helper/suppressor T‐lymphocytes, histaminemia,
increased free cortisol in blood and saliva.
• Defects in mucosal integrity.
Psychological stress and insufficient sleep;
• Associated with NG.
• Military personnel in wartime.
• New recruits for military services.
• Drug‐abusers during abstinence syndrome.
• Students during exam periods
• Patients with depression or other psychological conditions

31. • During these stress periods, not only the immune response is altered, but also the
subject’s behavior, leading to inadequate oral hygiene, poor diet or increased tobacco
consumption.
• Mechanism; a reduction in the gingival microcirculation and salivary flow and an
increase in serum and urine levels of 17‐hydroxycorticosteroid (17‐OHCS), which are
associated with an alteration in the function of polymorphonuclear leukocytes (PMN)
and lymphocytes, or even an increase in the levels of periodontal pathogens, such as P.
intermedia.
• In patients with NG, higher urine levels of 17‐OHCS have been reported, when
compared with healthy or treated patients.
• Patients with NG also contained PMNs with altered functions, since their bactericidal,
phagocytic and chemotactic capacities were depressed.

32. Inadequate oral hygiene, pre‐existing gingivitis and previous history of NPD;
• Plaque accumulation due to ulcer and crater lesions that may limit tooth brushing due to
pain.
• Usually occurs over a previously existing periodontal disease, usually chronic gingivitis.
Alcohol and tobacco consumption;
• Smoking is a risk factor.
• Mechanisms; effect of smoking on inflammation and tissue response, since smoking
interferes with both PMN and lymphocyte function and nicotine induces
vasoconstriction in gingival blood vessels.
• Alcohol consumption has also been associated with the physiological and psychological
factors favoring NPD.
Young age and ethnicity;
• In developed countries, young people are more prone to suffer NPD, mostly between 21-
24 years, usually combined with other predisposing factors, such as smoking and stress.
• NPD affects even younger people, being malnutrition and occurrence of infections.

33. Microbiology
• Spirochetes and fusiform bacteria Plaut et al, 1894 and Vincent et al, 1896 – Vincent’s
Infection
• Culture studies:- P. intermedia, and Treponema, Selenomonas and Fusobacterium species,
“constant flora”.
• In HIV patients:- along with other species, invasion of Candida albicans, herpes viruses or
superinfecting bacterial species.

34. Pathophysiology & Histological features
In NG lesions observed through light microscopy have shown a distinct pathology, with
presence of an ulcer within the stratified squamous epithelium and the superficial layer of the
gingival connective tissue surrounded with a non‐specific acute inflammatory reaction.
Four regions are:-
(1) Superficial bacterial area: [Fibrous mesh]
composed of degenerated epithelial cells, leukocytes, cellular rests, and a wide variety of
bacterial cells, including rods, fusiforms and spirochetes.

35. (2) Neutrophil-rich zone:
composed of a great number of leukocytes, especially neutrophils, and numerous
spirochetes of different sizes and other bacterial morphotypes located between the host
cells.
(3) Necrotic zone:
presence of disintegrated cells, together with medium and large size spirochetes and
fusiform bacteria.
(4) Spirochetal infiltration zone:
tissue components are adequately preserved, but infiltrated by large and medium size
spirochetes.

37. Diagnosis
Based on the clinical findings:
Necrotizing gingivitis:
• Based on the presence of necrosis and ulcers in the free gingiva.
• Start at the interdental papilla with the typical “punched‐out” appearance.
• A marginal erythema, named “lineal erythema”, may be present, separating the healthy
and the diseased gingiva.
• Necrotic lesions can progress to the marginal gingiva.
• Most typical location is the anterior teeth, especially in the mandible.
• Gingival bleeding is a frequent finding, usually spontaneous or after minimal contact.
• Painful with severity.

38. Other less common findings are:
• Pseudo‐membranous formation over the necrotic area. It consists on a meshwork of whitish-
yellow color, composed of necrotic tissue, fibrin, erythrocytes, leukocytes and bacterial
cells. When this “membrane” is removed, the underlying connective tissue becomes
exposed and bleeds.
• Halitosis.
• Adenopathies, if present, submandibular lymph nodes.
• Fever and a general feeling of discomfort.

40. Necrotizing periodontitis:
• Along with clinical features of NG; affects the periodontal ligament and alveolar bone,
leading to loss of attachment.
• On progression, the interdental papilla is divided in a buccal and a lingual/palatal part,
with a necrotic area in the middle, known as interproximal crater. If the craters are deep,
the interdental crestal bone becomes exposed and denudated. In addition, crater
formation favors disease progression by allowing the accumulation of more bacteria.
Interproximal necrotic areas spread laterally and merge with the neighboring areas,
creating an extensive zone of destruction.
• Immune‐compromised patients, bone sequestrum (necrotic bone fragments within the
tissues but separated from the healthy bone) may occur, mainly interdentally, but also in
buccal or lingual/palatal alveolar bone.

41. Necrotizing stomatitis:
• When bone denudation extends through the alveolar mucosa, larger bone sequestra may
occur, with large areas of osteitis and oral‐antral fistulae.
• Severity of these lesions is associated with severely compromised systemic patients,
including AIDS patients and severe malnutrition.
Problems in 1999 Classification
1. Did not consider the huge differences in prevalence, risk of progression, and extent and
severity of NPD among patients with different predisposing conditions.

42. 2017 Classification

43. Differential diagnosis / Other Acute Conditions in Periodontium
Gingival lesions of specific bacterial origin
• Group B streptococci → Gingival lesion- Streptococcal gingivostomatitis
Treated with re-hydration, resting, systemic antimicrobials
• Staphylococci aureus → with vesicles & desquamation, affecting lips, oral mucosae.
Appearance similar to multiform erythema or impetigo.
Treated with, systemic antimicrobials.
• Neisseria gonorrhoeae → white‐yellowish plaques or pseudo‐membranes when
removed → bleeding ulcer
Salivary flow ↓ → denser saliva
Treated with, systemic antimicrobials
Erythematous Erosive

44. • Treponema pallidum → Primary syphilis → chancre on the lips, tongue or tonsils.
Secondary syphilis → gingiva later with presence of plaque
(elevated papillae with central erosion)
Tertiary syphilis → affect palate and tongue
Treated with, specific systemic antimicrobials.
 Virus infections
• Varicela → Herpusvirus varicella (HSV-3) → Vesicles in oral cavity, including
gingiva
Treated with, antiviral agents & adequate nutritional support.
• Recurrent herpetic infection → Herpessimplex virus type 1(HSV-1) → Primary
Herpetic Gingivostomatitis
Intraoral or labial, itching & stinging feelings.
Erythema, grouped lesions break forming an erosion in oral mucosae gingiva or lip.
DD to recurrent aphthous stomatitis. Treated with, antiviral agents.

45. • Epstein Barr Virus (EBV) → Herpessimplex virus type 4 (HSV-4), Cytomegalovirus
or Herpes Simplex Virus Type-5 (CMV or HSV-5) or Coxsackie virus → specific
oral manifestations: infectious mononucleosis (HSV-4) or hand, foot & mouth
disease (Coxsackie).
Fungal infections
• Candidiasis → in immunocompromised patients.
Treated with, antifungal agents →Nystatin, Amphotercin B or Miconazole in solution
or gels.
Gingival manifestations of systemic conditions
• Mucocutaneous disorders →Chronic autoimmune disease →Vesicle-bullous lesions
with liquid content.
Present in gingiva as desquamative gingivitis, erythematous, vesicle-bullous or erosive
lesions. Reddness in attached and free gingiva.
Treated with, application of topical or systemic corticoids.

46. • Lichen planus → Reticular oral lesions on buccal and cheek mucosa. Erosive forms
in tougue and gingiva cause pain and tenderness, as well as bleeding.
Seen as desquamative gingivitis on attached gingiva.
• Pemphigus →Vulgaris →Desquamative gingivitis.
• Pemphigoid →Benign mucous membrane pemphigoid or Cicatrical phemphigoid
→Desquamative gingivitis including periods of exacerbation & remission.
Allergic reactions
• Exudative erythema multiforme →Desquamative gingivitis.
• Contact allergy →Erythematous & edematous gingival tissues
Treated by, removal of the allergen.

47. Traumatic lesions
• Physical (mechanical & thermal) injury →Erosions or ulcer, associated with gingival
recessions. Hyper-quertosis, vesicles or bullae.
• Ionizing radiations →Mucositis, with erythema followed by epithelial necrosis with
whitish plaques, leaves bleeding surface after dislodging.
• Chemical & pharmacological injury →Macular, vescicles, erosions or ulcers.

48. Treatment
The treatment should be organized in successive stages, including the treatment of the
acute phase and a subsequent treatment phase that should include the treatment of
the pre‐existing condition, the corrective treatment of the disease sequelae, and the
supportive or maintenance phase.
Treatment of the Acute Phase:
Two main objectives- 1) To arrest the disease process and tissue destruction.
2) To control the patient´s general feeling of discomfort and pain, which is interfering
with nutrition and oral hygiene practices.

49. Superficial debridement: Westergaard J et al, 1994
• To remove the soft and mineralized deposits.
• Power‐driven debridement devices (e.g. ultrasonics) are usually recommended exerting
minimum pressure over the ulcerated soft tissues.
• The debridement should be performed daily, getting deeper as the tolerance of the
patient improves, and lasting for as long as the acute phase lasts (normally, 2‐4 days).
• Mechanical oral hygiene measures should be limited, in order to avoid pain, since
brushing directly in the wounds may impair healing.
• During this period the patient is advised to use chlorhexidine‐based mouth rinses (at
0.12‐0.2%, twice daily), 3% hydrogen peroxide diluted 1:1 in warm water, and other
oxygen‐releasing agents.
If unsatisfactory response to debridement or systemic effects (fever,malaise)

50.  Systemic antimicrobials:
• Metronidazole, at 250mg, every 8 hours, may represent the first alternative, due to its
action over strict anaerobes.
• Other systemic drugs have also been proposed, with acceptable results, including
penicillin, tetracyclines, clindamycin, amoxicillin or amoxicillin plus clavulanate.
• Conversely, locally delivered antimicrobials are not recommended, due to the large
amount of bacteria present within the tissues, where the local drug will not be able to
achieve adequate concentrations.
• These patients have to be followed‐up very closely, daily if possible, and as the
symptoms and signs improve, strict mechanical hygiene measures should be enforced, as
well as complete debridement of the lesions can be scheduled.

51. Treatment of the pre‐existing condition: Cohen ME et al, 1995
• Once the acute phase has been controlled, the treatment of the pre‐existing chronic
condition should be implemented, including professional prophylaxis and/or scaling and
root planing.
• Oral hygiene instructions and motivation should be enforced.
• Existing predisposing local factors, such as overhanging restorations, interdental open
spaces and tooth malposition should be carefully evaluated and treated.
• At this stage, and also during the acute phase, attention should be paid to the control of
the systemic predisposing factors, including smoking, adequate sleep, reduction of stress
or treatment of the systemic conditions

52. Corrective treatment of disease sequelae: Westergaard J et al, 1994
• The correction of the altered gingival topography caused by the disease should be
considered, since gingival craters may favor plaque accumulation and disease recurrence.
• Gingivectomy and/or gingivoplasty procedures may be helpful to treat superficial
craters; for deep craters, periodontal flap surgery, or even regenerative surgery represent
more suitable options.

53. Supportive or maintenance phase:
• During this phase, the main goal becomes the compliance with the oral hygiene
practices and the control of the predisposing factors.

54. Specific considerations for HIV‐positive patients:
• Occurrence of NPD in systemically healthy individuals is suggestive of HIV infection,
and therefore the affected individuals should be screened for HIV.
• The specific management of NPD in HIV‐positive patients includes debridement of
bacterial deposits combined with the irrigation of the site with iodine povidone, based
on its hypothetic anesthetic and bleeding control effects.
• Careful consideration should be made regarding the use of systemic antimicrobials, due
to the risk of over-infections with Candida spp.
• Metronidazole has been recommended due to its narrow spectrum, with limited effects
on Gram‐positive bacteria, which prevent Candida spp. overgrowth, although HIV-
positive patients may not need antibiotic prophylaxis for the treatment of NPD.
• In non‐responding cases, the use of antifungals may be beneficial, including
clotrimazole lozenges, nystatin vaginal tablets, systemic fluoconazole or itraconazole,
mainly in cases of severe immunesuppression.

55. CONTENTS - PART 3
 Endo-Perio Lesions
• Clinical Presentation
• Etiology
• Microbiology
• Risk factors
• Pathophysiology & Histological features
• Classification
• Diagnosis
• Problems in 1999 Classification
• 2017 Classification
• Treatment

56. Clinical Presentation
Involves both the pulp and periodontal tissues and may occur in acute or chronic forms.
Signs and symptoms:
• Deep periodontal pockets reaching or close to the apex and negative or altered response
to pulp vitality tests.
• Bone resorption in the apical or furcation region, spontaneous pain or pain on palpation
and percussion, purulent exudate, tooth mobility, sinus tract, crown and gingival color
alterations.

57. Etiology
Primary etiology:
(1) Endodontic and/or periodontal infections
(2) Trauma and/or iatrogenic factors
(1) Endo-periodontal lesions associated with endodontic and periodontal infections:
Might be triggered;
(i) by a carious lesion that affects the pulp and, secondarily, affects the periodontium;
(ii) by periodontal destruction that secondarily affects the root canal;
(iii)or by both events concomitantly. Less frequently, “true-combined” or “combined”
lesion. Develop in subjects with periodontal health or disease.

58. (2) Endo-periodontal lesions associated with trauma and iatrogenic factors:
Poor prognosis as they affect the tooth structure.
Most common lesions are:
(1) root/pulp chamber/furcation perforation
(2) root fracture or cracking
(3) external root resorption
(4) pulp necrosis draining through the periodontium
Microbiology
Great similarity between the microbiota found in the root canals and periodontal pockets.
Mainly “red” and “orange” complexes, such as P. gingivalis, T. forsythia,or Parvimonas
micra, and species from the genera Fusobacterium, Prevotella and Treponema.

59. Risk factors
• Advanced periodontitis
• Trauma
• Iatrogenic events
• Presence of grooves
• Furcation involvement
• Porcelain-fused-to-metal crowns
• Active carious lesions
In high level of bone destruction around the affected
tooth, and anatomic problems worsen the prognosis

60. Pathophysiology & Histological features
The dental pulp and the periodontium have different communication pathways
• Apical radicular foramina
• Accessory (or lateral) canals, and
• Dentinal tubules
Accessory canals are more prevalent at the apical third of the roots, and furcation regions.
Pathological communication between these structures, includes the migration of
microorganisms and inflammatory mediators between the root canal and the periodontium.

61. Classification
(1) Primary endodontic lesions;
(2) Primary endodontic lesions with secondary periodontal involvement;
(3) Primary periodontal lesions;
(4) Primary periodontal lesions with secondary endodontic involvement; and
(5) “True” combined lesions.
Simon et al, 1972
The three main prognostic groups for a tooth with an EPL are:
(1) hopeless, (2) poor, and (3) favorable.

62. Diagnosis
1. Patient history for occurrence of trauma endodontic instrumentation or post
preparation.
2. Clinical and radiographic examinations presence of perforations, fractures, and
cracking or external root resorption.
If not identified radiographically initially full-mouth periodontal assessment,
including probing depth, attachment level, bleeding on probing, suppuration and mobility, as
well as tooth vitality and percussion tests.
The presence of a periodontal pocket reaching or close to the apex combined with absence of
pulp vitality would indicate the presence of an EPL.

63. Problems in 1999 Classification
(1)Grouping all EPL under a single section entitled “Periodontitis Associated with Endodontic
Lesion” was not ideal, as these lesions may occur in subjects with or without periodontitis.
(2)The single category presented, “Combined Periodontal-Endodontic Lesions”, was too
generic and not sufficiently discriminative to help the clinician to determine the most
effective treatment for a particular lesion.
EPL should be classified according to signs and symptoms feasible to be assessed at the time
that the lesion is detected and that have direct impact on their treatment, such as presence or
absence of fractures and perforations, presence or absence of periodontitis, and the extent of
the periodontal destruction around the affected teeth.

66. REFERENCES
1. David Herrera, Belén Retamal-Valdes, Bettina Alonso, Magda Feres; Acute periodontal
lesions (periodontal abscesses and necrotizing periodontal diseases) and endo-periodontal
lesions; 2017 WORLD WORKSHOP; J Periodontol. 2018;89(Suppl 1):S85–S102.
2. Barry Eley, Mena Soory, J. D. Manson; Periodontics Textbook 6th Edition.
3. Perry R. Klokkevold and Fermin A. Carranza; Acute Gingival Infections.

67. THANKYOU