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 ABOUT THE BOOK:
•The book Is complete, condse, comprehensive and easy to read book on the subjects of perlodontologyand oral

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lmplantology.

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ett briefly explains all the topics of the MDS In Periodontics according to the Curriculum of Dental coundl of Ind/a.
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with the/r reasonlng on the latest trends and updates In the field of perladantalogy and lmplantalagy.

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estep.lJy-step procedures and pre<entatlans ornumerous problems In perladantology with their possible therapeutic

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solutions.
eFresh perspectives on key topics and new Information throughout the book that gives the up-to-date coverage of
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complete spectrum In pertodontalogy and oral implantology. .
ett targets the undergraduates, post graduates and din/clans

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SARANRAJ JPS PUBLICATION DR. SYED WALi PEERAI

Bl. IAITHIIEYAI IAMAL/lliAM
Essentials of
PERIODONTICS &
ORAL IMPLANTOLOGY

DR. SYED WALi PEERAN

DR. KARTHIKEYAN RAMALINGAM
Essentials Of
PERIODONTICS & ORAL IMPLANTOLOGY
Published by Dr. Syed Wali Peeran and Dr. Karthikeyan Ramalingam @
Saranraj JPS Publication,
Tamil Nadu, India

© Dr. Syed Wali Peeran &

Dr. Karthikeyan Ramalingam
1st Edition 2021
ISBN: 978-81-950475-4-3
All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or
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Note: As new information becomes available, changes become necessary. The editors/author/contributors and the publishers have,
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of human error or advances in medical science neither the editor nor the publisher nor any other party who has been involved in the
preparation or publication of this work warrants that the information contained herein is in every respect accurate or complete. Readers
are strongly advised to conirm. This book is for sale in India only and cannot be exported without the permission of the publisher in
writing. Any disputes and legal matters to be settled under Chennai jurisdiction only.

Published in India
 Dr. Syed Wali Peeran is Professor of Periodontology and Oral lmplantology.
He finished his postgraduation in Periodontology in 2008 and has a doctoral degree.
He has a postgraduate certificate in advanced oral implantology and a
fellowship from international congress of oral implantologists.
He is the Editor in Chief and the founding editor for the journals-
Dentistry & Medical Research and Case Reports in Odontology.
He has over 63 national and international publications to his credit.
He has attended various national and international conferences and workshops.
He has also authored "Perio-Quest- MCQs in Periodontics with Self-Assessment
Picture Test" published by EMMESS publishers. He has been a reviewer for Libyan
Journal of Medicine,Journal of Nature, Biology and Medicine and various other
journals. He is a Life member of Indian Academy of Osseo Integration,
Indian Society of Periodontology, Indian immunological Society,
Indian Society of Oral lmplantologists and Indian Dental association.

Dr. Syed Wali Peeran, B.D.S, M.D.S (Peria), Ph.D. FICO/., PGCOI.
Professor, Department of Periodontics & Oral lmplantology,Faculty of Dentistry, Sebha
University, Sebha, Libya.

Dr. Karthikeyan Ramalingam is a Professor of Oral Pathology and Microbiology.

He finished his graduation and post graduation from Saveetha Dental College,
Chennai. He was the College topper in Part I and Part II postgraduate University
examinations.
He had secured the Gold medal in Pathology & Microbiology and Community
Dentistry in University examinations.He has guided postgraduates in oral pathology for
their seminars, research studies, journal discussions, library dissertations, thesis
preparation and in submitting articles for publication in various national and
international journals. He has also handled lectures and practical demonstrations
for undergraduates in oral histology,dental anatomy, forensic odontology, oral
pathology and microbiology. He has 65 international and national publications to his
credit. He is the Co-author of Textbook of Prosthodontics by Jaypee Brothers Medical
Publishers (P) Ltd. He has also contributed multiple choice questions and clinical
pictures to Perio-Quest- MCQs in Periodontics with Self-Assessment Picture Test by
EMMESS publishers. He is the Editor for Journals - Dentistry and Medical Research &
Case reports in Odontology.He is also the Reviewer for Journal of Oral and
Maxillofacial Pathology and North American Journal of Medical Sciences
(Indexed with PUBMED) and Journal of Cranio-Maxillary diseases.
He is a member of International Association of Oral Pathologists since 2016.
He is a Life member of Tamilnadu Dental Council since 2001, Life member of
Indian Association of Oral and Maxillofacial Pathologists since 2006 and a Life
member of Saveetha Dental College Old Students Association since 2001.
Dr. Karthikeyan Ramalingam, B.D.S, M.D.S
Professor, Department of Oral Pathology & Microbiology,Faculty of Dentistry, Sebha University,
Sebha,Libya
 Dr. ABDULNASIR MAQBOOL AHMED.
MSc, FICOI (U.S.A), Private Practice,
U.A.E.
Dr. Abhilash.
P.R. M.D.S
(Oral Pathology and Microbiology),
Reader, Department of Oral Pathology
and Microbiology,
Oxford Dental College & Hospitals,
Bangalore, Karnataka, India.
Dr. Ahmed Taher El-Hassan.
M.Sc (Oral Sciences-Periodontics),
Diplomate of American Board of
Periodontics, NOBE, WREB.
Assistant Professor, Benghazi University,
Benghazi, Libya.
Dr. Aisha Ahmed.
MB.ChB
ECFMG Certified Physician.
Department of Medicine, Faculty of
Medicine, Sebha University, Sebha,
Libya.
Dr. Bandar M.A. AL-Makramani.
BOS, HOD, MDSc, Ph.D
Assistant Professor, Fixed Prosthodontics,
Department of Prosthodontics, College
of Dentistry, Jazan University, Kingdom
of Saudi Arabia.
Dr. Fatma Mojtaba Al Said.
BOS., MPH (USA),
Faculty of Dentistry, Sebha University,
Sebha, Libya.
Dr. Franciso AL.
College of Dentistry, Jizan University,
KSA
Dr. Fuad Al Sanabani.
MSc, PhD
Department of Oral and Maxillofacial
Prosthodontics, Jazan University, Jazan,
Kingdom of Saudi Arabia
Dr. Ismail Abbas Darout.
DDS, Ph.D. (Dr .odont),
Postdoc Peria, Associate Professor
and Head, Department of Preventive
Dental Sciences, College of Dentistry,
Jazan University, Kingdom of Saudi
Arabia.
Dr. Khaled Awidat Abdalla.
B.D.S., C.E.S., DuODF (France),
Assistant Professor, Department of
Oral Biology and Orthodontics,
Sebha University, Sebha, Libya.
Dr. Manohar Murugan
M.Sc. (Microbiology), Ph.D.,
Assistant Professor, Department of
Medical Microbiology, Faculty
of Medicine, Sebha University, Sebha,
Libya.
Powered by TCPDF (www.tcpdf.org)
Dr. MOHAMMAD NAZISH ALAM.
BOS., MOS.
Asst. Prof, Department of Periodontics,
College of Dentistry, Jazan university
Dr. Nagabushan.
B.D.S., M.D.S
(Oral Medicine and Radiology),
Department of Oral Medicine and Radiology,
India.
Dr. Neha.
MOS.,
Department Of Periodontics and lmplantology,
Surendera Dental College and Research Institute,
Sriganganagar, Rajasthan.
Dr. R. Ganesh.
B.D.S., M.D.S. (Pedodontics)
Reader, Department of Pediatric and
Preventive dentistry, SRM University,
Tamil Nadu, India.
Dr. Rashmi Rai.
BOS., MOS.
Senior lecturer, public health dentistry,lndex
institute of dental sciences, Indore
Dr. Santosh Kumar.BB
BOS, MOS (Peria), M.Perio RCSEd (U.K),
MICOI (U.S.A) ), Specialist Periodontist and
lmplantologist, Kuwait.
Dr. Salhya Selhuraman.
B.D.S, M.A, PG0CA,
Surendra Dental College and Research
Institute, Sriganganagar, Rajasthan. India.
Dr. Shaesta Begum.
BOS, MOS (Periodontics),
Reader, Depatment of Periodontics, Farooqia
Dental College & Hospital, Mysore, Karnataka.
India.
Dr. Shamimul Hasan.
BOS, MOS
Assistant Professor, Department of Oral
Medicine and Radiology, Faculty of Dentistry,
Jamia Milia lslamia, New Delhi.India
Dr. Soumya K Nair.
B.D.S., MOS.,
Private practitioner, Mysore, India.
Dr. Suchelra N. Malleshi.
B.D.S., M.D.S (Oral Medicine and Radiology),
Department of Oral Medicine and Radiology,
J.S.S Dental College, Karnataka, India.
Dr. Supriya Ebenezer.
BOS., MOS.
Reader, Department of Periodontics,
Mathrusri Ramabai Ambedkar Dental
College and Hospital, Bangalore, India.
Dr. Syed Ali Peeran.
M.D.S. (Prostho)., MBA(HA), M.Phil (H.A),
Department of Prosthodontics, Assistant
Professor, Jazan University, Jazan, KSA.
Dr. Syed Kuduruthullah. S.K
M.0.S.(Oral Path)
Lecturer, Ajman University,
Ajman, U.A.E.
Dr. Syed Nahid Basheer.
BOS., MOS.
Assistant Professor, Department of Restorative
Dental Science, College of Dentistry, Jazan
University, Gizan, Kingdom of Saudi Arabia.
Dr. Syeda Nikhat Mohammadi.
BOS., MOS.
Senior lecturer, public health dentistry,
Pravara institute of dental sciences, Loni.
Maharashtra.
Dr. Tazeen.D
B.D.S., M.D.S (Peria).
Assistant Professor, Department of Periodontics,
Jazan University, Jazan, KSA.
Prof. Dr. Abdul Hafeez Khan
M.Sc., Ph.D.
Chairman, Department of Parasitology, Faculty
of Medicine, Sebha University, Sebha, Libya.
Prof. Dr. Abdul Hafeez Khan
M.Sc., Ph.D.
Chairman, Department of Parasitology, Faculty
of Medicine, Sebha University, Sebha, Libya.
Prof. Dr. Madhumala Thiruneervannan
BOS., M.D.S (Peria),
Head, Department of Periodontics, Vinayaka
Mission's Sankarachariyar Dental College,
Salem, India.
Prof. Dr. Marei Hamad Al Mugrabi.
B.D.S., M.Dent.Sc. (Periodontics-Dublin),Ph.D.
Head, Department of Periodontics, Benghazi
University, Libya.
Prof. Dr. Nurgul KOMERIK.
DDS., Ph.D.
Post Doc. Biruni University, Dental School,
Dept. of Oral Surgery, Istanbul, TURKEY
Prof. Dr. P.G. Naveen Kumar.
B.D.S., M.D.S., (Community Dentistry),
Head, Department of Community and
Preventive dentistry, College of Dental
Sciences, Davangere, Karnataka, India.
Prof. Dr. PC Anila Namboodiripad.
BDS, MDS., Department of Oral and M axillofacial
Pathology, India
Prof. Dr. R Thiruneervannan
BDS., MDS.
Principal, Vinayaka Mission's Sankarachariyar Dental
College, Salem, Tamil Nadu, India.
Prof. Dr. Syed Khalid Alla!.
MDS.
Associate Fellow AAID, Department of oral
mplantology, Vivekenanda dental college,
TN, India
Prof. Dr. V.Gopinalh.
M.D.S.
Professor, Department of Periodontology and
lmplantology, Chhattisgarh dental college
and research institute, Rajnandgaon, India
Prof. DR.V.HARIKRISHNA.
M.D.S.
Department of Orthodontics and Dentofacial
Orthopaedics. Chhattisgarh Dental college
and research institute, Rajnandgaon, India.
Chapter 6 Periodontal Pocket
CHAPTER

13 Periodontal Pocket

Syed Wali Peeran &

Karthikeyan Ramalingam

Chapter Outline

• Classification of Periodontal pocket • Root surface wall

• Clinical features • Detection of pockets
• Histopathologic features • Relation of loss of attachment and bone loss to pocket depth
• Pathogenesis of pockets • Treatment
• Micro-topography of the gingival pocket wall • Review Questions:
• Pocket contents • Principal references and suggested further reading:

The periodontal pocket is defined as a

pathologically deepened gingival sulcus. (Carranza)
It is the primary and definitive sign of all forms of
periodontitis except necrotizing ulcerative periodontitis.
Classification:
According to the morphology:
1. Gingival Pocket (Pseudo pocket or False pocket or
Relative pocket): This type of pocket is formed by
gingival enlargement without destruction of the
underlying periodontal tissues. The sulcus is
deepened because of the increased bulk of gingiva
especially of the marginal gingiva. Pathological
changes are confined to the gingival compartment.
Fig 13.1: Gingival Pocket
Gingival pocket: A pathologically deepened
gingival crevice that does not involve loss of
connective tissue attachment. Frequently
observed when there is gingival enlargement.
(Glossary of Periodontal terms, 2001)

Periodontics & Oral Implantology 1

Etiopathogenesis of periodontal diseases
Fig. 13.2: Gingival Pocket
PSEUDO POCKET: A deepening of the
gingival crevice resulting primarily from an increase
in bulk of the gingiva without apical migration of
the junctional epithelium or appreciable destruction
of the underlying tissue. (Glossary of Periodontal terms, are involved.There is direct communication between
2001)
2. Periodontal Pocket (True pocket or Absolute
pocket): This is the type of pocket that occurs with
the destruction of the supporting periodontal tissue.
Loss of attachment can be measured. The pathological
changes have reached beyond the confines of the
gingival compartment; its base has advanced apically.
Periodontal Pocket is defined as “A pathologic fissure
between a tooth and the crevicular epithelium, and
limited at its apex by the junctional epithelium. It is an
abnormal apical extension of the gingival crevice caused by
migration of the junctional epithelium along the root as the
periodontal ligament is detached by a disease process. According to the relationship to the adjacent
(Glossary of Periodontal terms, 2001)
Fig. 13.3: Periodontal pocket
2 Periodontics & Oral Implantology
Section - III
Fig. 13.4: Periodontal pocket
According to the involvement of tooth surfaces:
1. Simple Pocket: Pocket may involve only one tooth
surface. In such a case, there is free communication
between the base of the pocket and the surface.
2. Compound Pocket: Two or more tooth surfaces
the base of the pocket and the gingival margin on
each of the involved surface. Pockets can be of
different depths and types on different surfaces of
the same tooth and approximating surfaces of the
same interdental spaces.
3. Complex Pocket: It is a spiral originating on one
tooth surface and twisting around the tooth to
involve one or more additional surfaces. The only
communication with the gingival margin is at the
surface where the pocket originates. These types are
most common in furcation areas.
tissue:
1. Suprabony pocket (Supracrestal or supraalveolar):
The bottom of the pocket is coronal to the alveolar
bone crest. It is seen along with horizontal bone
loss.
SUPRA BONY POCKET: A periodontal
pocket with a base coronal to the alveolar bone.
(Glossary of Periodontal terms, 2001)
2. Infrabony pocket (Intra bony, subcrestal or
intraalveolar): The base of the pocket has progressed
apical to the alveolar bone crest and is laterally bound
by it. Hence is seen along with vertical bone loss.
Chapter 13 Periodontal Pocket

INTRABONY POCKET: A periodontal pocket 4. Cup-shaped defect.

that extends into an intrabony periodontal defect. With the increase in the number of walls and
(Glossary of Periodontal terms, 2001)
decrease in the width of the defect, the prognosis
According to the According to the shape improves.
number of bony walls A periodontal pocket can at times be oedematous
and at times fibrotic. Moreover, it can be at times
Three-wall bony pocket Narrow associated with clinical signs of inflammation where
Two-wall bony pocket. it is referred to as active and in the intermittent
phase of quiescence, it is termed as passive.
Two-wall bony pocket. Broad Periodontitis is a chronic inflammatory condition,
Cup-shaped bony defect and a repair component is familiar finding in
chronic diseases. Hence, long-standing pockets
Fig. 13.5: Infrabony pocket often appear fibrotic. Thus the terms fibrotic,
1. Three-wall bony pocket have a remaining proximal wall, oedematous, active and passive represents bouts
a buccal and a lingual wall. It has better prognosis. of disease activity and presentation rather than
certain types of periodontal pocket. It is worth
2. Two-wall bony pocket has two remaining bony noting that, in particular, chronic periodontitis is a
walls. cyclic disease state with cycles of progression and
3. One-wall bony pocket has a remaining wall and is not a stability.
good candidate for periodontal regenerative
procedures.
Table13-1: Differences between suprabony and infrabony pocket
S. No. Suprabony pocket Infrabony pocket
1 The base of the pocket is coronal to the level of The base of the pocket is apical to the level of alveolar
the alveolar bone. bone.
2 The pattern of the underlying bone destruction The pattern of underlying bone destruction is vertical
is horizontal. (angular).
3 Interproximally the transseptal fibers that are Interproximally the transseptal fibers that are restored
restored during progressive periodontal disease during progressive periodontal disease are arranged in an
are arranged horizontally between the base of oblique direction and extend from the base of the pocket
the pocket and alveolar bone. to the adjacent tooth.
4 On the facial and lingual surface, the periodon-
On the facial and lingual surfaces, the periodontal ligament
tal ligament fibers beneath the pocket follow
fibers beneath the pocket follow an angular pattern similar
the normal horizontal oblique course between
to the adjacent bone.
the tooth and bone.
3. A break in the continuity of the interdental gingiva.
Clinical features:
4. Shiny, discoloured, puffy gingiva associated with
Clinical signs: exposed root surface.
1. Enlarged bluish red marginal gingiva with a rolled 5. Gingival bleeding on gentle probing.
edge separated from the tooth surface. 6. Purulent exudate (pus) appears spontaneously or on
2. A reddish-blue discoloration of the gingival margin application of digital pressure.
seen extending upto the attached gingiva. 7. Looseness, extrusion and migration of the teeth.

Periodontics & Oral Implantology 3

 Etiopathogenesis of periodontal diseases Section - III

Symptoms: 2. In such cases, fibrotic changes predominate over

8. Localized pain or sensation of pressure after
eatingwhich gradually decreases.
9. Foul taste in localized areas.
10. A tendency to suck material from the interproximal
surfaces.
11. Radiating pain deep into the bone.
12. A gnawing pain or feeling of itchiness in the gums.
13. An urge to dig a pointed instrument into the gums
with the relief obtained from the resultant bleeding.
14. Complains that the food sticks between the teeth
and preference to eat on the other side.
15. Sensitivity to heat and cold, toothache in the absence
of caries.
Histopathologic features:
1. The discoloration is caused by circulatory stagnation,
the flaccidity, by destruction of the gingival fibers and
surrounding tissues, the smooth, shiny surface, by the
atrophy of the epithelium and oedema, the pitting on
pressure, by oedema and degeneration.
exudation and degeneration, particularly in relation
to the outer surface of the pocket wall. However,
despite the external appearance of health, the
inner wall of the pocket invariably presents some
degeneration and is often ulcerated.
3. Ease of bleeding results from increased vascularity,
thinning and degeneration of the epithelium, and
the proximity of the engorged vessels to the inner
surface.
4. Transmigration of polymorphonuclear leukocytes
through the pocket epithelium.
5. Loss of collagen and invasion of subepithelial
connective tissue compartment by inflammatory
leukocytes.
6. Pain on tactile stimulation is due to ulceration of the
inner aspect of the pocket wall.
7. Pus occurs in pockets with suppurative inflammation
of the inner wall.
Pathogenesis of pockets:
The periodontal pocket formation is initiated by the
microbial assault on the tissues along with the susceptible
host response.

Inflammation: Degradation of Junctional epithelium Junctional epithelium Junctional epithelium

collagen proliferation detachment: detachment:
• Inflammatory
invasion of the • Collagenases, • Apical and lateral • JE detaches from • JE detaches from
connective tissue MMPs released proliferation the tooth. the tooth.
apical to junctional from the cells. • Intraepithelial • Intraepithelial
epithelium • Fibroblasts clevage within clevage within
phagocytose the junctional the junctional
collagen epithelium. epithelium.

Fig.13-6: Pathogenesis of periodontal pocket

4 Periodontics & Oral Implantology

Chapter 6 Periodontal Pocket

Gingival Proliferation of
inflammation gingival marginal Gingival pocket
connective tissue

Fig.13-7: Pathogenesis of gingival pocket

In association with the inflammation, the junctional Table13-2: Correlation between clinical features and
epithelium proliferates along the root surface (apically), histopathological features of periodontal pocket
and the coronal portion detaches from the root due to S. Histopathologic
Clinical features
increased inflammatory cells and oedema causing further No. features
detachment coronally and migration apically. With 1 Gingival wall of the peri- Circulatory stagnation,
continued inflammation, the gingiva increases in bulk and odontal pocket may show destruction of gingival
the gingival margin extends toward the crown surface. The bluish red discolouration, fibers, atrophy of epi-
junctional epithelium continues to migrate along the root flaccidity, pitting on pres- thelium and oedema.
and separate from it. Extension of inflammation into the sure. Oedema and degen-
epithelium takes place causing degeneration and necrosis. eration.
The junctional epithelium continues to migrate along the 2 The gingival wall is pink Fibrotic changes pre-
root and separate from it. The epithelium of the lateral and firm. dominate over exuda-
wall of the pocket proliferates to form bulbous, cord-like tion and degeneration.
extensions into the inflamed connective tissue. Leukocytes
3 Bleeding on probing. Increased vascularity.
and oedema from the inflamed connective tissue infiltrate
the epithelium lining the pocket resulting in various degrees 4 Pain on probing. Ulceration of the inner
of degeneration and necrosis. Pocket epithelium is a unique aspect of the pocket
pathological setting continuously challenged by accumulating wall.
plaque mass and insulted by the periodontopathic bacteria. 5 Exudation on the applica- Suppurative inflam-
The formation of a periodontal pocket is an irreversible tion of finger pressure. mation of the pocket
process. Mature periodontal pockets appear to be plasma wall.
cell-dominated lesion mediated by Th2 cells.
MICRO-TOPOGRAPHY OF THE GINGIVAL
POCKET WALL:
Gingival Scanning electron microscopy reveals the following areas.
inflammation
1. Areas of relative quiescence.
2. Areas of bacterial accumulation.
3. Areas of emergence of leukocytes.
Plaque Pocket
Accumulation Formation 4. Areas of leukocytes-bacterial interaction.
5. Areas of intense epithelial desquamation.
6. Areas of ulceration.
Fig.13-8: Pathogenesis of periodontal pocket 7. Areas of haemorrhage.

Periodontics & Oral Implantology 5

 Etiopathogenesis of periodontal diseases Section - III

Pocket contents: I. Structural changes: The following structural changes

in cementum are seen.
Periodontal pockets contain debris that is principally
a. The presence of pathologic granules; Areas of
1. Microorganisms and their product (enzymes, collagen degeneration or areas where collagen
endotoxins): The micro-organisms at each level in fibrils have not been fully mineralized.
the pocket are different and are associated with
b. Areas of increased mineralization: As a result of
the concomitant plaque. Subgingival spirochaetes
an exchange, upon exposure to the oral cavity
on a given root surface significantly increased
of minerals and organic components at the
apically. Pocket depth and pocket oxygen tension are
cementum-saliva interface.
inversely related. Pockets are increasingly populated
by anaerobic microorganisms towards the base with c. Areas of demineralization: They are probably
deeper pockets being increasingly associated with related to root caries. Exposure of oral fluid
anaerobic bacteria. and bacterial plaque results in theproteolysis
of the embedded Sharpey’s fibers, cementum,
2. Gingival crevicular fluid-exudate.
may be softened and undergo fragmentation
3. Food remnants. and cavitation. Root caries tends to progress
4. Salivary mucin. around rather than into the tooth. Active root
caries lesions appear as well defined yellowish or
5. Desquamated epithelial cells. light brown areas, covered by plaque and have a
6. Leukocytes: Presence of Polymorphonuclear softened or leathery consistency on probing.The
neutrophils is a consistent finding adjacent to the predominant organism is Actinomyces viscosis. The
pocket-lining epithelium, and they migrate through tooth may be painful, but an exploration of the
this pocket lining epithelium and into the gingival root surface reveals the presence of the defect
sulcus where they form a barrier between the plaque and penetration of the involved area with a
biofilm and the tissues. probe cause pain. Caries of the root may lead to
pulpitis, sensitivity to sweets and thermal changes
7. Yeast: Candida albicans is a common finding in saliva
or severe pain. Pathologic exposure of the pulp
and oral mucosa of healthy individuals. The presence
occurs in severe cases. Root caries may be the
of yeasts esp Candida spp in periodontal pockets has
cause of toothache inpatient’s with periodontal
regularly been noted. However, the exact role played
disease and no evidence of coronal decay.
by them if any is still unclear.
II. Chemical changes: The mineral content of cementum
Plaque-covered calculus usually projects from the tooth
is increased. Following minerals are increased on
surface. Purulent exudates (Pus) if present, consists of
the diseased root surface; Calcium, Magnesium,
living, degenerated and necrotic leukocytes, living and dead
Phosphrous and Flourine. Exposed cementum may
bacteria, serum and fibrin. The presence of pus signifies
absorb them from its local environment, making
an ongoing destructive process and is a secondary sign.
possible the development of a highly calcified layer
PURULENT EXUDATE: Characterized by resistant to decay.This ability of cementum to absorb
an abundance of polymorphonuclear leukocytes, substances from its environment may be harmful if
resulting in pus formation at the site of injury. the absorbed materials are toxic.
(Glossary of Periodontal terms, 2001)
III. Cytotoxic changes: Bacterial penetration into the
Root surface wall: cementum is seen. In addition, bacterial products
The root surface wall of the periodontal pockets often such as endotoxins have also been detected.
undergo changes that are significant because they may
perpetuate the periodontal infection, cause pain and
complicate periodontal treatment.
6 Periodontics & Oral Implantology
Chapter 13 Periodontal Pocket

Detection of pockets Treatment:

♦ Residual pockets with Pocket depth ≥ 6mm were
♦ The periodontal probe (graduated). Six points
risk factors for both disease progression and tooth
(mesiobuccal, mid-buccal, distobuccal, distolingual,
loss. Practical implications: Residual Pocket depth ≥
mid-lingual and mesiolingual) along each tooth are
6mm represent an incomplete periodontal treatment
probed. Three sites per tooth (MB, B, DL) have been
outcome and need further therapy.
advocated for large-scale epidemiological purposes
as they showed very small bias in estimating disease ♦ BOP at the same site during supportive periodontal
severity and were quite sensitive in estimating disease therapy (SPT) was found to be a parameter with a
severity. Moreover, it was also shown right-handed, limited, but statistically significant positive predictive
and left-handed persons probe similarly. Pocket value for attachment loss.
probing can be at times painful especially when the ♦ Clinical attachment loss (CAL) is a reliable
pockets are inflamed. In cases of mobile teeth and measurement to detect the changes in periodontal
teeth with inflamed gingiva, the probing measurements status than the probable pocket depth.
may be exaggerated due to lesser resistance offer
Pocket formation, provoked by micro bacterial plaque,
by the underlying supracrestal tissue. Probing with
seemed to be initiated by the degenerative changes in
a manual probe has a resolution of 1 mm, and
the second or third cell layers from the innermost cells in
that with electronic probes may have a resolution of
the most coronal part of the junctional epithelium facing
up to 0.2 mm.
the microbial plaque. Consequently, an intraepithelial
♦ Pockets are not detected by radiographic examination cleavage was formed followed by the degeneration and
as the pocket is a soft tissue change. So radiographs desquamation of the cells lining the split. This resulted in a
detect the areas of bone loss where pockets may be deep crevice and gingival pocket formation in both early and
suspected, and they do not show pocket or depth. established lesions. In advanced lesions, the deep pocket
Radiographs may show horizontal as well as vertical epithelium was exposed for such a long distance adjacent
bone loss. Deep intra bony pockets can seldom be to the plaque and calculus, that the epithelium could be
without radiographic changes. directly affected by toxic bacterial products and mechanical
♦ Guttapercha points or calibrated silver points can be irritation of calculus. Finally, the epithelium became very
used with radiograph thin and ulcerated, and a typical periodontal pocket was
formed. The disruption of the epithelial barrier along with
Relation of loss of attachment and bone loss to
the concomitant penetration of bacteria and their toxic
pocket depth:
products were considered to be the most significant
The severity of attachment loss is correlated with the depth factors related to the conversion of an established lesion
of the pocket. The degree of attachment loss (recession) to an aggressive lesion.
depends on the location of the base of the pocket on the
root surface.Whereas the depth is the distance between the Review Questions:
base of the pocket and the crest of the gingival- so pocket
Essay Questions:
of the same depth may be associated with different degrees
of attachment loss. In addition, pocket of different depths 1. Define and classify pockets. Write about the clinical
may be associated with the same amount of attachment features and contents of the pockets.
loss. The severity of bone loss is correlated with pocket Short notes:
depth (but not always). The extensive bone loss may be
associated with shallow pocket, and slight bone loss can 2. Enumerate the differences between suprabony and
occur with deep pockets. The radius of the action of the infrabony pockets.
plaque bacteria is 0.5 to 2.5mm i.e. this distance is generally 3. The pathogenesis of periodontal pocket.
observed between the plaque front and the alveolar bone.
4. Enumerate the differences between pocket and
clinical attachment loss.
Periodontics & Oral Implantology 7
 Etiopathogenesis of periodontal diseases
5. Root surface changes in periodontal pocket
6. The microtopography of the soft tissue wall of the
periodontal pocket.
Principal references and suggested further
reading:
♦ Allahyari S, Kadkhoda.Z, Comparison of right-handed
and left-handed dental students in measurement
of periodontal pocket depth Journal of Dental
Medicine-Tehran University of Medical Sciences 2010;
23(4):256-264.
♦ Andrea Mombelli, Clinical parameters: biological
validity and clinical utility. Periodontology 2000, Vol.
39, 2005, 30–39.
♦ Bryan S. Michalowicz, James S. Hodges, Bruce Lee
Pihlstrom. Is change in probing depth a reliable
predictor of change in clinical attachment loss? JADA
144(2) http://jada.ada.org February 2013. 171-178.
♦ Carranza.FA and Camargo PM.The periodontal
pocket.Newman.MG, Takei.HH, Klokkevold.PR,
Carranza.FA. Carranza’s Clinical Periodontology. 10th
edition. 2006, Saunders, St Louis, Missouri.
♦ Glossary of Periodontal Terms, 4th Edn,The American
Academy of Periodontology, 2001
♦ Grant MM, Kolamunne RT, Lock FE, Matthews
JB, Chapple ILC, Griffiths HR. Oxygen tension
modulates the cytokine response of oral epithelium
to periodontal bacteria. J Clin Periodontol 2010; 37:
1039–1048.
♦ Houshmand M, Holtfreter B, Berg MH, Schwahn
C, Meisel P, Biffar R, Kindler S, Kocher T. Refining
definitions of periodontal disease and caries for
prediction models of incident tooth loss. J Clin
Periodontol 2012; 39: 635–644.
♦ Kingman A, Susin C, Albandar JM. Effect of partial
recording protocols on severity estimates of
periodontal disease. J Clin Periodontol 2008; 35:
659–667.
8 Periodontics & Oral Implantology
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Section - III
♦ Lang, N. P., Joss, A., Orsanic,T., Gusberti, F. A. & Siegrist,
B. E. (1986) Bleeding on probing. A predictor for the
progression of periodontal disease? Journal of Clinical
Periodontology 6, 590–596.
♦ Matuliene G, Pjetursson BE, Salvi GE, Schmidlin K,
Bra¨gger U, Zwahlen M, Lang NP.Influence of residual
pockets on progression of periodontitis and tooth
loss: Results after 11 years of maintenance. J Clin
Periodontol 2008; 35: 685–695.
♦ Michael Smith, Gregory J. Seymour & Mary P. Cullinan.
Histopathological features of chronic and aggressive
periodontitis. Periodontology 2000, Vol. 53, 2010,
45–54
♦ Neiderud A-M, Ericsson I and Lindhe J: Probing pocket
depth at mobile/nonmobile teeth. J Clin Periodontol
1992; 19: 754-759.
♦ Nesse W, Abbas F, van der Ploeg I, Spijkervet FKL,
Dijkstra PU, Vissink A. Periodontal inflamed surface
area: quantifying inflammatory burden. J Clin
Periodontol 2008; 35: 668–673.
♦ Omar AA, Newman HN. Bulman J and Osborn J:
Darkground microscopy of subgingival ptaque from
the top to the bottom of the periodontal pocket. J
Clin Periodontol 1990: 17: 364-370.
♦ Philippe P. Hujoel, Joana Cunha-Cruz, Herbert Selipsky
& Barry G. Saver Abnormal pocket depth and gingival
recession as distinct phenotypes. Periodontology
2000,Vol. 39, 2005, 22–29
♦ Rajendran R, Shafer’S Textbook Of Oral Pathology
(6Th Edition)
♦ Reynaud AH, Nygaard-Østby B, Bøygard G-K, Eribe
ER, Olsen I, Gjermo P: Yeasts in periodontal pockets.
J Clin Periodontol 2001; 28: 860–864. C Munksgaard,
2001.
♦ Takata T, Donath K. The mechanism of pocket
formation. A light microscopic study on undecalcified
human material. J Periodontol. 1988; 59(4):215-21.