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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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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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•The authors have excellent academic records and hold reputable positions In their respective fields

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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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diagnosis, treatment planning and management.
estep.lJy-step procedures and pre<entatlans ornumerous problems In perladantology with their possible therapeutic

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solutions.
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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
mechanical, including photocopy, recording or any information storage and retrieval system without the permission in writing from the
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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 1 Bone Loss and Patterns of Bone Destruction
CHAPTER

14 Bone Loss and Patterns

of Bone Destruction

Syed Wali Peeran &

Karthikeyan Ramalingam

Chapter Outline
• Pathway of Spread of Inflammation from Gingiva to Supporting Periodontal Tissues In Periodontitis:
• Radius of action: • Bone morphology in periodontal disease: • Osseous craters:
• Rate of alveolar bone loss: • Normal variation: • Bulbous bone
• Periods of destruction: • Exostoses: contours:
• Mechanisms of bone destruction: • Patterns of bone destruction in periodontal disease • Review Questions:
• Classification of bone defects and patterns of bone loss • Horizontal bone loss: • Principal References
• Bone destruction caused by Trauma from occlusion: • Osseous defects: and Suggested
• Bone destruction caused by systemic disorders: • Vertical/ Angular defects Further Reading:

Gingivitis always precedes periodontitis, but around the blood vessels, through the transseptal fibers,
gingivitis does not always progress to periodontitis. and then into the bone through vessel channels that
The crest of the alveolar bone is located perforate the crest of the interdental septum.
approximately 2mm apical to the cemento-enamel ♦ The site at which the inflammation enters the bone
junction. Periodontitis is characterized with theloss of depends on the location of vessels channels.
attachment. The alveolar bone loss is a hallmark of
periodontitis and represents the apical sequel of ** It may enter the interdental septum at the centre
periodontitis. of the crest, towards the side of the crest or at
the angle of the septum, and it may enter the bone
PATHWAY OF SPREAD OF INFLAMMATION through more than one channel.
FROM GINGIVA TO SUPPORTING
After reaching the marrow spaces, the inflammation
PERIODONTAL TISSUES IN PERIODONTITIS: may return from the bone into periodontal
Pathway of the spread of inflammation is significant ligament. Less frequently, the inflammation spreads
because it affects the pattern of alveolar bone destruction from the gingiva directly into the periodontal ligament
in periodontal disease. and from there into interdental septum.
Though the pathway of spread of inflammation is not Facial and lingual spread:
confirmed, there are suggested pathways of spread of
inflammation including interproximal, facial and lingual The inflammation from the gingiva spreads along the
directions. outer periosteal surface of the bone and penetrates into
the marrow spaces through vessel channels in the outer
Interproximal Spread cortex.
The inflammation spreads in the loose connective tissue ♦ From the alveolar bone, it travels to the periodontal
ligament.
Periodontics & Oral Implantology 1
 Etiopathogenesis of periodontal diseases Section - III

♦ Less frequently it travels from the periodontal of the radius of effectiveness is more important than the
ligament to alveolar bone. actual radius distance as it may slightly vary depending on
tolerance of the host, location and pathogenic potential of
Bone involvement: the plaque biofilm, pre-existing anatomical abnormalities,
After inflammation reaches the bone, it spreads into the abscess formation, or frank bacterial invasion of periodontal
marrow spaces and replaces the marrow with a fluid tissues which may be seen in aggressive periodontitis.
exudate, leukocytes, new blood vessels, and proliferating Rate of alveolar bone loss:
fibroblasts. Multinuclear osteoclast and mononuclear
phagocytes increase in number, and the bone surfaces are
lined with resorption lacunae.
In the marrow spaces, resorption proceeds from within,
first a thinning of the surrounding bony trabeculae and
enlargement of marrow spaces, followed by destruction of
the bone and a reduction in bone height.

Primary Etiology Rate of progres- Loss of Percentage

S. No sion of periodon- attachment/ of individu-
tal disease year als studied
• Dental plaque/Biofilm: It is the primary cause
of alveolar bone loss. 1 Rapid progression 0.1-1.0mm 8
Moderate pro-
2 0.05-0.5mm 81
Predisposing factors gression
Minimal or no
• Plaque-retaining elements-Anatomic anamolies. 3 0.05-0.09mm 11
progression
• Close proximity between adjacent root surfaces.
• Trauma from occlusion. Periods of destruction:
• Food Impaction. Destruction of periodontium is cyclic and episodic in
Fig 14-1:Etiology of alveolar bone loss nature. Periodontal destruction is interspersed with long
intermittent periods of inactivity or quiescence.
Radius of action: Plaque is the primary cause of alveolar
bone loss. Page & Schroeder postulated that this The reasons why and how these destructive periods start
microbial plaque ‘‘radius of effectiveness’’ in combination is not clearly understood.The following theories have tried
with variable dimensions of bone adjacent to infected root to explain these periods of periodontal breakdown as
surfaces resulted in the wide range of intraosseous and follows
furcation defects in periodontitis. Destruction of alveolar 1. Bursts of destructive activities are associated with
bone usually radiates from the plaque to a distance ranging subgingival ulcerations and an acute inflammatory
from 1.5mm to 2.5mm. An intra bony defect occurs reaction, resulting in rapid loss of alveolar bone.
adjacent to infected root surfaces where the distance 2. Bursts of destructive activity coincide with the
from the cribriform plate to either the external cortex conversation of a predominately T-lymphocyte lesion
or neighbouring root surface exceeds this radius of to one with predominance of B-lymphocyte plasma
effectiveness. Thus when interproximal/radicular bone is cell infiltrate.
wider than 2.5 mm, vertical defects form. If the interproximal
/radicular bone is narrower than 2.5 mm the hypothesis 3. Periods of exacerbation are associated with an
predicts the loss of all bone opposing the infected root increase of the loose, unattached, motile, gram-
surface leading to horizontal bone defects. This concept negative, anaerobic pocket flora, and periods of
2 Periodontics & Oral Implantology
Chapter 14 Bone Loss and Patterns of Bone Destruction

remission coincide with formation of a dense,

unattached, nonmotile, Gram-positive flora with through a noncellular mechanism.
tendency to mineralise. 3. Plaque products stimulate gingival cells, causing them
4. Tissue invasion by one or several bacterial species to release mediators, which in turn induce bone
is followed by an advanced local host defence that progenitor cells to differentiate into osteoclasts.
controls the attack. 4. Plaque products cause gingival cells to release agents
Mechanisms of bone destruction: that can act as cofactors in bone resorption.
5. Plaque products cause gingival cells to release agents
The following possible pathways by which plaque products
that destroy bone by direct chemical action, without
could cause alveolar bone loss in periodontal disease were
osteoclasts.
listed by Hausmann (1974):
However, as of now we know that all alveolar bone
1. Direct action of plaque products on bone progenitor
resorption is mediated by osteoclasts and the bacterial
cells induces differentiation of these cells into
products do not directly damage the alveolar bone
osteoclasts.
directly.
2. Plaque products act directly on bone, destroying it

Fig. 14-2: Mechanism of Alveolar bone loss

Periodontics & Oral Implantology 3

 Etiopathogenesis of periodontal diseases Section - III

Classification of bone defects and patterns of bone loss:

Goldman and cohen (1958)
• One wall defect
• Two-wall defect
• Three-wall defect.
• Combination defect.
Goldman and cohen (1958) Manson (1976)
• Thickened margin • Ossoeus bone defects were
• Interdental crater grouped under three clearly
• Hemispetum distinguishable groups:
• Infrabony defect with three • Intra-alveolar defects.
osseous walls (other than a • Marginal defects.
marginal gutter) • Perforations.
• Infrabony defect with two
osseous walls (other than
an interdental crater)
• Infrabony defect with one
osseous wall (other than a
hemispetum)
• Marginal gutter
• Furcation involvement
• Irregular bone margin
• Dehiscence
• Fenestration
• Exostosis

osseous contours produced by periodontal disease.

Bone destruction caused by Trauma from
occlusion:
In the absence of inflammation (plaque), trauma from
occlusion leads to angular defects without pocket
formation. These changes reverse as trauma from occlusion
is removed.
♦ In the presence of existing periodontitis (local factors),
trauma from occlusion has a compounding effect on
periodontal bone loss and destruction.
Bone destruction caused by systemic
disorders:
(b) Exostoses: They are outgrowths of bone of varied
The alveolar bone loss may occur in generalized skeletal
disturbances such as Hyperthyroidism, Leukemia, and
Langerhans cell histiocytosis.
Bone morphology in periodontal disease:
(a) Normal variation: The normal variations in the
morphologic features of alveolar bone affect the
The bone features that substantially affect the bone
destructive pattern in periodontal disease include
the following:
Alveolar bone:
• The thickness, width, and crestal angulation of the
interdental septa and alveolar plates.
• The presence of fenestrations and or dehiscence.
Tooth and root:
• Teeth alignment, Root length, root trunk anatomy
and root position
size and shape. Palatal exostoses have been found in
40% of human skulls. They can occur as small nodules,
large nodules, sharp ridges, spike-like projections, or
any combination of these.
EXOSTOSIS: A benign, bony growth projecting
outward from the surface of a bone.(Glossary of
Periodontal terms, 2001)

4 Periodontics & Oral Implantology

Chapter 14 Bone Loss and Patterns of Bone Destruction

HYPEROSTOSIS: A localized overgrowth of oral function or the replacement of a denture base or

bone. (Glossary of Periodontal terms, 2001) framework.
TORUS: An elevation, a swelling, a bulging
projection, a protuberance. (Glossary of
Periodontal terms, 2001)
TORUS PALATINUS: A bony
protuberance occurring at the midline of the hard
palate. (Glossary of Periodontal terms, 2001)
Bone exostoses and tori are localized peripheral
overgrowths of bone that arise from the cortical
plate and sometimes from the spongy layer due
to some unknown cause. Although the aetiology
is unknown, a hereditary basis is suspected.
These developmental anomalies are not pathologically Fig. 14.3: Torus Palatinus
significant, and frequently develop in skeletal jaw. In
TORUS MANDIBULARIS: A bony exostosis on
this respect, different types of exostoses have been
the lingual aspect of the mandible, generally in the
described; torus palatinus and torus mandibularis are
premolar molar region; commonly bilateral. (Glossary
two of the most common intraoral exostoses. The
of Periodontal terms, 2001)
other types of exostoses such as buccal or palatal
exostoses are less commonly encountered. Torus mandibularis (TM) which has reportedly been
usually bilaterally located in the lingual surfaces of the
Torus Palatinus(TP) is an exostosis of the hard
palate that is localized along the median palatine cusped/premolar area of the mandible and superior to the
suture and involves both the processi palatini and os mylohyoid ridge. The lingual tori are unnecessary bony
palatinum. TP contains compact and cancellous bone extensions, which may limit tongue space and create
and is formed by hypertrophy of the spongy and oral phonetic difficulties. Therefore, the tori may require
compact layers while the nasal compact layer surgical removal for prosthetic reasons. Removal of
remains unchanged. these exostoses can also assist with flap adaptation
TP is asymptomatic, grows slowly during the second during periodontal surgery. Tori are highest among
and third decades of life, and often goes unnoticed Eskimos. The TM are usually nodular in shape.
until middle age. Although much research has tried
to clarify the influence of genetic, environmental,
nutritional, and climatologic factors, there is still
no consensus regarding the etiology of TP.
TP occurs in about 20% of the population. It has
also been reported that females demonstrate a
higher prevalence of TP.
TP is a bony prominence that occurs along the
middle third of the midline of the hard palate. It
forms different shapes, including flat, spindle,
nodular, and lobular. This oral exostosis is not a
disease or a sign of disease. However, if TP is large, it
may be problematic for the construction or wearing
of dentures.
TP is not pathologically significant; surgical removal is Fig. 14.4: Madibular tori
required if it causes chronic trauma or interferes with
Periodontics & Oral Implantology 5
 Etiopathogenesis of periodontal diseases
(c) Trauma from occlusion: May cause thickening of
the cervical margin of alveolar bone or a change in
the morphology of the bone (e.g., angular defects and
buttressing bone).
(d) Buttressing bone formation: Buttressing
Bone: Marginal linear aspect of bone, which
may be formed in response to heavy occlusal
forces.(Glossary of Periodontal terms, 2001)
-Central buttressing bone formation: It occurs
within the jaws.
-Peripheral buttressing bone formation
(Lipping): It occurs on the external surface. This
may cause bulging of the bone contour.
(LIPPING): Bone formation sometimes occur
in an attempt to reinforce bony trabeculae
weakened by resorption.
Fig: 14.5: Peripheral buttressing bone formation
(e) Food impaction: The forceful wedging of food
into the interproximal space by chewing
pressure (vertical impaction) or the forcing of
food interproximally by tongue or cheek
pressure (horizontal impaction).(Glossary of
Periodontal terms, 2001)
Interdental bone defects often occur where proximal
contact is abnormal or absent. Pressure and irritation
from food impaction contribute to inverted bone
architecture. In some instances, the poor proximal
relationship may be the result of a shift in tooth
position because of extensive bone destruction
6 Periodontics & Oral Implantology
Section - III
that preceded food impaction. In such cases, food
impaction is a complicating factor rather than the
cause of bone defect.
(f) Aggressive periodontitis: Around first molars,
a vertical or angular pattern of alveolar bone
destruction is found.
Patterns of bone destruction in periodontal
disease:
Furcation Invasion:
Pathologic resorption of bone within a furcation.
Classification of Furcation Invasions:
Class I: Incipient loss of bone limited to the furcation flute
that does not extend horizontally.
Class II: A variable degree of bone loss in a furcation, but
not extending completely through the furcation.
Class III: Bone loss extending completely through the
furcation.
Hemiseptal Defect: A vertical defect in the presence
of adjacent roots; thus, half of a septum remains on one
tooth.
Intrabony Defect: A periodontal defect surrounded
by two or three bony walls or a combination of these.
(a) Horizontal bone loss:
It occurs where progression of bone loss takes place
at an even rate leading toa symmetrical reduction in
the height of the alveolar bone.In this type of bone
loss, the bony architecture appears relatively flat. It is
the mostcommon pattern of alveolar bone loss.
It can be regularly seen at sites where the interdental
bone is thin. Supra-bony pockets accompany the
horizontal bone loss. Horizontal bone loss can be
seen on radiographs. Regenerative procedures
with periodontal horizontal bone loss are not
undertaken.
Osseous Defects
Periodontal Bony Defects: Alterations in the
morphological features of the bone. Osseous defects
may be subcategorized as follows:
Chapter 14
Circumferential Defect: A vertical defect
that includes more than one surface of a tooth,
e.g., a vertical defect that includes the mesial and
lingual surfaces of a tooth. (Glossary of Periodontal
terms, 2001)
Crater: A cup- or bowl-shaped defect in the
interalveolar bone with bone loss nearly equal on
the contiguous roots. The facial and lingual palatal
walls may be of unequal height. A type of intrabony
defect, a crater also may be classified by the number
of bony walls (i.e., a one-, two-, or three-walled);
combination defects also exist. (Glossary of
Periodontal terms, 2001)
Funnel-Shaped Defect: An Intrabony
resorptive lesion involving one or more surfaces of
supporting bone; may appear moat-like. (Glossary of
Periodontal terms, 2001)
Fig. 14.6: Types of Bone loss
Table 14.2: Differences between Horizontal and vertical
bony defects
(b) Vertical/ Angular defects (Intra bony defects):
It occurs where bone loss develops around adjacent
teeth/surfaces at different rates. It primarily affects a
tooth and not it is adjacent. Bone loss takes a vertical-
angular-cuneiform when there is an adequate volume
of alveolar bone surrounding the root/roots. They
occur in an oblique-slanting direction with rapid bone
resorption progressing into the bone adjacent to the
root surface. They have a funnel shaped-trench like
appearance-hallowed trough-shaped presentation.
Vertical defects can occur inter-proximally or on the
radicular surface of tooth surface.
Periodontics & Oral Implantology
Bone Loss and Patterns of Bone Destruction
Sometimes they are difficult to be seen on the
radiographs. They increase with age.
These vertical defects are classified based on the
residual bony walls as follows:
Three-wall bony defect
• They are bordered by one tooth surface and three
bony surfaces. It was originally called intra bony
defect. It may be difficult to visualize this defect on the
radiograph. It yields the best results with periodontal
regeneration. They are frequently observed on the
mesial surfaces of the molars.
Two-wall bony defect
• It is enclosed by two tooth surfaces and two osseous
surfaces (buccal and palatal/lingual). The cortical
bone is generally intact. It may be difficult to visualize
this defect on the radiograph. It is located between
adjoining posterior teeth.
One-wall bony defect / Hemiseptum
• Only one bony wall remains facing the involved
tooth surface. It occurs generally when considerable
amount of interdental septum is lost.
Combined bony defect/combined osseous defect/
combination bony defect
• The number of bony walls apically at the level of base
of vertical defect can be more the occlusal aspect.
Horizontal bony
Vertical bony defect
defect
Bone level is essentially Bone level is essentially
equal interdentally equal interdentally
The bone loss is equal One tooth has more bone
across teeth. loss than the adjacent teeth.
Measured as the percent- Measured as the attach-
age of bone lost. ment loss at a site.
An individual tooth can have combination bone loss
consisting of both horizontal component and vertical
component.
7
 Etiopathogenesis of periodontal diseases
Fig. 14.7: Vertical defect
(Courtesy: Dr.Marei Hamad al Mugrabi)
Fig. 14.8: Cup shaped defect
(Courtesy: Dr.Marei Hamad al Mugrabi)
(c) Osseous craters: These are concavities in the
crest of interdental bone or peripheral radicular
bone. They are centred beneath the contact point of
the neighbouring teeth and are often saucer/ cup/
bowl shaped. These defects are confined by the
facial and lingual/palatal walls probably of unequal
heights. The defect affects the adjacent root surfaces
similarly. They are common in posterior teeth. It is
the most common bony lesion encountered in
periodontal disease.
Ochsenbein divided osseous craters into three
types based on the depth of the crater from the
crest of facial/lingual bone as follows:
• Shallow crater: 1-2mm.
• Medium crater: 3-4mm.
8 Periodontics & Oral Implantology
Section - III
• Deep crater: 5mm or more.
Why are interdental craters so common?
• Plaque: The difficulty in removal of plaque from
the interdental area.
• Morphology of interdental septum: The normal
flat or even concave faciolingual shape of the
interdental septum in lower molar may favour
crater formation.
• Pathway for inflammation: Vascular patterns from
the gingiva to the centre of the crest.
(d) Bulbous bone contours:
• These are bony enlargement caused by
exostoses.
• They occur as an adaptation to function or
buttressing bone formation.
• Prevalence: Maxilla > Mandible.
Architecture: A term with an appropriate
modifier, commonly used in periodontics to
describe gingival and/or bony form.(Glossary of
Periodontal terms, 2001)
Physiologic Architecture: A concept of soft
tissue or bony form that includes positive
architecture in a vertical dimension, buccal-lingual
contours devoid of ledges and exostoses, and
interradicular grooves. (Glossary of Periodontal terms,
2001)
Positive Architecture: When the crest of
the interdental gingiva or bone is located coronal
to its midfacial midlingual margins.(Glossary of
Periodontal terms, 2001)
Reverse Architecture: When the crest of
the interdental gingiva or bone is located apical
to its midfacial and mid-lingual margins.
(Glossary of Periodontal terms, 2001)
(e) Reversed architecture:
These defects are produced by loss of the interdental
bone crest, including the facial and/or lingual plates,
without concomitant loss of radicular bone, thereby
reversing the normal scalloped architecture.
• It is also called as inconsistent bony margin.
• It is more common in Maxilla.
Chapter 14 Bone Loss and Patterns of Bone Destruction

Fig. 14.9: Reverse architecture

(f) Ledges: It is plateau-like bone margin caused by
resorption of thickened bony plates.
Resorption: A loss of substance from tissues that
normally are calcified, such as the dentin or
cementum of teeth, or of the alveolar process. The
condition may be physiologic or pathologic.
(Glossary of Periodontal terms, 2001)
Bone Resorption: Bone loss due to osteoclastic
activity. (Glossary of Periodontal terms, 2001)
Cavernous Resorption: Bone loss leaving hollow
spaces. (Glossary of Periodontal terms, 2001)
Idiopathic Resorption: Loss of calcified tissues
without apparent cause. (Glossary of Periodontal
terms, 2001)
(g) Furcation involvement: It refers to the invasion
of bifurcation and trifurcation of multi-rooted teeth
by periodontal disease. (Carranza)
FURCATION INVASION: Pathologic resorption
of bone within a furcation. (Glossary of Periodontal Fig. 14.10: Classification of furcation involvement
terms, 2001) (Glickman’s classification) G-Gingiva, AB-Alveolar Bone

♦ Mandibular 1st molar are the most common site, and

maxillary premolars are the least common site.
♦ Diagnosis of Furcation involvement is made by clinical
examination and careful probing with Nabers probe.
♦ Furcation involvements have been classified by
Glickman as
♦ Grade I: incipient bone loss
♦ Grade II: partial bone loss (cul-de-sac)
♦ Grade III: total bone loss with through-and-through
opening of furcation.
Periodontics & Oral Implantology 9
Etiopathogenesis of periodontal diseases Section - III

♦ Grade IV: Grade III with gingival recession exposing the furcation clinically to view.

Fig. 1.10: Through and through furcation involvement

Clinically Radiographic

Periodontal Probing: It gives Two-dimensional (2D)

an indirect measure of the depth radiographic diagnosis
of the defect by providing methods: (bitewing and
the clinical attachment periapical radiographs):
loss measure. Advantages: They can be easily
acquired, cheap and provide high-
Disadvantage: The defect
resolution images.
cannot be visulaized as the
shape and size of the defect Disadvantages: They are limited
remains unknown. by overlapping anatomical
structures, difficult to standardize
and underestimating the size and
Transgingival
occurrence of bone defects.
probing/Sounding:
It provides the
understanding of the Cone beam CT (CBCT)
shape and size of the Advantages: It allows for an
underlying defect. analysis of the buccal and
Disadvantage: It requires lingual/palatal surfaces and
probing under anesthesia provides improved
hence remains an invasive
procedure and cannot be It allows visualization of the
carried over regularly. morphology of the defect.
Disadvantages: Expensive and
cannot be afforded regularly.

Fig14-11: How to detect the bone defects ?

10 Periodontics & Oral Implantology

Chapter 14
Review Questions:
Essay Questions:
1. What is an osseous defect? Classify and describe the
osseous defects.
Short Questions:
2. Buttressing bone formation.
3. Discuss the mechanism of bone loss in Periodontitis.
4. Osseous craters
5. Osseous defects in periodontal disease
6. Radius of action
7. Revised architecture
8. Transgingival Probing.
Principal References and Suggested Further
Reading:
♦ Al-Quran FA,Al-Dwairi ZN.Torus palatinus and torus
mandibularis in edentulous patients. J Contemp Dent
Pract 2006; 7: 112-9.
♦ Bartold PM, Cantley MD, Haynes DR. Mechanisms
and control of pathologic bone loss in periodontitis
.Periodontology 2000,Vol. 53, 2010, 55–69.
♦ Belsky JL, Hamer JS, Hubert JE, Insogna K, Johns W.
Torus palatinus: a new anatomical correlation with
bone density in postmenopausal women. J Clin
Endocrinol Metab 2003;88: 2081e6.
♦ Benedicto Egbert Corrˆea de Toledo, ElianeMarc¸on
Barroso, Alex TadeuMartins, and Elizangela Partata
Zuza. Prevalence of Periodontal Bone Loss in Brazilian
Adolescents through Interproximal Radiography.
International Journal of Dentistry Volume 2012,
Article ID 357056, 5 pages
♦ Cagirankaya LB, Kansu O, Hatipoglu MG. Is torus
palatinus a feature of a well-developed maxilla? Clin
Anat 2004;17: 623e5.
♦ Cantley MD, Bartold PM, Marino V, Fairlie DP, Le GT,
Lucke AJ, Haynes DR. Histone deacetylase inhibitors
and periodontal bone loss. J Periodont Res 2011; 46:
697–703. 2011 John Wiley & Sons A/S
Periodontics & Oral Implantology
Bone Loss and Patterns of Bone Destruction
♦ Carranza, Newman. Clinical Periodontology. 8th edi.
Philadelphia, PA.WB Saunders Co., 1996.
♦ D.T. Graves1, J. Li, and D.L. Cochran. Inflammation and
Uncoupling as Mechanisms of Periodontal Bone Loss.
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♦ De Faria Vasconcelos K, Evangelista K, Rodrigues
C, Estrela C, de Sousa T, Silva M. Detection of
periodontal bone loss using cone beam CT and
intraoral radiography. Dentomaxillofacial Radiology
2012; 41(1):64-69.
♦ Demetries Z, Maria B, Panayiotis P. Concurrence of
torus palatines with palatal and buccal exostoses:
case report and review of the literature. Oral Surg
Oral Med Oral Pathol Oral Radiol Endod 1998;85:
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♦ Eggen S, Natvig B, Gasemyr J. Variation in torus
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♦ Glossary of Periodontal Terms, 4th Edn, The American
Academy of Periodontology, 2001
♦ Gorsky M, Bukai A, Shohat M. Genetic influence on
the prevalence of torus palatinus. Am J Med Genet
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♦ Hassan KS, Alagl AS, Abdel-Hady A.: Torus
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♦ Haugen LK. Palatine and mandibular tori. A
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♦ King DR, Moore GE. The prevalence of torus palatinus.
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Etiopathogenesis of periodontal diseases
♦ Manson JD. Bone morphology and bone loss in
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♦ Neville BW, Damm DD, Allen CM, Bouqout JE,
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♦ Newman et al, Carranza’s Clinical Periodontology,
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♦ Page RC, Schroeder HE. Periodontitis in man and
other animals. A comparative review. Basel: Karger,
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♦ PAPAPANOU PN, TONETTI MS. Diagnosis and
epidemiology of periodontal osseous lesions.
Periodontology 2000,Vol. 22, 2000, 8–21
♦ Regezi JA, Sciubba JJ. Oral pathology: clinical–
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Co.; 1989. p. 386–387.
♦ Reichart PA, Neuhaus F, Sookasem M. Prevalence of
torus palatinus and torus mandibularis in Germans
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♦ Sapp JP, Eversole LR, Wysocki GP, editors.
Contemporary oral and maxillofacial pathology. St.
Louis: Mosby; 1997 . p.106–7.
♦ Sisman Y, Gokce C, Tarim Ertas E, Sipahioglu M,
Akgunlu F. Investigation of elongated styloid process
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♦ SismanY, Tarim Ertas E, Gokce C,Akgunlu F. Prevalence
of torus palatinus in Cappadocia region population in
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♦ Şişman Y., Gökçe C., Sipahiolu M.H., Tarım Ertaş E.,
Ünal A., Oymak O., Utaş C., “Torus Palatinus In End-
Stage Renal Disease Patients Receiving Peritoneal
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♦ Tran KT, Shannon M. Images in clinical medicine: torus
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♦ Yildiz E, Deniz M, Ceyhan O. Prevalence of torus
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