Necrosis and degeneration

© Ramaiah University of Applied Sciences
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Faculty of Dental Sciences

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Necrosis and Degeneration
Presented by
Minnu Joe Ida
Dept of Periodontics
Guided by
Dr. Bhavya
Dept of Periodontics

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CONTENTS
• INTRODUCTION
• CAUSES OF CELL INJURY
• MECHANISMS OF CELL INJURY
• DEGENERATION
– Causes of impaired energy production
– Effects of defective energy production
– Ultrastructural changes of degeneration
– Patterns of degeneration
• NECROSIS
– Morphology
– Electron microscopy
– Types
• NECROTISING PERIODONTAL DISEASES
– NUG, NUP, NS
• RECENT STUDIES
• CONCLUSION
• REFERRENCES

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What happens when a cell under
homeostasis undergo stress ?

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Faculty of Dental Sciences©M. S. Ramaiah University of Applied Sciences
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Causes Of Cell Injury
Genetic
•Developmental defects
•Cytogenetic(karyotypic) defects
•Single gene defects
•Multifactorial inheritance disorders

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Acquired- due to alteration in the external environment
of cells by many injurious agents such as
1. Hypoxia and Ischemia
2. Physical agents
3. Chemical agents and drugs
4. Microbial agents
5. Immunologic reactions
6. Nutritional derangements
7. Aging
8. Iatrogenic factors

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Mechanisms of cell injury

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Irreversibilty
1. The inability to
correct mitochondrial
dysfunction
2. Profound
disturbances in
membrane function

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Causes of Impaired energy
production
HYPOGLYCEMIA HYPOXIA
ENZYME
INHIBITION
UNCOUPLING OF
OXIDATIVE
PHOSPHORYLATION

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Effects of defective energy production
Intra cellular
accumulation
of water and
electrolysis
Changes in
organelles
Anaerobic
metabolism

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Reversible injury / Degeneration:
Definition :
• The gradual deterioration of specific
tissues, cells, or organs with impairment or loss
of function, caused by injury, disease or aging.
or
• the accumulation of metabolites or other
substances in a cell damaged by preceding
injury.

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Ultra structural changes of reversible injury

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Morphologic patterns of reversible
injury
• Cellular swelling
• Fatty change
• Hyaline change
• Amyloidosis
• Pathologic calcification
– Dystrophic calcification
– Metastatic calcification

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Cellular swelling

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•Leukoedema
•Lichen planus

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Fatty change
(steatosis)

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Hyaline change
•Extracellular
•Intracellular

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Amyloidosis

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Congo red
staining
Amyloid : pink to red
Nucleus: blue
In Polarizing Microscope:
Red to green bifringence

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Pathologic calcification
• Deposition of calcium salts, together with
smaller amounts of Mg, Fe and other mineral
salts is called pathologic calcification.
1. Dystrophic calcification
2. Metastatic calcification

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Dystrophic
calcification
Of aortic valves
Periapical and Pulpal pathosis

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Metastatic
calcification
Gross pathology and
histology of lung of a
Pt with high serum
calcium level
(hypercalcemia)

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NECROSIS
• Definition
It refers to the death of a
group of contiguous cells
within a living tissue or
organ, followed by
morphological changes
within the cell that affect
both the nucleus and
cytoplasm.

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Morphology of necrosis
• The changes that involve
the necrotic cell are :
a) Increase in the
eosinophilia.
b) more glassy &
homogenous appearance.
c) The cytoplasm becomes
vacoulated.

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• discontinuities in plasma and
organelle membranes.
• marked dilation of
mitochondria
• disruption of lysosomes
• intracytoplasmic myelin
figures
• profound nuclear changes
By electron microscopy

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Nuclear changes

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Types of Necrosis
Coagulative necrosis
Liquefactive necrosis
Caseous necrosis
Fat necrosis
Fibrinoid necrosis

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Coagulative necrosis
• basic tissue architecture is
preserved for atleast
several days.
• The foci - pale, firm and
slightly swollen
• more yellowish, softer and
shrunken
• Denaturation of structural
proteins and enzymes
• infarcts of solid organs
except the brain

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Histology of renal infarct
Eosinophilic
cytoplasm

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Liquefactive necrosis
• bacterial / fungal
infections
• autolysis or
heterolysis
predominates
protein denaturation
• cerebral infarcts
Focus of liquefactive necrosis in
liver

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• The necrotic liquid -pus.
• Cyst
• gliosis -brain
• proliferating fibroblasts
abscess cavity.
Liquefactic necrosis
of the brain
Cerebral infarction
leading to
encephalomalacia

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Caseous necrosis
• foci of tuberculous
infection
• caseous - friable
yellow white
appearance of the
area of necrosis.

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Pulmonary TB – Caseous necrosis

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Fat necrosis
• Breast
• Omental and
Mesentric fat in
cases of acute
hemorrhagic
pancreatitis.

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The areas of chalky white deposits represent foci of fat necrosis with
calcium soap formation (saponification) at sites of lipid breakdown in
the mesentry.
Fat necrosis in acute pancreatitis

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Fibrinoid necrosis
• Immune
reactions
involving blood
vessels.
• Ag –Ab
complexes are
deposited in the
walls of arteries.
• Fibrinoid (fibrin-
like).

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Pathological changes associated with
necrosis
• Acute inflammation with
neutrophils infiltration
• Healing by regeneration or
organization
• Calcification
• Gangrene of necrotic tissue if it
is infected by putrefactive
organisms

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Fate of necrotic tissue
Acute
inflammation
subsides
Macrophages,
lymphocytes &
plasma cells
Formation of
granulation
tissue
Heterolysis/
Autolysis
Phagocytosis
Collagen
formation
Scar formation

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Necrotising Periodontal Diseases
• Necrotising Ulcerative
Gingivitis (NUG)
• Necrotising Ulcerative
Periodontitis (NUP)
• Necrotising Stomatitis
(NS)
• Various stages of
same disease process
( Horning & Cohen
1995 )

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Nomenclature
Ulceromembranous gingivitis
Trench mouth ( Pickard 1973,Johnson & Engel 1986, Horning &
Cohen 1995)
Phagedenic ginigvitis
fusospirillosis
Fusospirochetal periodontitis
Vincent’s gingivostomatitis

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Clinical features
 NUG
• Ulcerated necrotic papilla
• Interproximal craters
• Linear erythema
• Pseudomembranous slough
• Spontaneous gingival
hemorrhage
• Halitosis

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NUP
• Involves PDL, alveolar
bone
• Loss of attachment
• Sequestrum formation.
May involve facial
cortical bone

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NS
• beyond MGJ
• Immunocompromised
individuals
• Hiv seropositive &
malnuorished
• Severe suppression of
CD4 cells
• Oro-antral fistula and
osteitis
• Similar to cancrum
oris (Noma).

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Clinical course of the disease by Pindborg et al
Erosion of Tip of interdental papilla
Marginal gingiva
Attached gingiva
Bone exposure

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Stages of oral necrotising disease by
Horning & Cohen
Stage 1
• Necrosis of tip of interdental papilla
Stage 2
• Necrosis of entire papilla
Stage 3
• Necrosis extending to gingival margin
Stage 4
• Necrosis extending to attached gingiva
Stage 5
• Necrosis extending to labial and buccal mucosa
Stage 6
• Necrosis exposing alveolar bone
Stage 7
• Necrosis perforating skin of cheek

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Etiology
• Plaut & Vincent : fusiform bacillus & spirochetal organism
• Loesche et al : P.intermedia,treponema sp., selenomonas sp. &
fosubacterium sp.
• Chung et al : increased antibody titres for spirochetes &
P.intermedia in NUG Pts.
• Spirochetes and fusobacteria - epithelium (Heylings 1967)
• endotoxins (Kristoffersen et al 1970)
• Spirochetes - connective tissue (Listgarten 1965)
Role of microorganism
• NUG not found in well nourished individuals with fully functioning
immune system
• immuno suppression
• Cohen et al : marked depression in PMNL chemotaxis and
phagocytosis
Role of host response

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• Poor oral hygiene
• Pre existing gingivitis
• Smoking : Pindborg et al : 98% of his patients with NUG
were smokers that the frequency of disease increases with
increased exposure to smoking
• Injury to gingiva
Local predisposing factor
• Malnutrition
• Immunodeficiency
• Debilitating diseases : AIDS, syphilis, anemia, leukemia,
ulcerative colitis, blood dyscrasias
• Psychological stress and sleep deprivation
• Alcohol & drug abuse
Systemic predisposing factors

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Diagnosis
• Based on clinical findings
• Bacterial studies are useful in differential diagnosis
Treatment
• Antibiotic therapy : metronidazole 250mg TID (Loesche
et al 1982) reduces acute pain and promotes rapid
healing (Scully et al)
• H2O2 (3%) is used for debridement in necrotic areas
and also used as mouth rinse
[1:1 - H2O2 (3%) and warm water]

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Pulp necrosis and Periodontitis
Necrosis
of pulp
Bone
resorption
Periodontal
lesions
abscess
Cyst/granuloma
Lateral/accessory
canal lesion

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Endodontic Rx complications –
periodontal defects
Perforations
Resorption
• Internal
• External
Vertical root fractures

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Pontes et al
• accidental injection of sodium hypochlorite into the
lingual gingiva of a female patient - gingival and bone
necrosis

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OsteoNecrosis of Jaw (ONJ) in patients
treated with bisphosphonates (BPNs)
Suppression of bone
turn over
Infection
Tissue hypoxia Cellular toxicity
MOA of BPNs

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Perrotta et al , 2010
• Hyperactive osteoclastic bone resorption
• Direct cytotoxic effect of BPNs on bone tissue
• Induction of osteocyte cell death
Brooks et al, 2015
• BPNs related osteonecrosis of hard palate after the
harvesting of a subepithelial connective tissue graft for
treatment of ginigval recession in the mandible
• Medical history of BPNs

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Degenerative periodontal diseases and
oral osteonecrosis
Baldi et al , 2008
• Chronic degenerative dentistry diseases including
periodontal diseases and oral osteonecrosis ---
environmental genotoxic risk factors and genetics of
individual
• genes encoding metalloproteinases (periodontal tissue
remodelling and degradation), cytokines(inflammation),
prothrombin and DNA repair activities

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Orthodontic forces and periodontal
ligament degeneration
Vinod Krishnan et al, 2006
• Cellular, molecular and tissue level reactions to
orthodontic forces
• orthodontic forces induce remodelling of PDL and
gingival connective tissue matrices
Rygh & Brudvick
• great increase in vascularity in areas of PDL tension.
• beyond a certain level of stress, the vascular supply to
the PDL decreases, with cell death occuring between
stretched fibres

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 Pressure side - narrowing of PDL space & deformation of
the alveolar crest bone .
 Light pressure - direct bone resorption
 Heavy forces - hyalinisation
 Tissue changes in compressed PDL –
– edema
– gradual obliteration of blood vessels
– breakdown of the walls of veins
– leakage of blood constituents into the extravascular space
Orthodontic forces and periodontal
ligament degeneretion

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Orthodontic forces and periodontal ligament
degeneretion
• Fibroblasts
– Moderate swelling of ER
– Formation of vacuoles
– Rupture & loss of cytoplasm
Attal et al
• periodontal vasculature showed similar changes in
pressure and tension areas
• large diameter vessels are unaffected by mechanical
loading

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Lowney et al
• quantity of paradental TNF , found in human gingival
sulcus , is elevated during tooth movement

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Bruxism and Periodontium

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Bruxism and Periodontium
When inflammation
extends to
supporting
periodontal tissues,
plaque induced
inflammation enters
the zone influenced
by occlusion which
Glickman has
called as zone of
co-destruction

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Macapanpan and Weinmann, 1954
Reported that
excessive pressure and
tension produce
alterations in PDL
Inflammation is passed
to the altered area and
resulted in necrosis of
periodontium.
This necrotic tissue
would act as a barrier
preventing
inflammation from
extending in to
underlying periodontal
tissues.
Postulated that when
inflammation spreads
beyond marginal
gingiva and when
combined with occlusal
trauma , they become
interrelated co-
destructive factors in
periodontitis

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Free gingival graft and necrosis
Lopez et al,2013
• very thin graft has great chances of necrosis and
exposure of the receptor area
• However, if the graft is very thick, its superficial layer
may be at risk, since the excess of tissue will hinder an
adequate nutrition
Mormann et al 1981
• rapid revascularization can be expected when uniform
grafts of thin to intermediate thickness. An uneven, thick
graft placed on a site of denuded bone favored a
prolonged period of revascularization and delayed
healing

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Tissue damages caused by lasers
•Result from the thermal
interaction of radiant energy
with tissue proteins
•Temperature elevations  cell
destruction by denaturation of
cellular enzymes and structural
proteins
•Additionally, exposures of 1 sec or greater can
interfere with vascular perfusion
•Laser- induced tissue injury  dependant on extent of
absorption of incident radiation by tissue

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•It is important, therefore, to recognise the factors that
may influence the extent of laser- tissue interaction
-Relative amount of absorption, transmission &
scatter of particular wavelength
-Pulse duration and pulse repetition rate
-Level of radiant exposure (energy density or
exposure dose)
-Relative degree of vascularity of the tissue

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CONCLUSION
Knowledge of the etiology, mechanism and process of cell
injury and necrosis can help in prevention and better
management of the same.
A dentist should therefore be familiar with the signs and
symptoms of necrotizing periodontal diseases, of their potential
sequelae and of the need for immediate therapeutic
intervention.
Also care should be taken to avoid iatrogenic cell injuries which
have been discussed.

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References
• Pathologic basis of diseases 8th ed –Robbins & Cotran
• Textbook of Pathology 5th ed Harsh Mohan
• Boyd’s textbook of pathology 9th ed Vol II A.C.Ritchie
• Carranza’s clinical periodontology 11th ed Newman et al
• Clinical periodontology and imlpant dentistry 4th ed Jan Lindhe
• Khammissa, R.A.G., Ciya, R., Munzhelele, T., Altini, M., Rikhotso, Ε. and
Lemmer, J., 2014. Oral medicine case book 65: Necrotising stomatitis. South
African Dental Journal, 69(10), pp.468-470.Mcculloch, C.A., Lekic, P. and
Mckee, M.D., 2000. Role of physical forces in regulating the form and
function of the periodontal ligament. Periodontology 2000, 24(1), pp.56-72.
• Krishnan, V. and Davidovitch, Z.E., 2006. Cellular, molecular, and tissue-level
reactions to orthodontic force. American Journal of Orthodontics and
Dentofacial Orthopedics, 129(4), pp.469-e1.

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• Lowney, J.J., Norton, L.A., Shafer, D.M. and Rossomando, E.F., 1995.
Orthodontic forces increase tumor necrosis factor α in the human gingival
sulcus. American Journal of Orthodontics and Dentofacial
Orthopedics, 108(5), pp.519-524.
• Perrotta, I., Cristofaro, M.G., Amantea, M., Russo, E., De Fazio, S., Zuccalà,
V., Conforti, F., Amorosi, A., Donato, G., Tripepi, S. and Giudice, M., 2010.
Jaw osteonecrosis in patients treated with bisphosphonates: an
ultrastructural study. Ultrastructural pathology, 34(4), pp.207-213.
• Izzotti, A., Menini, M., Pulliero, A., Dini, G., Cartiglia, C., Pera, P. and Baldi,
D., 2013. Biphosphonates-associated osteonecrosis of the jaw: the role of
gene-environment interaction. Journal of preventive medicine and
hygiene, 54(3), p.138.
• Baldi, D., Izzotti, A., Bonica, P., Pera, P. and Pulliero, A., 2009. Degenerative
periodontal-diseases and oral osteonecrosis: the role of gene-environment
interactions. Mutation Research/Fundamental and Molecular Mechanisms of
Mutagenesis, 667(1), pp.118-131.

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• Lavigne, G.J., Khoury, S., Abe, S., Yamaguchi, T. and Raphael, K., 2008.
Bruxism physiology and pathology: an overview for clinicians. Journal of
oral rehabilitation, 35(7), pp.476-494.
• Brooks, J.K., Kleinman, J.W., Younis, R.H. and Reynolds, M.A., 2015.
Alendronate-Associated Osteonecrosis of the Hard Palate After Harvesting of
a Connective Tissue Graft: A Case Report. Clinical Advances in
Periodontics, 5(3), pp.171-177.
• Mörmann, W., Schaer, F. and Firestone, A.R., 1981. The Relationship
Between Success of Free Gingival Grafts and Transplant Thickness:
Revascularization and Shrinkage—A One Year Clinical Study. Journal of
Periodontology, 52(2), pp.74-80.
• Macapanpan, L.C. and Weinmann, J.P., 1954. The influence of injury to the
periodontal membrane on the spread of gingival inflammation. Journal of
dental research, 33(2), pp.263-272.

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