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The coagulation system, or clotting cascade, converts soluble fibrinogen into fibrin, creating a
protective protein mesh at the injury site. Coagulation factor XII (Hageman factor) activates the
coagulation, kinin and fibrinolytic systems.
The fibrinolytic system opposes the coagulation system, balances clotting and produces
many inflammatory mediators. Fibrinolysis by plasmin may have a local effect on vascular
permeability.
12.6 Pro-inflammatoryCytokines
Cytokines are a vast and diverse group of pro- or anti- inflammatory proteins grouped into families based on their structural homology or receptors(4). Cytokines are key modulators of inflammation (pro- inflammatory cytokines) produced in response to invading pathogens.
Pro- inflammatory cytokines are secreted from T helper (Th1) cells, CD4+ cells, macrophages
and dendritic cells. They generally regulate the growth, cell activation and differentiation and
attract immune cells to the sites of infection to control and eradicate intracellular pathogens.
Cytokines are responsible for the production of several Interleukins (IL), tumour necrosis factor
(IFN- γ and TNF- α) and chemokines (CXC, CC, CX3C and XC).
12.6.1 Interleukins
IL- 1, IL- 6 and TNF- α are key pro- inflammatory cytokines:
● IL- 1 is a potent pro- inflammatory cytokine. It is induced mainly by lymphocytes, macrophages
and monocytes responding to microbial molecules(4).
● IL- 6 is a cytokine that affects the immune system. It acts in other biological systems and many
physiological events, including regulating cell growth and gene activation, proliferation, survival
and differentiation. Monocytes, fibroblasts and endothelial cells produce IL- 6. Many additional
cell types (mast cells, macrophages, T cells, B cells, glial cells, eosinophils, keratinocytes and
granulocytes) secrete IL- 6 upon stimulation. IL- 6 is essential in inducing B cells to differentiate
into antibody- forming cells (plasma cells)(4).
12.6.2 TumourNecrosisFactor-α(TNF-α)
Like other pro- inflammatory cytokines, TNF- α is vital in the inflammatory response locally and in
the circulation. TNF- α triggers the expression of vascular endothelial cells, resulting in the
enhancement of the leucocyte adhesion molecules. These molecules stimulate immune cell infiltration and participate in the early response against viral infection by improving the infiltration of
lymphocytes to the site of infection(4).
12.6.3 Chemokines
Chemokines are cytokines with chemotactic activities. They are classified into four main
subfamilies: CXC, CC, CX3C and XC chemokines, which play a crucial role in regulating the
movement and localisation of lymphocytes. The CXC chemokines recruit immune cells
to the site of inflammation, whereas the homeostatic chemokines mediate homeostatic
migration and homing of lymphocytes. However, some chemokines can be inflammatory and
anti- inflammatory(4).
t.me/Dr_Mouayyad_AlbtousH
12.7 CardinalSignsofInflammation
Cardinal signs of inflammation include (i) Tumour (swelling), (ii) Dolor (pain), (iii) Rubor (redness),
(iv) Calor (heat) and (v) Functio laesa (loss of function). These are often observed in acute inflammation.
● Tumor (swelling) is caused by the gradual accumulation of fluid (oedema) outside the blood
vessels.
● Dolor (Pain) is due to the mechanical action of tissue tension and pressure on nerve endings or
direct response to prostaglandin, serotonin and bradykinin reactions.
● Rubor (redness) is due to vasodilation of the damaged area.
● Calor (Heat) is due to hyperaemia, increased metabolic activity and pro- inflammatory media-
tors that increase local temperature.
● Functio laesa (loss of function) is due to pain and oedema. These are cardinal signs of inflam-
mation, often observed in acute inflammation.
Common clinical responses during systemic inflammation include altered body temperature
(fever), elevated pulse rate, elevated respiratory rate and abnormal white blood cell count.
Other, mostly non- specific symptoms of inflammation include fatigue, weakness, loss of appetite and exhaustion. These symptoms are believed to be related to the action of mediators of inflammation such as IL- 1 or TNF. These are known as acute- phase reactants.
12.8 ClassificationofInflammation
181
Inflammation can be acute, subacute or chronic(5–7).
● Acute inflammation is of sudden onset and short duration.
● Chronic inflammation is of prolonged duration. These two types of inflammation also differ
in the kind of cells involved in the inflammatory process.
● Subacute inflammation is a state between acute and chronic inflammation and has some
characteristics of each.
● Granulomatous inflammation is a particular type of infection in chronic infectious diseases
such as tuberculosis, leprosy and syphilis. Foreign- body granuloma is an example of granuloma-
tous inflammation caused by a foreign body. Granulomatous inflammation is characterised by
the formation of granulomas consisting of localised microscopic collections of macrophages,
epithelioid cells and multinucleated giant cells. A brief description of these types of inflamma-
tion is given below.
12.8.1 Acute Inflammation
Acute inflammation is an immediate and initial response to an injurious agent(5–7). This usually
lasts for a short period, minutes, hours or days, depending on the severity of the injury. Acute
inflammation is typically non- specific. It is characterised by the release of fluid and plasma proteins and the arrival of white blood cells, starting with neutrophils and later macrophages, at the
injury site.
Acute inflammation is categorised into two primary responses: early vascular (microcirculatory)
and late cellular responses.
t.me/Dr_Mouayyad_AlbtousH
(a) (b)
182
12.8.1.1 EarlyVascularResponse
Sudden and temporary vasoconstriction is the first change in microcirculation(5–7). This response
is due to neurogenic or chemical stimulation. This early vascular response is followed by marked
dilatation of the arterioles, capillaries and venules. Initial vasodilation causes increased blood flow
to the area, a phenomenon called hyperemia. After hyperemia, vascular permeability in the postcapillary veins increases, leading to increased accumulation of protein- rich fluid in soft tissues
(exudate/oedema). As a result, the existing dilated blood vessels are now filled with red blood cells,
leading to slow blood circulation and stasis (Figure12.1a,b). In acute inflammation, chemical
mediators mediate vascular events.
12.8.1.2 LateCellularResponse
Usually, blood cells, especially erythrocytes in venules, are found in the central (axial) zone, while
plasma is found in the peripheral zone(5–7). In acute inflammation, due to increased vascular
permeability (as discussed in the Vascular Events section above), many neutrophils migrate and
congregate in the peripheral zone of the endothelium. The key cells in the acute inflammatory
response are PMN. They are attracted to the site of injury by the action of chemical mediators. The
cellular response includes the following steps:
● Stage 1. Margination, rolling, pavementings and adhesion of leukocytes
● Stage 2. Transmigration of leukocytes
● Stage 3. Chemotaxis
● Stage 4. Phagocytosis
12.8.1.2.1 Stage1
● Margination: In normal circulation, cells are confined to the blood vessels central (axial) flow.
When inflammation occurs, blood flow slows due to fluid loss in blood vessels and increased
plasma viscosity. Consequently, neutrophils flock into the plasmatic zone. This process results in
a peripheral localisation of white blood cells (mainly neutrophils) along the vascular endothelial
cells(5–7).
Figure12.1 Acute inflammation showing polymorphonuclear cell infiltrate and engorged vessels.
Courtesy of Professor D F Wilson, Adelaide, Australia.
t.me/Dr_Mouayyad_AlbtousH
● Rolling: Rows of white blood cells come into contact with the endothelium through rolling. The
purpose of rolling and slow rolling is to bring the leukocytes into contact with the endothelial
cells so chemokines and other pro- inflammatory agents can further activate them on the
endothelial cells(5–7).
● Pavementing: In normal circulation, neutrophils randomly contact the endothelial lining but do
not adhere to it. In acute inflammation, neutrophils line endothelial cells, which is called pave-
menting. This phenomenon explicitly occurs in venules(5–7).
● Adhesion: The next event is white blood cells’ binding (adhesion) to endothelial cells. Cell adhe-
sion molecules (CAMs) such as selectins, immunoglobulins and integrins support this phenom-
enon, which causes leukocytes to adhere to endothelial cells(5–7).
12.8.1.2.2 Stage 2
12.8.1.2.2.1 TransendothelialMigrationofLeukocytes
Transendothelial migration (TEM) is
the process whereby the leukocytes squeeze in an ameboid fashion across the endothelial
cells(5–7). The active ameboid movement of leukocytes occurs by extending pseudopodia
through the gap between endothelial cells and then through the basal lamina (basement
membrane) into the vessel wall. This process is called diapedesis. The most important mechanism of leukocyte emigration is the widening of interendothelial junctions after endothelial
cell contractions. The basement membrane is disrupted and resealed immediately after
this event.
183
12.8.1.2.3 Stage 3
12.8.1.2.3.1 Chemotaxis of Neutrophils
Chemotaxis is when an extracellular gradient of
chemicals determines the direction of a cell’s locomotion. Newly extravasated leukocytes
migrate to the injury site along soluble chemical mediators’ gradients (Chemotactic factors).
This process is known as chemotaxis. Some chemotactic factors are secreted by host cells at or
near the injury site, while others may be microbial components. The most critical chemotactic
factors for neutrophils are complement system components (C5a), bacterial mitochondria and
leukotriene B4 (products of arachidonic acid metabolism) and cytokines (IL- 8). All granulocytes, monocytes and lymphocytes (to a lesser extent) respond to chemotactic stimuli. Receptors
on the cell membranes of leukocytes react with the chemoattractants, activating phospholipase
C that ultimately releases cytosolic calcium ions, which trigger cell movement towards the
stimulus(5–7).
12.8.1.2.4 Stage 4
Phagocytosis: Phagocytosis is the process of engulfment and internalisation by specialised cells of
particulate material, which includes invading microorganisms, damaged cells and tissue debris
(Figure 6.2). These phagocytic cells include polymorphonuclear leukocytes (mainly neutrophils), monocytes and tissue- resident macrophages(5–7).
Recognition and Attachment: Phagocytosis is enhanced if the material to be phagocytosed is coated
with specific plasma proteins called opsonins. These opsonins promote the adhesion between
the particulate material and the phagocyte’s cell membrane. The three significant opsonins are
the Fc fragment of the immunoglobulin, components of the complement system C3b and C3bi,
and the carbohydrate- binding proteins–lectins. Thus, IgG binds to receptors for the Fc piece of
the immunoglobulin (FcR), whereas 3cb and 3bi are ligands for complement receptors CR1 and
CR2, respectively(5–7).
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184
Engulfment: Once recognised by a neutrophil or macrophage, a foreign particle is engulfed by the
phagocytic cell to form a membrane- bound vacuole called a phagosome, which fuses with
lysosomes to create a phagolysosome(5–7).
Killing or Degradation: The ultimate step in phagocytosis is killing and degradation. There are two
forms of bacterial killing: oxygen- independent and oxygen- dependent mechanisms.
● Oxygen- independent Mechanism: This is mediated by the constituents of the primary
and secondary granules of polymorphonuclear leukocytes. These include Bactericidal
permeability- increasing (BPI) proteins, lysozymes, lactoferrin and major essential protein
(MBP). The lysosomal enzymes are necessary for degrading dead organisms within
phagosomes(5–7).
● Oxygen- dependent Mechanism: The formation of reactive oxygen species (ROS) is involved in
the killing of oxygen- dependent killing of bacteria. These include hydrogen peroxide (H
superoxide (O
) and hydroxyl ion (HO−). These react with molecules in the cell membrane or
2
nucleus to cause damage. There are two types of oxygen- dependent killing mechanisms:
non- myeloperoxidase- dependent and myeloperoxidase- dependent(5–7).
– Non- myeloperoxidase- dependent Mechanism: The formation of ROS is involved in killing
oxygen- dependent microorganisms. These species include hydrogen peroxide (H
superoxide (O
) and hydroxyl ion (OH−). These species react with molecules in the cell
2
membrane or nucleus to cause damage(5–7).
– Myeloperoxidase- dependent Mechanism: The bactericidal activity of H
lysosomal enzyme myeloperoxidase, which converts H
the presence of halide ions. This H
–halide–myeloperoxidase system is neutrophils’
2O2
to hypochlorous acid (HOCI) in
2O2
involves the
2O2
most efficient bactericidal system. A similar mechanism is also effective against fungi,
viruses, protozoa and helminths(5–7).
2O2
2O2
),
),
12.8.2 SubacuteInflammation
Subacute inflammation is a state between acute and chronic inflammation that has some characteristics of each. It may last a few days and is less symptomatic than acute inflammation.
Microscopically, subacute inflammation comprises a mixture of acute and chronic inflammatory
cell infiltrate (Figure12.2).
12.8.3 ChronicInflammation
● Chronic inflammation is characterised by a prolonged duration, usually spanning weeks,
months or years. In chronic inflammation, tissue injury, active inflammation and the
Figure12.2 Subacute inflammatory
response in granulation tissue
showing mixed acute and chronic
inflammatory cell infiltrate.
Courtesy of Professor D F Wilson,
Adelaide, Australia.
t.me/Dr_Mouayyad_AlbtousH
Figure12.3 Chronic inflammation
shows mixed lymphocytic and plasma
cell infiltration. Courtesy of
Professor D F Wilson, Adelaide,
Australia.
healing processes proceed simultaneously, and the predominant cell types involved include
mononuclear cells, macrophages, lymphocytes and plasma cells (Figure12.3). Products of
inflammatory cells cause tissue destruction, and the reparative process involves angiogenesis and fibrosis(5–7).
● Chronic inflammation can result from several causes, namely (i) failure to eliminate the agent
causing acute inflammation, (ii) exposure to a low- level irritant or foreign material that cannot
be eliminated by enzymatic breakdown or phagocytosis, (iii) an autoimmune disorder, (iv)
adefect in the inflammation mediating cells (v) recurrent episodes of acute inflammation and
(vi) inflammatory and biochemical inducers are causing oxidative stress and mitochondrial
dysfunction(5–7).
● Acute inflammation may progress to chronic inflammation when the injurious agent persists or
the normal healing process is interfered with. Some chronic inflammatory conditions may occur
from the onset without the preceding acute phase. The main features of chronic inflammation
include infiltration of macrophages, lymphocytes and plasma cells at the site of injury. These
cells produce inflammatory cytokines, growth factors and enzymes contributing to the progression of tissue damage and secondary repair, including fibrosis, and in some infections, granuloma formation(5–7).
185
12.8.4 TypesofChronicInflammation
● Non- specific Proliferative: This condition is characterised by non- specific granulation tissue.
Microscopically, granulation tissue comprises the infiltration of mononuclear cells (lymphocytes, macrophages, plasma cells) and the proliferation of fibroblasts, connective tissue, vessels
and epithelial cells. Examples are inflammatory polyp- like nasal polyps, lung abscesses and pyogenic granuloma (Angiogranuloma) of the gingivae(6, 7).
● Granulomatous Inflammation: Granulomatous inflammation is a specific type of chronic
inflammation characterised by the formation of granulomas. These lesions are usually nodular and formed with the aggregation of activated macrophages or epithelioid cells, which
are usually surrounded by lymphocytes. The granuloma macrophages often coalesce to form
multinucleated giant cells (Langhans cells in tuberculosis or foreign- body giant cells)
(Figure12.4). There are two types of granulomas: Foreign- body granuloma (e.g. silicosis
related) or granuloma due to T- cell mediated immune response, for example, tuberculosis
and leprosy(6, 7).
t.me/Dr_Mouayyad_AlbtousH
186
Figure12.4 Foreign- body
granuloma. Distinct foreign- body
material is seen within a background
of inflamed fibrous connective tissue
and multinucleate giant cells (arrows).
Courtesy of Professor
D F Wilson, Adelaide, Australia.
12.9 MorphologicPatternsofInflammation
● Fibrinous Inflammation:Fibrinous Inflammation is a general morphological pattern of acute or
chronic inflammation. There is extensive fluid leakage from the vasculature, thus allowing for
the passage of large plasma proteins, mainly fibrinogen, into tissue. This is commonly seen
in bacterial infections such as streptococcal infection of the throat, bacterial pericarditis and
bacterial pneumonia. Ultimately, the organisation of the fibrinogen can occur when rigid
fibrous tissue is laid down. Fibrinous inflammation should be differentiated from serous
inflammation(6, 7).
● Suppurative (purulent) Inflammation:Suppurative Inflammation is a general morphological pat-
tern of acute or chronic inflammation. Inflammation results in a large amount of pus, which
consists of neutrophils, dead cells and fluid. Infection by pyogenic bacteria such as staphylococci
is characteristic of purulent inflammation. Abscesses are characterised by a localised collection
of pus enclosed by surrounding tissues(6, 7).
● Serous Inflammation:Serous Inflammation is a general morphological pattern of acute or chronic
inflammation. It is characterised by exudating serum generated from mildly leaky vasculature or
synthesised by mesothelial cells. Examples include pneumonia, skin blisters caused by herpes
virus infections or burns, serous pericarditis, pleuritis and joint fluid in rheumatoid arthritis(6, 7).
● Ulcerative Inflammation: Inflammation occurring on an epithelial surface (skin or mucosa) can
result in the necrotic loss of tissue, exposing deeper layers. Examples include gastric or duodenal ulcers. An ulcer is a general morphological pattern of acute or chronic inflammation(6, 7).
● Catarrhal inflammation is a form affecting mainly mucosal surfaces, marked by a non-
suppurative, copious discharge of mucous and epithelial debris. Examples include acute rhinitis
and catarrhal bronchitis(6, 7).
● Pseudomembranous inflammation is a form of ulcerative/exudative inflammation involving
mucous and serous membranes. The exudate of fibrin, pus, cellular debris and mucus forms a
pseudomembrane on the surface of the ulcers. Examples include pseudomembranous colitis
and pseudomembrane in the throat in diphtheria(6, 7).
The formation of granulomas characterises granulomatous inflammation; they result
fromalimited but diverse number of diseases, such as tuberculosis, leprosy, sarcoidosis and
syphilis(6, 7).
t.me/Dr_Mouayyad_AlbtousH
12.10 ClinicalConsiderations:Organ-specificInflammatoryResponses
Inflammatory diseases are designated with the suffix ‘itis’. For example, inflammation of the liver is
called hepatitis, and inflammation of the gums is called gingivitis. There are exceptions, however,
such as pneumonia, typhoid fever and paronychia (nail bed infection due to infection). Inflammation
has long been recognised as a significant cause of disease, including cancer. Some 15% of human
cancers are estimated to be associated with chronic infection and inflammation(8, 9).
Acute and chronic inflammation- mediated tissue injury occurs in several organs, including the
heart, pancreas, liver, kidney, lung, brain, intestinal tract, reproductive system, oral mucosa, jawbones, salivary glands, dental pulp and periodontal tissues.
● Heart: Inflammatory mediators play a role in atherosclerosis. Myocardial infarction, the com-
mon cause of cardiac injury, commonly results from coronary atherosclerosis (10). Necrotic
cardiac cells initiate the inflammatory response to clear dead cells and debris from the infarct
(8, 11, 12).
● Pancreas: Inflammation of the pancreas is called pancreatitis. Some causes of pancreatitis
include pancreatic duct obstruction, trypsinogen gene mutation or alcoholism(8, 13). Prominent
features of pancreatitis are Acinar cell destruction and activation of inflammatory cells (mac-
rophages, neutrophils and granulocytes), which secrete inflammatory cytokines(8, 13).
● Liver: Inflammation in the liver (hepatitis) is a defensive mechanism that protects this organ
from infection and injury. However, excessive inflammation leads to hepatic damage due to
extensive loss of hepatocytes, ischaemia- reperfusion injury and metabolic alterations (8, 14).
Inflammation can destroy hepatic parenchymal cells and increase the risk of chronic liver dis-
eases. Some examples of hepatitis include non- alcoholic fatty liver disease (NAFLD) and viral
hepatitis (Hepatitis B and Hepatitis C hepatitis)(8, 14).
● Lung: A general term used for inflammation of the lung is pneumonitis. Exposure to bacterial
and viral pathogens and environmental pollutants causes respiratory system inflammation.
Excessive acute inflammation can cause pulmonary fibrosis, which causes an impairment in gas
exchange. Some examples of inflammatory pulmonary diseases include bronchitis, bronchial
asthma, bronchiectasis and cystic fibrosis(8, 10, 15).
● Kidney: Kidney inflammation can cause glomerulonephritis, end- stage renal disease, or acute or
chronic kidney disease (CKD)(8, 10). Viral infections, bacterial infections, autoimmune disor-
ders and toxins cause glomerulonephritis.
● Intestinal Tract: Inflammatory bowel disease (IBD) refers to two main inflammatory diseases:
ulcerative colitis (UC) and Crohn’s disease (CD)(8, 16).
● Reproductive System: Physiological reproductive processes, including menstruation, ovulation,
implantation and parturition, are associated with inflammation (8, 17). These can trigger the
inflammatory cascade.
● Brain: Inflammation causes several central nervous system diseases. These include autoimmune
diseases and neurodegenerative diseases such as Alzheimer’s (AD), Parkinson’s disease (PD)
and epilepsy(8, 18, 19).
187
12.11 InflammatoryLesionsoftheOro-facialComplex
The following table (Table12.2) provides definitions and causes of inflammatory lesions of the
oro- facial complex.
t.me/Dr_Mouayyad_AlbtousH
Table12.2 Inflammatory lesions ofthe oro- facial complex.
Downloaded from https://onlinelibrary.wiley.com/doi/ by ibrahim ragab - Oregon Health & Science Univer , Wiley Online Library on [07/10/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
Pulpal,periapical,gingival,
andperiodontal
inflammatory conditions Definition Causes/riskfactors
Pulpitis Inflammation of the dental pulp Caries
Traumatic exposure of the pulp
Fracture of the crown or cusp.
Cracked tooth.
Thermal or chemical irritation
Chronic hyperplastic
pulpitis
Acute apical periodontitis Inflammation of the periodontal ligament surrounding the
Periapical granuloma Formation of granulation tissue surrounding the apex of a
Chronic inflammation of the exposed pulp characterised by an
overgrowth of granulation tissue often covered by epithelium
seen in the open carious (molar) tooth in children
apex of the tooth
non- vital tooth arising in response to pulpal necrosis
Chronic low
Infection, bacterial products, and other irritants
Bacterial invasion from the pulp.
Occlusal trauma from the high spots of restorations.
- grade irritation
Irritants and inflammatory mediators from the necrotic pulp.
Endodontic procedures (iatrogenic)
Dentoalveolar abscess An odontogenic infection is characterised by the localisation
of pus surrounding the roots of involved teeth
Condensing osteitis Focal areas of bone sclerosis associated with apices of teeth. Low
Radicular, lateral radicular
and residual cysts
located at the apex of a non
periapical cyst
Lateral radicular cyst: a radicular type of cyst located at the
lateral surface of a non
Residual radicular cyst: a radicular cyst that has persisted
after extraction of the causative non
- vital tooth, also known as a
- vital tooth
- vital tooth
Secondary to dental caries, trauma or failed root canal treatment.
Bacteria and their toxic products enter the periapical tissues via the apical
foramen and induce acute inflammation and pus formation
- grade inflammatory stimulus from an inflamed dental pulp
Radicular cyst: caused by the proliferation of odontogenic epithelium in a
periapical granuloma due to stimulation derived from chronic
inflammation from non
Lateral radicular cyst is caused by the proliferation of odontogenic
epithelium in the periodontal tissues at the lateral aspect of a non
Stimulation for chronic inflammation is derived from the non
Residual radicular cyst is caused by the proliferation of odontogenic
epithelium in a radicular cyst that has persisted after extraction due to
inadequate curettage.
Cystic expansion in all three types of cysts occurs because of the effects of
osmotic gradient within the epithelial lining layers and mediators of
inflammation
- vital pulp
- vital tooth.
- vital tooth
t.me/Dr_Mouayyad_AlbtousH
0005802307.INDD 188 09-13-2024 17:45:25
Downloaded from https://onlinelibrary.wiley.com/doi/ by ibrahim ragab - Oregon Health & Science Univer , Wiley Online Library on [07/10/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
Acute and chronic
gingivitis
Necrotising periodontal
disease
Plasma cell gingivitis A rare inflammatory condition characterised by dense
- body gingivitis Inflammatory condition of the gingiva associated with the
Foreign
Desquamative gingivitis A descriptive term (not a disease) used for non
Chronic periodontitis Chronic inflammation of the periodontal tissues arising
A reversible gingival inflammatory condition Cause: Bacterial plaque
A spectrum of conditions that affect the periodontium
(gingiva, periodontal ligament and alveolar bone) through
necrosis and ulceration
There are two types of ulcers: necrotising ulcerative
gingivitis and necrotising ulcerative periodontitis.
plasma cell infiltrate in the gingival connective tissue
secondary to hypersensitive reaction
presence of foreign material in the gingival connective
tissues
gingival manifestation characterised by gingival
desquamation, seen clinically as diffuse erythema of the
marginal and keratinised gingiva, associated with different
dermatological and vesiculoerosive diseases
- existing the gingival inflammatory process
from pre
destroying periodontal ligament and resorption of crestal
bone
- specific
Risk factors:
Poor oral hygiene
- breathing
Mouth
during sleep
Xerostomic medications and conditions that cause xerostomia.
Tobacco/smokeless tobacco habits
Stress
Mental health issues such as depression
- existing
Pre
conditions such as diabetes
Pregnancy/puberty
Cause: mixed bacterial flora (Fusobacterium nucleatum, Borrelia vincentii,
Prevotella intermedia, Porphyromonas gingivalis, and Selenomonas
sputigena)
Predisposing factors: Malnutrition, viral infections, immune defects (HIV),
stress, leukaemia, lymphoma, and smoking.
Hypersensitivity to a variety of agents used in chewing gums or toothpaste
Allergens, including mint, cinnamon, cloves, cardamom, red chilli peppers,
khat and pumice used in prophy paste
Dental materials implanted in the gingival connective tissue during dental
procedures (iatrogenic)
Not a cause but a manifestation of mucous membrane pemphigoid,
pemphigus vulgaris, mucous membrane pemphigoid, systemic lupus
erythematosus, lichen planus, linear immunoglobulin A disease, dermatitis
herpetiformis, psoriasis and erythema multiforme
Long
- term persistence of gingivitis (chronic gingivitis)
Predisposing factors: Advancing age, poor oral hygiene, calculus, traumatic
occlusion, poor interdental contact, smoking, diabetes mellitus
(Continued)
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