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Figure11.33 This frozen section stained with haemotoxylin and eosin is another field of the tissue in
Figure11.31. This field shows a subepithelial clefting process of mucous membrane pemphigoid.
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Figure11.34 Direct immunofluorescence study shows linear deposit of IgG at the basement membrane.
and fibrinogen deposits at the basement membrane (Figures11.34– 11.36). The current hypothesis
on the etiopathogenesis of this condition is explained by the epitope spreading theory that the
inflammation and T- cell mediated immune response of lichen planus results in the exposure of
sequestered antigens that further trigger an autoimmune response. Region 4within the C- terminal
of the NC16 A domain of the BP180 antigen is identified as this antigen. IgG reactivity against this
novel epitope results in MMP(13). Oral LPP is a mild immunobullous and erosive condition managed with topical steroids.
11.4.5 Chronic Ulcerative Stomatitis
CUS is an oral mucosal erosive and ulcerative condition that may be clinically misdiagnosed as
erosive lichen planus (Figure11.37). It affects women predominantly. The mean age is 60 years.
While any part of the oral cavity may be affected, gingival erosive lesions are the most common.
Symptoms include pain, soreness, difficulty eating, bleeding and intolerance to acidic and spicy
foodstuffs. Biopsy of non- ulcerated areas shows features of lichen planus such as hyperkeratosis
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172
Figure11.35 Direct immunofluorescence study shows linear deposits of C3 at the basement membrane.
Figure11.36 Direct immunofluorescence study shows shaggy deposits of fibrinogen at the basement
membrane.
Figure11.37 Right buccal mucosa shows erosive and ulcerated lesion of chronic ulcerative stomatitis.
t.me/Dr_Mouayyad_AlbtousH
References
Figure11.38 Direct immunofluorescence study shows deposits of IgG in the nuclei of basal and
suprabasal cells of the epithelium.
with hyperplasia or atrophy, basal cell degeneration, Civatte bodies, sawtooth- like epithelial rete
ridges and a band- like inflammatory cellular infiltrate of the lamina propria. This infiltration
shows plasma cells also. The diagnosis rests on the direct immunofluorescence findings that
include a dot- like deposition of IgG onto the nuclei of basal and suprabasal cells of the epithelium
(Figure11.38). The IgG is directed against the nuclear protein ΔNp63α. CUS does not respond to
conventional treatment such as corticosteroids. Antimalarials have helped cause remission of disease activity. Patients need to be monitored closely for side effects of therapy(14).
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11.5 Summary
Immune dysfunctions include a range of conditions, from hypersensitivity disorders to autoimmune diseases to immunodeficiencies. Oral involvement is frequent and, in some cases, the first
and only site of disease activity. Some conditions are mild and easily recognised and treated. Others
are potentially life- altering and cause of death. Many conditions also have overlapping clinical
syndromes, and diagnosis requires additional disease- specific testing because the management of
patients with diverse conditions is different. Recognition of the complexity of these diseases,
including their complications and management strategies, is essential in dental practice to facilitate patient triage to an appropriate specialist for definitive care.
References
1 Suddock JT, Crookston KP. Transfusion Reactions. [Updated 2023 August 8]. In: StatPearls
[Internet]. Treasure Island (FL): StatPearls Publishing; 2023January. PMID: 29489247.
2 Hall V, Avulakunta ID. Hemolytic Diseases of the Newborn. [Updated 2022November 22].
In:StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023January. PMID: 32491355.
3 Berentsen S, Barcellini W. Autoimmune hemolytic anemias. N Engl J Med. 2021;385(15):1407– 19.
https://doi.org/10.1056/NEJMra2033982.
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4 Crow MK. Pathogenesis of systemic lupus erythematosus: risks, mechanisms and therapeutic
targets. Ann Rheum Dis. 2023;82(8):999– 1014. https://doi.org/10.1136/ard- 2022- 223741.
5 Wang DH, Wallace DJ. New insights into systemic lupus erythematosus therapies: 2010- 2020.
JClin Rheumatol. 2022;28(1):e217– 21. https://doi.org/10.1097/RHU.0000000000001603.
6 Notarangelo LD. Primary immunodeficiencies. J Allergy Clin Immunol. 2010;125(2 Suppl 2):
S182–94. https://doi.org/10.1016/j.jaci.2009.07.053.
7 Tuano KS, Seth N, Chinen J. Secondary immunodeficiencies: an overview. Ann Allergy Asthma
Immunol. 2021;127(6):617– 26. https://doi.org/10.1016/j.anai.2021.08.413.
8 Chinen J, Shearer WT. Secondary immunodeficiencies, including HIV infection. J Allergy Clin
Immunol. 2010;125(2 Suppl 2):S195– 203. https://doi.org/10.1016/j.jaci.2009.08.040.
9 Sultan AS, Villa A, Saavedra AP, Treister NS, Woo SB. Oral mucous membrane pemphigoid and
pemphigus vulgaris retrospective two- centre cohort study. Oral Dis. 2017;23(4):498– 504.
https://doi.org/10.1111/odi.12639.
10 Saccucci M, Di Carlo G, Bossù M, Giovarruscio F, Salucci A, Polimeni A. Autoimmune diseases
and their manifestations on oral cavity: diagnosis and clinical management. J Immunol Res.
2018;2018:6061825. https://doi.org/10.1155/2018/6061825.
11 Cheng YS, Gould A, Kurago Z, Fantasia J, Muller S. Diagnosis of oral lichen planus: a position
paper of the American Academy of Oral and Maxillofacial Pathology. Oral Surg Oral Med Oral
Pathol Oral Radiol. 2016;122(3):332– 54. https://doi.org/10.1016/j.oooo.2016.05.004.
12 Al- Hashimi I, Schifter M, Lockhart PB, Wray D, Brennan M, Migliorati CA, etal. Oral lichen
planus and oral lichenoid lesions: diagnostic and therapeutic considerations. Oral Surg Oral Med
Oral Pathol Oral Radiol Endod. 2007;103(S25):e1– e12. https://doi.org/10.1016/j.tripleo.2006.11.001.
13 Sultan A, Stojanov IJ, Lerman MA, Kabani S, Haber J, Freedman J, etal. Oral lichen planus
pemphigoides: a series of four cases. Oral Surg Oral Med Oral Pathol Oral Radiol. 2015;
120(1):58–68. https://doi.org/10.1016/j.oooo.2015.03.012.
14 Schroeder FMM, Palma VM, Rados PV, Visioli F. Clinical and immunological features of
chroniculcerative stomatitis: a systematic review. J Oral Pathol Med. 2022;51(6):501– 9.
https://doi.org/10.1111/jop.13279.
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12
Pathology of Inflammation and Inflammatory Diseases
oftheOro-FacialComplex:AnOverview
S. R. Prabhu
School of Dentistry, University of Queensland, Brisbane, Queensland, Australia
12.1 Introduction
Inflammation is a natural response our bodies produce when we are injured. It is like a team of
white blood cells and plasma proteins rushing to the scene to fight off any harmful organisms or
chemicals. The main job of inflammation is identifying and eliminating these harmful substances
and repairing any damage they have caused. The process can vary depending on the type of injury
and how severe it is. But no matter what, inflammation always involves changes in blood vessels,
the arrival of white blood cells and the release of certain chemicals that help heal.
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12.2 Aetiology
Inflammation can be caused by microbial, physical, chemical, biological, immune and genetic/
metabolic factors. Infectious organisms include viruses, bacteria, fungi and parasites. Physical
agents include mechanical injuries, extremes of temperature and electrical injuries. Inflammation- causing chemicals include organic, inorganic, industrial chemicals, drugs and toxins.
Immunological causes include hypersensitivity reactions, autoimmunity and immunodeficiency
states. Examples of genetic/metabolic causes include gout and diabetes. Inborn errors of the innate
immune system can cause a condition known as constitutive inflammation(1).
Inflammation is initially beneficial as the body responds to an injurious stimulus. This ‘physiological’ aspect of inflammation occurs by (i) improving immunity and repairing the body,
(ii)assisting the body in containing the cause of inflammation and (iii) healing damaged organs
and depends on endogenous inhibitors of pro- inflammatory signalling pathways. Uncontrolled
inflammation, however, can lead to apoptosis, necrosis, fibrosis and eventual or chronic organ
damage when physiological inhibitors fail.
Pathological Basis of Oral and Maxillofacial Diseases, First Edition. Edited by S. R. Prabhu, Syed Ali Khurram,
Omar Kujan and Merva Soluk Tekkesin.
© 2025 John Wiley & Sons Ltd. Published 2025 by John Wiley & Sons Ltd.
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12.3 CellularResponsesinInflammation
Cells in the inflammatory process include polymorphonuclear neutrophils (PMN), eosinophils,
basophils, mast cells, macrophages, plasma cells, lymphocytes and platelets (2, 3). Their
morphological features are listed below and shown in Table12.1.
● Polymorphonuclear Neutrophils (PMNs): PMNs are the most abundant white blood cells in
circulation (60–70% of all circulating white blood cells). • PMNs are the first cell line recruited at
the inflammation site after chemotactic stimuli. • PMNs have segmented nuclei and numerous
granules in the cytoplasm (hence, the name neutrophilic granulocytes). • PMNs are the most
prominent cell type and are the first to appear in inflammation. • PMNs are highly mobile and
capable of phagocytosis. They contain bactericidal agents in their cytoplasmic granules and
secrete inflammatory mediators (cytokines).
● Eosinophils: 2–3% of all circulating white blood cells. • Eosinophils are present in the res-
piratory, gastrointestinal and urinary tract and are less abundant than neutrophils. • The
nucleus of the eosinophil is divided into two lobes, and the cell contains cytoplasmic
granules (stains pink with eosin, hence the name ‘eosinophil’). • It is mobile, phagocytic and
bactericidal. • Have an important role in allergies and parasitic infections. • May be associated with chronic infections.
● Basophils: Less than 1% of circulating white blood cells. • The most essential cells in allergic
reactions mediated by immunoglobulin E (IgE). • Have a bean- shaped nucleus and cytoplasmic
granules. • Contain vasoactive substances (histamine). • Basophils are mast cell precursors
(tissue basophils). • These cells are not phagocytic.
● Mast Cells: Resident connective tissue cells contain granules rich in histamine (inflamma-
tory mediator) and heparin (anticoagulant). • Histamine increases vascular permeability;
degranulation promotes blood clotting, and PDGF promotes the proliferation of connective
tissue cells. • Round nucleus, granulated cytoplasm. • These cells arenot phagocytic.
● Monocytes/Macrophages: Monocytes circulate in peripheral blood, can migrate to the inflamma-
tory site, and transform themselves into tissue macrophages (histiocytes). • They have a beanshaped nucleus. • Have capacity for phagocytosis and release of inflammatory mediators
(cytokines). • Cell types of chronic inflammation.
● Plasma Cells: Derived from differentiated B lymphocytes. • Oval eccentrically located round
nucleus with a characteristic cartwheel or clock face arrangement. • Rich in the rough endoplasmic reticulum (RER), the site of production of immunoglobulins.
● Lymphocytes: 20–40% of all white blood cells in the bloodstream. • Derived from bone marrow
pre- lymphoid stem cells. • Present in blood and lymphoid tissues (spleen, tonsils, lymph
nodes) and mucosa- associated lymphoid tissues (MALT) (including gastrointestinal and
bronchial mucosa). • Small cells with minimal cytoplasm and round nuclei. • Two types:
Tlymphocytes (matured in the thymus) and B lymphocytes (derived from bone marrow or
bursa). • T cells are involved in cellular immunity, while B cells are primarily responsible for
humoral (antibody- related) immunity.
● Platelets: Platelets participate in coagulation, bleeding control and defence against infectious
agents. • There is no nucleus, and the cytoplasm contains vacuoles and membrane- bound
granules. • The granules contain histamine, clotting (coagulation) proteins, cytokines and
platelet- derived growth factor (PDGF).
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Table12.1 Describes thecharacteristics andlocation ofcells involved inthe innate immune system.
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
Celltype Characteristics Location Image
Mast cell Dilates blood vessels and induces inflammation through release
Connective tissues, mucous membranes
of histamines and heparin. Recruits macrophages and
neutrophils. Involved in wound healing and defence against
pathogens but can also be responsible for allergic reactions.
Macrophage Phagocytic cell consumes foreign pathogens and cancer cells.
Migrates from blood vessels into tissues.
Stimulates response of other immune cells.
Natural killer cell Kills tumour cells and virus- infected cells. Circulates in blood and migrates into tissues.
Dendritic cell Presents antigens on its surface, thereby triggering adaptive
immunity.
Present in epithelial tissue, including skin,
lung and tissues of the digestive tract. Migrates
to lymph nodes upon activation.
Monocyte Differentiates into macrophages and dendritic cells in response
to inflammation
Stored in spleen, moves through blood vessels
to infected tissues.
(Continued)
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Table12.1 (Continued)
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
Celltype Characteristics Location Image
Neutrophil First responders at the site of infection or trauma, this
abundant phagocytic cell represents 50–60% of all leukocytes.
Releases toxins that kill or inhibit bacteria and fungi and
recruits other immune cells to the site of infection.
Migrates from blood vessels into tissues.
Basophil Responsible for defence against parasites. Releases histamines
Eosinophil Releases toxins that kill bacteria and parasites but also cause
Source: Rice University/https://openstax.org/books/biology- 2e/pages/42- 1- innate- immune- response/last accessed on February 03, 2024/CC BY 4.0.
that cause inflammation and may be responsible for allergic
reactions.
tissue damage.
Circulates in blood and migrates to tissues.
Circulates in blood arid migrate to tissues.
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0005802307.INDD 178 09-13-2024 17:45:22
12.4 Cell-derivedInflammatoryMediatorsinInflammation
Chemical mediators of cellular origin include histamine, lysosomal compounds, prostaglandins,
leukotrienes, 5- hydroxytryptamine (serotonin) and chemokines(2, 3).
Histamine is derived from mast cells; it causes immediate vasodilation and increases vascular
permeability.
Lysosomal compounds are derived from neutrophils. These also contribute to increased
vascular permeability.
Prostaglandins are derived from arachidonic acid. Prostaglandins are synthesised in many cell
types. Macrophages, endothelial cells and several different cells make prostaglandins. They are
crucial in the vascular and systemic effects of inflammation and enhance increased vascular permeability. Cyclooxygenases (COX- 1 and COX- 2) are the catalysts responsible for the production of
prostaglandins(2).
Leukotrienes are derived from arachidonic acid. As inflammatory mediators, these have vasoactive properties.
5- Hydroxytryptamine (serotonin): In response to inflammatory substances such as cytokines,
the platelet- activating factor (PAF) and the complement system, 5- hydroxytryptamine is released
by platelets, mast cells and basophils. Serotonin acts as a chemotactic agent, which increases
pro- inflammatory cytokine secretion (interleukins IL- 1, IL- 6, NFκB) and enhances phagocytosis.
Chemokines are a family of signalling proteins secreted by cells that induce the directional
movement of leukocytes and other cell types, including endothelial and epithelial cells. This protein selectively attracts white blood cells to the affected area (see below under cytokines).
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12.5 Plasma-derivedInflammatoryMediatorsinInflammation
Plasma has four enzymatic cascade systems, namely the complement system, the kinin system, the
coagulation system and the fibrinolytic system(2, 3).
The complement system, or the complement cascade, a part of the immune system, enhances
the ability of antibodies and phagocytic cells to eliminate bacteria and damaged cells from the
body. It also promotes inflammation and attacks the cell membranes of pathogens. The proteins in
the complement system work together to ‘complement’ the action of the immune system (antibodies) to kill bacteria. These proteins circulate in the blood in an inactive form. During the inflammatory response, complements are activated.
The major functions of the complement process include (i) opsonisation, (ii) chemotaxis,
(iii)cell lysis and (iv) agglutination.
● Opsonisation is a process in which an opsonin (such as an antibody molecule) binds to the sur-
face of an antigen so that the antigen is easily identified, engulfed, and destroyed by phagocytes.
● Chemotaxis attracts macrophages and neutrophils via inflammation caused by inflammatory
mediators.
● Cell lysis ruptures the membrane with the formation of membrane attack complexes (MACs).
● Agglutination leads to the clustering and binding of pathogens. Activated complement proteins
can also increase vascular permeability, cause histamine release from mast cells and act as
chemoattractants for neutrophils.
The kinin system comprises blood proteins that play a role in inflammation, blood pressure
control, clotting and pain. Bradykinin and kallidin are inflammatory mediators, vasodilators and
chemical pain mediators in acute inflammation.
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