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Table12.2

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

 (Continued)

Gingivalandperiodontal inflammatory diseases Definition Causes/riskfactors

● Aggressive periodontitis Characterised by the rapid attachment loss coupled with

● Peripheral giant cell

granuloma (Giant cell epulis)

Pyogenic granuloma/ Angiogranuloma/ Pregnancy epulis

● Inflammatory gingival

hyperplasia

● Generalised gingival

hyperplasia in pregnancy

Gingival and periodontal abscesses

bone destruction in otherwise healthy individuals

A tumour

- like reactive hyperplastic lesion of the gingival

margin located anterior to the permanent molars

A highly vascular, localised inflammatory tumour with abundant granulation tissue

- like lesion

A chronic inflammatory process resulting in generalised gingival enlargement

Inflammatory gingival hyperplasia between the 14th and 30th weeks of pregnancy

Gingival abscess is a localised purulent infection that involves the marginal gingiva or interdental papilla without involving the periodontal ligament or alveolar bone

Periodontal abscess is the result of acute inflammation of the periodontal pocket, resulting in the collection of pus alongside a vital tooth

Several complex interactions, including host factors, microbiology, and genetics.

- negative microbes are the chief etiological agents

Gram Local irritation or trauma

Local low- grade irritation or trauma Female hormones in pregnancy can be precipitating factors

Poor oral hygiene. The irritant could be microbial deposits in dental plaque and calculus. Systemic factors include hormonal disturbances or blood dyscrasias, which

can render gingiva susceptible to microbial flora and contribute to inflammatory gingival enlargement.

Dental plaque accumulation Increased levels of oestrogen and progesterone accentuate the gingival

response to plaque. Between the Gingival, inflammation increases between the 14th and 30th

weeks of pregnancy. Gingival abscess: Plaque or foreign body entrapped in the gingival sulcus.

Periodontal abscess: Acute exacerbation of untreated chronic periodontitis Foreign body (such as toothbrush bristle or fishbone) in the periodontal

pocket Food impaction between the teeth with poor contact points. Pericoronitis.

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0005802307.INDD 190 09-13-2024 17:45:25

● Pericoronitis An inflammatory process of the soft tissues around a

● Osteomyelitis of the

jaws:

Acute suppurative osteomyelitis

Chronic suppurative osteomyelitis

Sclerosing osteomyelitis

Proliferative periostitis (Garre’s osteomyelitis)

● Cervicofacial cellulitis/

Ludwig’s angina

partially erupted or impacted tooth

An acute inflammatory process that involves the bone marrow and the surrounding jawbone

Chronic inflammatory process that causes necrosis of mineralised and marrow tissues, suppuration, and resorption

Characterised by the process of sclerosis of bone due to low

- grade non- suppurative inflammation

Sclerosing osteomyelitis has two types: Focal (condensing osteitis) and diffuse

Proliferative periostitis is the proliferation of new bone formation, resulting in the expansion of the mandibular cortex as a periosteal reaction to low children and adolescents

Acute inflammation of the soft tissue spaces of the facial and cervical region due to spreading odontogenic infection

- grade inflammation in

Entrapment of plaque and food debris between the crown of the tooth and the overlying gingival flap or operculum

Oral streptococci and various anaerobic species

Causative microbes: predominantly anaerobes: Bacteroides, Porphyromonas, Prevotella species, and staphylococci in early stages

Predisposing factors include diabetes mellitus, malnutrition, and immunosuppression

Sources of infection: periapical infections, infected periodontal pocket, acute necrotising ulcerative gingivitis or pericoronitis, bone fracture, radiation damage

- grade infection with Staphylococcus aureus and aerobic Gram- negative

Low bacilli

Odontogenic infection (most common) Post- extraction complication Infected periodontal pocket

Focal sclerosing osteomyelitis: low individual with a strong host defensive response

Diffuse sclerosing osteomyelitis: periapical or periodontal chronic infection around the bone

Periapical/dentoalveolar low

Anaerobic bacteria from odontogenic sources (mandibular molars in particular)

- grade periapical infection in an

- grade chronic infection

(Continued)

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0005802307.INDD 191 09-13-2024 17:45:26

 (Continued)

Table12.2

Inflammatory conditions of the oral mucosa and salivaryglands Definition Causes

Recurrent aphthous stomatitis

Oral lichen planus An inflammatory chronic cell

Oral lichenoid lesions An oral chronic inflammatory lesion causing lichen

Pemphigus vulgaris Pemphigus is a blistering autoimmune disorder that affects

Mucous membrane pemphigoid

Erythema multiforme An acute, self

A common inflammatory condition characterised by multiple recurrent, painful, round ulcers with circumscribed margins, surrounded by an erythematous halo and a central yellow or grey floor

mucocutaneous response

planus

- like lesions due to hypersensitivity to local or

systemic agents

- mediated immune

the skin and mucous membranes

An autoimmune subepithelial blistering disease predominantly affects the mucous membranes associated with antibodies that target the basement membrane zone

conditions are considered type associated with certain infections, medications or other triggers

- limiting, and sometimes recurring skin

- IV hypersensitivity reactions

Many implicated factors include hormonal changes, trauma, drugs, food hypersensitivity, nutritional deficiency, stress and tobacco.

Genetic predisposition has been noted (family history in about 30% of patients) Immunodysfunction may be a factor (antibody

cytotoxicity reaction) Immunologically mediated T- cell disorder targeting basal keratinocytes;

antigen unknown Oral lichenoid lesions are caused by known triggers such as restorative

materials and agents such as amalgam, gold, and composites Drugs causing hypersensitivity reactions include sulfasalazine, angiotensin-

converting enzyme inhibitors, non- steroidal anti- inflammatory drugs (NSAIDs), beta

An autoimmune disease. IgG antibodies are directed against desmoglein 1 or 3 proteins of the

desmosomes in the epithelium. Circulating antibodies bind to epithelial desmosomes and cause the cells to

detach, forming intraepithelial vesicles. Antibodies are directed against basement membrane zone antigens

(namely, bullous pemphigoid 180 antigen, integrins, laminin and type VII collagen)

A cell It may be triggered by herpes simplex virus infection (cold sore), genital

recurrent herpes, mycoplasma’ pneumonia, varicella zoster infection, drugs such as sulphonamides, antibiotics, analgesics, phenolphthalein containing laxatives, barbiturates, radiation, and chemotherapy

- dependent cellular

- blockers, gold, antimalarial sulfonylurea compounds and other drugs.

- mediated hypersensitivity reaction

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0005802307.INDD 192 09-13-2024 17:45:26

Lupus erythematosus It is a chronic autoimmune connective tissue disorder with

- Versus- Host Disease

Graft (GVHD)

Traumatic ulcer An ulcer caused by trauma. Physical, thermal, or chemical injuries. Occasionally iatrogenic and also

Chronic ulcerative stomatitis

- induced

Radiation mucositis

Medication stomatitis

Actinic cheilitis Actinic cheilitis is an inflammatory keratotic lesion

Primary Herpetic Gingivostomatitis

- induced

two main clinical types: systemic lupus erythematosus (SLE) and chronic cutaneous lupus erythematosus (discoid lupus erythematosus)

A complication of haematopoietic stem cell transplantation. This usually affects multiple organs and tissues, including the oral tissues. In the chronic form, the oral cavity is most commonly affected

A rare autoimmune mucosal disorder characterised by lichen planus- like lesions. Affects predominantly females

Inflammation of the mucosa due to damage caused by ionising radiation

Oral mucositis followed by ulceration in patients receiving medication for various conditions

commonly occurring in the lower lip due to intense and chronic sun damage in susceptible individuals

Inflammation of the gingival and oral mucosal tissues predominantly in children with infection of the herpes simplex virus (HSV) type I

An autoimmune disorder

Human leukocyte antigen (HLA) incompatibility

due to biting after dental local anaesthetic injections. Autoimmune disorder

Radiation to the head and neck region for cancer therapy

Groups of ulcerogenic drugs include cytotoxic drugs used for cancer therapy,

- blockers, immunosuppressants, anticholinergic bronchodilators, platelet

beta aggregation inhibitors, vasodilators, protease inhibitors, antibiotics, NSAIDs, anti

- retroviral agents, and anti- hypertensive drugs (e.g. potassium channel

activator nicorandil). Chronic sun damage: ultraviolet radiation (range: 290–320

lip of people who are fair complexioned

HSV type 1 (90–95%) and type 2 (5–10%) are the causative agents. The transmission mode is physical contact with the contaminated source

(oral secretions)

nm) to the lower

(Continued)

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0005802307.INDD 193 09-13-2024 17:45:26

 (Continued)

Table12.2

Inflammatory conditions of the oral mucosa and

glands Definition Causes

salivary

Recurrent Herpetic stomatitis

The secondary infection with HSV- 1 characterised by the vesicular lesions of the vermillion border and adjacent skin

(Herpes labialis) Gonococcal stomatitis A sexually transmitted bacterial disease causes inflamed

Oral tuberculous ulcers Tuberculosis (TB) is a chronic specific granulomatous

Syphilitic oral lesions (Primary, secondary and

tertiary stages).

Sialadenitis (Mumps) Inflammation of the salivary glands, mainly in parotid

Sjögren’s syndrome An autoimmune disorder of salivary glands characterised by

erythematous, pustular, erosive, or ulcerated oral mucosa lesions

infection caused by Mycobacterium tuberculosis. Oral lesions of TB include chronic non

- healing socket, or stomatitis.

non Oral mucosal sites include the tongue (mid

lateral borders), gingiva, lips, buccal mucosa, and soft and hard palate

- healing ulcer,

- dorsal surface or

Syphilis is an infectious sexually transmitted disease. Non

- specific chronic inflammation with plasma cells and

lymphocytes Granulomatous inflammation with giant cells and

histiocytes in the tertiary stage

glands in children

dry eyes, dry mouth and other systemic manifestations

Reactivation of the latent virus in the nerve ganglion causes recurrent herpetic stomatitis

Caused by Neisseria gonorrhoeae

Causative agent: Acid At

- risk individuals include those with:

● HIV infection

● Substance abuse

● Silicosis

● Diabetes mellitus

- fast bacillus M. tuberculosis.

Spirochete Treponema pallidum is the causative agent. Syphilis is transmissible by sexual contact. Maternal infection is from

mother to foetus in utero. Infection via blood product transfusion is possible but rare

Caused by paramyxovirus (mumps virus)

The exact cause is unclear Genetic and environmental (possibly viral) factors may play a role An autoimmune disorder attacks all exocrine glands, including those of the

skin, vagina, lungs and pancreas Increased prevalence of human leukocyte antigen DR/DQ alleles Autoantibody production against nuclear antigens SS

- A and SS- B

t.me/Dr_Mouayyad_AlbtousH

0005802307.INDD 194 09-13-2024 17:45:26

References

12.12 Summary

Inflammation is a biological response of the immune system. Pathogens, injured cells and toxic compounds can trigger the inflammatory process. An overview of inflammatory reactions has been presented, focusing on the types, aetiology, cardinal signs, mechanisms and organ- specific inflammatory responses, including those of the oro- facial complex.

References

1 Hawiger J, Zienkiewicz J. Decoding inflammation, its causes, genomic responses, and emerging

countermeasures. Scand J Immunol. 2019;90:e12812.

2 Kanova M, Kohout P. Serotonin— Its synthesis and roles in the healthy and the critically Ill.

Int J Mol Sci. 2021;22(9):4837. https://doi.org/10.3390/ijms22094837.

3 Alharbi KS, Alenezi SK, Gupta G. Chapter1- Pathophysiology and pathogenesis of inflammation.

In: Prasher P, Zacconi FC, Withey JH, Rathbone M, Dua K, editors. Recent Developments in Anti- Inflammatory Therapy. Academic Press; 2023, pp. 1–9.

4 Zlotnik A, Yoshie O. The chemokine superfamily revisited. Immunity. 2012;36:705–16. 5 Takeuchi O, Akira S. Pattern recognition receptors and inflammation. Cell. 2010;140:805–20. 6 Kumar V, Abbas AK, Aster JC. Chapter3. Inflammation and repair. In: Robbins Basic Pathology,

edition. Philadelphia: Elsevier; 2018, pp. 57–93.

7 Burt AD, Fleming S. Chapter4. Cell injury, inflammation and repair. In: Levison D, Reid R, Burt

AD, Fleming S, editors. Muir’s Textbook of Pathology, 14 pp. 47–76.

8 Rohrmann S, Pestoni G. Using dietary indices— what’s next? Nutrients. 2020;12(7):2161. 9 He G, Karin M. NF- κB, STAT3- key players in liver inflammation and cancer. Cell Res. 2011;21:159–68. 10 Inflammatory responses and inflammation- associated diseases in organs | Oncotarget.

https://www.oncotarget.com/article/23208/text/

11 Pfeffer MA, Braunwald E. Ventricular remodelling after myocardial infarction. Experimental

observations and clinical implications. Circulation. 1990;81:1161–72.

12 Opie LH, Commerford PJ, Gersh BJ, Pfeffer MA. Controversies in ventricular remodelling. Lancet.

2006;367:356–67.

13 Manohar M, Verma AK, Venkateshaiah SU, Sanders NL, Mishra A. Pathogenic mechanisms of

pancreatitis. World J Gastr Pharmacol Therapeut. 2017;8:10–25.

14 Kumar P, Liu Y, Shen Y, Maher J, Cingolani F, Czaja M. Mouse liver injury induces hepatic

macrophage FGF23 production. PLoS One. 2022;17(3):e0264743.

15 Ernandez T, Mayadas TN. The changing landscape of renal inflammation. Trends Mol Med.

2016;22:151–63.

16 Goswami B, Rajappa M, Sharma M, Sharma A. Inflammation: its role and interplay in cancer

development, with special focus on gynaecological malignancies. Int J Gynecol Cancer. 2008;18:591–9.

17 Nelson PT, Soma LA, Lavi E. Microglia in diseases of the central nervous system. Annals Med.

2002;34:491–500.

18 Vezzani A, Granata T. Brain inflammation in epilepsy: experimental and clinical evidence.

Epilepsia. 2005;46:1724–43.

19 Prabhu SR. Inflammation: an overview. In: Textbook of General Pathology for Dental Students.

Springer Nature; 2023, pp. 39–47.

edition. London: CRC Press; 2008,

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196

Cellular andMolecular Mechanisms ofHealing ofCutaneous andOral Mucosal Wounds

H. Ibrahim Korkmaz1 and Susan Gibbs

Molecular Cell Biology and Immunology, Amsterdam University Medical Centre, Amsterdam, Netherlands

Academic Center for Dentistry Amsterdam (ACTA), Amsterdam, Netherlands

13.1 Introduction

Wound healing is a physiological response to tissue injury involving a complex interaction between cellular and molecular processes and the vascular system (1). The biological process of wound healing in the human body consists of overlapping phases, i.e. the inflammatory phase (haemostasis and inflammation), the proliferation phase and the remodelling phase. Specific cellular and molecular responses regulate these phases. Dysregulation, especially in the inflammatory phase (i.e. prolonged, overactive response), can result in detrimental effects like delayed wound closure and hypertrophic scars(2). Interestingly, oral mucosal wounds heal faster with less scarring than cutaneous wounds(3).

Cutaneous and oral mucosal wounds can be caused by trauma, surgery, infections or due to medical conditions. Understanding the underlying processes that govern wound healing is of scientific importance and holds significant clinical implications. Successful restoration of tissue integrity is paramount in preventing complications such as infections, scarring and impaired function of skin and mucosa. In addition, providing a comprehensive overview of the cellular and molecular mechanisms governing cutaneous and oral mucosal wound healing will give insights that may have significant implications in regenerative medicine, tissue engineering and therapeutic interventions.

This chapter delves into the cellular and molecular mechanisms that underlie the healing of cutaneous and oral mucosal wounds, from the unique structural characteristics and microenvironment to the intricate behaviour of various cell types, molecules and extracellular matrix components that enable the skin and mucosa to restore damaged tissue.

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.

t.me/Dr_Mouayyad_AlbtousH

      

Oral epithelium

Epidermi

Adipocyte

13.2 Tissue Architecture andMicroenvironment inSkin andOral Mucosa

13.2.1 Tissue Architecture

Skin and oral mucosa comprise a specialised tissue architecture that provides unique structural characteristics (Figure13.1).

The outermost layer of both skin and oral mucosa is a stratified epithelium (in the skin called the epidermis), which contains keratinocytes, melanocytes, Merkel cells and Langerhans cells (4). This layer provides a barrier against physiological and pathogenic external factors, e.g. body fluid loss, exposure to toxins and microbial invasion(5, 6). The skin epidermis is entirely keratinised, whereas the oral mucosa differs in the keratinised epithelium of the hard palate and gingiva and the non- keratinised epithelium of the buccal mucosa and soft palate. This can be explained by the fact that the hard palate and gingiva have to withstand mechanical forces during chewing, and both buccal mucosa and soft palate have to be flexible to stretch and withstand compression

Skin Oral mucosa

197

Dermis

Subcutis

Keratinocyte

Fibroblast

Langerhans cell

Dendritic cell

Macrophage

Figure13.1 Graphical illustration of skin (left) and oral mucosa (right) tissue architecture and cellular and

molecular composition. Source: Adapted from Biorender.com.

Collagen type I

Collagen type III

Elastin

Glucosaminoglycan

Blood vessel with single cell layer of endothelial cells

Lamina propria

Submucosa

t.me/Dr_Mouayyad_AlbtousH

 

198

forces(6, 7). Furthermore, the oral epithelium is thicker than the skin epidermis, consisting of more cell layers, 20– 30 and 5– 8living cell layers, respectively. Moreover, the cell proliferation rate in oral mucosa is also higher than in the skin(8).

In skin, the layer underneath the epidermis, named the dermis, consists of a network of extracellular matrix, i.e. collagen and elastic fibres, providing strength and elasticity to the skin. It contains blood vessels, nerve endings, immune cells and skin appendages, including hair follicles and sweat glands. The dermis can be subdivided into the superficial, thin papillary dermis and the deeper, thicker reticular dermis (9). The connective tissue layer underneath the oral mucosal epithelium is called the lamina propria, which can be subdivided into a superficial papillary layer and a deeper reticular layer. Like the skin dermis, the lamina propria contains blood vessels and immune cells, playing an essential role in the oral immune response(10). Both the dermis and lamina propria extracellular matrix mainly consist of collagen type I and III (in ratio 5:1); the lamina propria underneath the non- keratinised oral epithelium consists of extracellular matrix that has a looser structure and contains more elastin compared to skin dermis and lamina propria underneath keratinised oral epithelium(3, 11). This can also be explained by the fact that buccal mucosa and soft palate must be more flexible to withstand compression forces. The papillary layer of the lamina propria is formed by thin collagen fibres that are irregularly oriented and contain many capillary loops, providing nutrient transport. The underlying reticular layer is formed by thicker and parallel- oriented collagen fibres, giving strength to compression and shear to the oral mucosa(3, 11– 13).

The deepest skin later is the subcutis, also known as the hypodermis. This layer mainly consists of adipose tissue, providing energy storage and insulation and containing adipocytes, adipose stem cells and progenitor cells. In addition, the hypodermis connects the dermis with muscles and bones. In the oral submucosa, the lamina propria of the buccal mucosa and soft palate are similarly on top of an adipose tissue layer, i.e. submucosa. In contrast, the lamina propria of the hard palate and gingiva are directly attached to bone via mucoperiosteum(6, 9).

13.2.2 Cellular andMolecular Composition

The microenvironment in the skin and oral mucosa regulates the maintenance of tissue integrity, homeostasis and the immune response. Within this microenvironment, the interplay of cellular components, extracellular matrix, blood vessels and immune cells collectively regulate physiological processes, including wound healing(3, 14) (Figure13.1).

Regarding the cellular microenvironment, keratinocytes are the predominant cell type in the epidermis and oral mucosal epithelium, responsible for producing keratin that provides strength and water- resistant properties (15). Melanocytes in the epidermis produce the pigment melanin, which offers skin colour and protection against UV radiation(16). Oral mucosal melanin can neutralise toxins and bacterial products, thus acting as an extra defence barrier(17, 18). Langerhans cells, a type of dendritic cell in the epidermis and oral mucosal epithelium, are essential for the immune response by detecting and processing antigens that enter the skin(16). Merkel cells are specialised cells, also known as ‘touch cells’, essential for light touch sensation(19).

Both dermis and lamina propria contain blood vessels that provide oxygen, nutrition and immune cells and mediators; nerves that regulate sensation; lymphatic vessels that transport lymph fluid away from the tissue back to the circulatory system; and immune cells, e.g. dendritic cells, neutrophils, macrophages and mast cells, to protect against infections and modulate inflammatory responses(10, 16). The dermal layer of the skin also contains appendages such as hair

t.me/Dr_Mouayyad_AlbtousH

     

follicles and sweat glands. The oral mucosa contains various mucous glands, such as the minor salivary glands. These glands secrete mucus to lubricate the oral cavity and aid in digestion.

Fibroblasts, the most abundant cell type in the dermis and lamina propria, produce and deposit extracellular matrix components (e.g. collagen, elastin and proteoglycans). By secreting growth factors such as transforming growth factor- beta (TGF- β), cytokines including tumour necrosis factor- alpha (TNF- α), and enzymes such as matrix metalloproteinases (MMPs), fibroblasts regulate keratinocyte proliferation and differentiation, and extracellular matrix formation(20). Therefore, fibroblasts are crucial in tissue remodelling during wound healing of skin and oral mucosa.

The connective tissue, i.e. the extracellular matrix of the dermis and lamina propria, is composed of collagen, providing strength; elastin, maintaining elasticity; and proteoglycans, giving hydration and viscosity. MMPs, produced by fibroblasts, keratinocytes, neutrophils and mast cells, regulate the remodelling of the connective tissue.

The subcutis provides insulation, acts as an energy reservoir and has an endocrine function as it synthesises oestrone and leptin (15). The main cell type within it is the adipocyte. The subcutis forms a fibrous connective tissue with a rich microvascular network providing oxygen and nutrient exchange, nerves, and lymphatic vessels(16). Similarly, the submucosa comprises adipose tissue with minor salivary glands, blood vessels, nerves and lymphatic vessels(10).

Regarding the microenvironment of skin and oral mucosa, a significant difference is the microbiome and saliva in oral mucosa. The oral mucosa has a greater diversity of microbial species than skin(21, 22), and saliva plays a vital role in keeping the microbial balance(23). Around 700 unique microbial species have been identified in the healthy oral cavity(21, 22). The skin microbiome primarily consists of bacteria, e.g. Staphylococcus, Corynebacterium, Propionibacterium, and some fungi and viruses. In contrast, the oral mucosa includes bacteria, commonly Streptococcus, Actinomyces, and Veillonella, fungi and viruses.

199

13.3 Wound Healing inSkin andOral Mucosa

13.3.1 Cellular andMolecular Mechanisms

Wound healing in the skin and oral mucosa is a highly complex and well- coordinated sequence of processes where specific cellular and molecular processes regulate the haemostasis, inflammatory, proliferative and remodelling phases (Figure13.2).

After an injury, neutrophils are the first immune cells that arrive at the wound site in response to chemokine interleukin- 8 (IL- 8) secretion, followed by macrophages. These immune cells phagocytose dead tissue, i.e. debris, and possible pathogens, initiating the early inflammatory response by secretion of proinflammatory cytokines, e.g. IL- 1, IL- 6 and TNF- α(2, 3).

Platelet- derived growth factor (PDGF) stimulates fibroblast proliferation in the proliferation phase. Fibroblasts proliferate and migrate to the wound site and produce and deposit extracellular matrix, mainly collagen, forming the tissue repair framework. TGF- β stimulates collagen produc- tion and myofibroblast differentiation, which are responsible for wound contraction. In contrast, vascular endothelial growth factor (VEGF) promotes angiogenesis by endothelial cells to supply oxygen and nutrients to the healing tissue. Keratinocytes and other epithelial cells migrate from the wound edges, forming a new epidermal/epithelial layer(2, 3).

Fibroblasts and myofibroblasts continue with extracellular matrix (collagen) deposition during remodelling, leading to tissue maturation and scar formation. In contrast, MMPs are involved in the degradation and reorganising of the extracellular matrix(2, 3).

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