**Oral Pathology module**
**Physical and Chemical Injuries of the**
**Oral Cavity**
**DENT4217**
**A/Prof Omar Kujan**
**BDS DipOPath MDSc MFDS RCPS FHEA FRCPath PhD**
**Acknowledgement**
of country
The University of Western Australia acknowledges that its
campus is situated on Noongar land, and that Noongar
people remain the spiritual and cultural custodians of their
land, and continue to practise their values, languages, beliefs
and knowledge.
**Artist: Dr Richard Barry Walley OAM**
**Learning outcomes**
1. Describe common physical and chemical lesions of the
oral mucosa.
2. Identify the aetiology of the oral mucosa's associated
physical and chemical lesions.
The university logo and text **"THE UNIVERSITY OF WESTERN AUSTRALIA"** are also present in the top right corner.
**Cell injuries**
**Types of Injuries (aetiology)**
• Physical (e.g., surgical trauma)
• Chemical (e.g., exposure to caustic substances)
• Thermal (e.g., burns)
• Infectious (e.g., microorganisms)
• Clinically, the patient’s chief complaint includes a painful area
or a “lump”.
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**Physical**
**and**
**chemical**
**injuries**
**Traumatic**
**occlusion**
**Sharp**
**occlusal**
**anatomy**
**Thermal**
**injury**
**Radiation**
**induced**
**Acidic and**
**alkaline**
**compounds**
**Medications**
**Cell injuries**
**Types of cell injuries (biological response)**
**Reversible**
Hyperplasia
Hypertrophy
Atrophy
Metaplasia
Dysplasia
Intracellular pigments
**Irreversible**
Necrosis
Ischemia
Apoptosis
Free radical damage
Pathologic calcification
Cell ageing
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Definitions
• **Hyperplasia** is an increase in the size of an organ or tissue due to an increase in the
number of cells (physiologic or pathologic)
• **Hypertrophy** is an increase in size of a tissue or body part due to the increase in the
size of individual cells (physiologic or pathologic).
• **Atrophy** refers to decrease in size of cells, organs, tissues, or body parts because of
disease, hormonal alteration, injury, or lack of use (physiologic or pathologic).
• **Metaplasia** is caused by a stimulus that changes one cell type into another.
• **Dysplasia** is defined as lack of proper maturation of a tissue. When cells are unable
to mature, the tissue cannot properly develop.
**Table: Types of Cellular Adaptations – Physiologic vs. Pathologic**
| | **Physiologic** | **Pathologic** |
|----------------------|------------------------------------|-----------------------------------|
| **Normal cells** | | |
| **Hyperplasia** | A. Kidney regeneration | B. Gum hyperplasia |
| **Hypertrophy** | C. Pregnancy (uterine enlargement) | D. Cardiac hypertrophy in infant |
| **Atrophy** | E. Arm in sling (disuse atrophy) | F. Tongue muscle atrophy |
**Endogenous Intracellular Pigments**
• **Melanin** is produced by melanocytes located in the basal layer of the epithelium. It can be seen in the skin following lacerations and chronic inflammatory disorders as oral lichen planus.
• **Hemosiderin** is a pigment derived from hemoglobin of red blood cells. It is composed of ferric oxide. A localized deposit of hemosiderin is seen after bruising when the red blood cells break down and the hemoglobin is released into the surrounding tissues
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Definitions
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• **Ischemia** is a restriction in blood supply generally due to damaged blood vessels. The
result is damage, dysfunction, or death of tissue supplied by that blood vessel, called
infarction.
• **Necrosis** is the death of cells and tissues that fail to adapt to environmental changes.
Pathologic necrosis occurs when normal cell functions cannot be sustained due to
infection, toxins, trauma, or lack of oxygen.
• **Apoptosis** is the process of programmed or planned cell death (tumours and
inflammatory disorders). This contrasts with cell death due to injury.
• **Free radical damage**: Free radicals inflict damage when they react with cell membranes
or cellular DNA via peroxidation of membrane lipids, a process that has been implicated
in some diseases and ageing.
• **Pathologic calcification**: abnormal deposition of calcium and may be dystrophic or
metastatic. **Dystrophic calcification** can be observed in both vital and necrotic pulp
tissues. Causes include irritation, injury, and reaction to the caries process.
**Figure Description:**
- Diagram explaining the creation and impact of free radicals:
- (A) Shows formation of a free radical from a normal oxygen atom via loss of electron.
- (B) Illustrates cell damage by free radicals:
- Sources include ultraviolet rays, atmospheric pollution, stress, and poor nutrition.
- Free radicals damage the cell membrane and DNA.
- (C) Displays how antioxidants neutralize free radicals by donating an electron.
**Inflammation**
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**Table 2.2 Types of Inflammation**
| | Acute | Chronic | Granulomatous |
|----------------------|-----------------------------------|-----------------------------------------|-------------------------------------------------------|
| **Onset** | Sudden | Gradual | Gradual |
| **Duration** | Short | Long-standing | Long-standing |
| **Predominant cell type(s)** | Neutrophils, macrophages | Lymphocytes, plasma cells, macrophages | Epithelioid histiocytes, multinucleated giant cells, lymphocytes |
| **Clinical characteristics**| Pain, erythema, and edema; fever | Loss of function | Nonpainful enlargement; nodules |
| **Outcome** | Abscess; resolution; progression to chronic inflammation | Fibrosis; tissue destruction | Medical or surgical intervention |
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Physical and
chemical injuries
**Leukoedema**
This term should only be reserved for clinical
presentation; the histopathologic feature is
keratinocyte edema.
• **Clinical Findings**
• This is present in up to 90% of the
population and is more readily discerned in
dark-skinned individuals.
• Delicate lacy, grey-white lines are present
on the buccal mucosa or tongue
(nonkeratinized sites) that disappear with
stretching
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Histological images of epithelial tissue.
**Contact Desquamation**
* superficial injury to the mucosa caused by direct contact with a mild- to-moderately irritating or caustic toothpaste or mouthwash
* Strips of desquamated keratinocytes appear eosinophilic and degenerated or coagulated, and generally lie on the surface of the otherwise intact mucosa
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# Frictional Keratosis
**Frictional Keratosis**
---
##### THE UNIVERSITY OF WESTERN AUSTRALIA
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* **Frictional Keratosis:** benign reactive phenomenon occurs when the mucous membranes are repeatedly irritated over a prolonged period.
* It represents a protective mechanism that increases the thickness of the surface epithelium to protect the underlying tissues from persistent irritation.
---
[Image of oral cavity] **A**
[Microscopic image of tissue]
Excess keratin
Orthokeratinized stratified squamous epithelium
Connective tissue
**B** Inflammatory cells Normal keratinocytes
---
[Image of oral cavity]
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Histological images of epithelial tissue with acanthosis and spongiosis.
**Linea alba**
* Linea alba ("white line") is a specific form of
frictional keratosis seen as a thin, slightly
raised white keratotic line along the occlusal
plane on the buccal mucosa, and it is often
bilateral.
* Linea alba is a variation of normal anatomy
but may become prominent in some
individuals.
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**Morsicatio buccarum**
* Morsicatio buccarum, linguarum, and labiorum, are forms of frictional keratosis caused by habitual chewing or nibbling of the cheek (morsicatio buccarum), tongue (morsicatio linguarum), and lip (morsicatio labiorum).
* Extra surface keratin builds up (hyperkeratosis) to minimise damage to the deeper tissues. The surface appears white and somewhat shredded. Cessation of the habit usually leads to regression of the lesion.
Histological images of skin tissue under different conditions (labeled A–D).
**22**
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**Snuff dippers keratosis**
• **Snuff dippers keratosis** is seen in users
of smokeless tobacco. White plaques
develop in the vestibule where the
tobacco directly touches the tissues.
These lesions are characterised by
thickened white mucosa that is
typically wrinkled or corrugated.
• The clinical presentation may vary from
an ill-defined area of white wrinkled
thickening to deeply folded tissue with
red patches. In addition to mucosal
changes, gingival recession around the
teeth may be pronounced.
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**Black hairy tongue**
- Coated tongue is retention
keratosis caused by dehydration
with reduced watery and increased
mucous saliva, and poor diet low in
fresh fruits and vegetables, leading
to retention of keratin rather than
normal shedding.
- It is very commonly seen in
inpatients in the hospital.
- Antibiotics have been associated
with black hairy tongue but they
are not a direct effect of the
antibiotic. The patient is ill and
required antibiotic therapy and is
likely dehydrated and not eating
normally.
**BBR** **THE UNIVERSITY OF**
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Histological images of skin tissue under a microscope, showing hair follicles and layers of the epidermis and dermis.
**Amalgam tattoo**
The University of Western Australia
*Amalgam tattoos* result from accidental implantation of dental amalgam within the oral tissues.
Amalgam can be introduced into oral mucosa in several ways:
* During placement or removal of amalgam restorations or during crown preparation.
* Fracture of dental amalgams via trauma or tooth extraction may also leave residual amalgam within soft tissues.
* Endodontic treatment that involved placing amalgam at the apex of the tooth
Diagnosis is confirmed by x-ray.
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**Post-inflammatory pigmentation**
* Inflammation releases prostaglandins
and other inflammatory products that
stimulate melanocytes to increase
synthesis of melanin.
* Melanin becomes trapped by
macrophages, called *melanophages*.
* More common in individuals with darker
skin.
* Lesions disappear shortly after the
inflammatory process resolves.
* Hypermelanosis may present for many
years
* These lesions cause concern because
they may resemble early melanoma.
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**Smoker melanosis**
• **Smoker’s melanosis** is a condition
of excessive melanin pigmentation
found in the gingiva of about 20%
of smokers and seen more
frequently in females.
• Melanin deposition is considered a
protective mechanism.
• Melanosis is thought to be an
attempt by the body to protect
itself from toxins and heat
produced by smoking tobacco.
• Any mucosal surface can be
affected, but melanosis is most
commonly seen in the facial
anterior gingiva and rarely in the
molar areas
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**Traumatic ulcer**
* **Ulcer:** the loss of surface epithelium with exposure of the underlying connective tissues.
* Ulcers are one of the most common injuries to the human body.
* Traumatic ulcers are almost always of acute onset, immediately following the traumatic event.
* The lateral border of the tongue and labial mucosa are the most common locations.
* Lesions will appear as round to ovoid depressions with yellow necrotic centers and erythematous irregular borders.
* Patients complain of pain that slowly subsides as the lesion heals over 7 to 10 days.
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Traumatic ulcer
## **Table 2.8 Traumatic Ulcerations of the Oral Mucosa**
| Etiology | Clinical Features |
|---|---|
| Traumatic ulcer | Physical injury such as biting the tongue or contact with sharp object | Usually single, well-defined area of erythema surrounding yellow fibrinopurulent membrane; slightly raised border; tender/painful; resolves in 7 to 10 days with removal of etiology |
| Traumatic ulcerative granuloma | Traumatic ulcer that receives persistent mild chronic trauma | Long duration; raised rolled border; crater with **yellow** fibrino-purulent membrane; nonpainful or mildly tender; slow to resolve with removal of etiology; often requires surgical excision and healing by primary intention |
| Denture ulcer | New denture with ill-adapted flange; prolonged denture wearing | Ovoid erythematous area with **yellow** necrotic center; contacts irregular area of denture; resolves with denture adjustment |
| Anesthetic necrosis | Ischemia from epinephrine in local anesthetic or trauma during injection | Usually on hard palate at injection site; painful well-defined intense **red** area with central necrosis; heals without treatment in 10 to 14 days |
| Thermal burn | Contact with hot foods such as pizza | Painful **yellow** to **white** zone of necrosis of surface mucosa of palate or buccal mucosa; tissue sloughs; patient reports etiologic event; resolve with no treatment |
| Electrical burn | Contact with live electrical cord or extension cord | **Yellow** to **black** painless area that gradually becomes edematous; sloughs and bleeds; usually on lips of children |
| Chemical burn | Contact with caustic medications, dental materials, improper use of analgesics, mouth rinses | Superficial **white** corrugated or "cracked" appearance; epithelium sloughs leaving **red** painful surface; resolves without treatment in 10 to 14 days |
| | | |
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**Anesthetic necrosis**
* Anesthetic necrosis is an unusual traumatic ulceration typically seen in patients who receive an injection in the greater palatine foramen for dental procedures on the maxillary teeth. It is believed that the epinephrine in the local anesthetic causes mild ischemia, leading to localized necrosis.
* Anesthetic necrosis appears as a well-defined tender-to-painful lesion at the injection site.
* The lesion heals without treatment in 7 to 10 days.
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**Burns**
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• **Burns** to the oral mucous membranes destroy surface
epithelium and are usually very painful.
• Burns can be thermal or chemical and are of acute
onset following exposure to the source.
• **Thermal burns** can be induced by contact with hot
foods or liquids. Hot foods that contact the lips or oral
cavity mucosa may result in acute tissue destruction.
• Palatal burns from eating hot pizza are a common
example. Occasionally, accidental contact with live
electrical wires can cause deep burns to the face
and/or oral cavity.
**Electrical burns** of the lips and commissures can be seen in young children who accidentally
chew or bite into electrical cords. Electrical burns to the lips are often severe, involving
extensive tissue damage and requiring special reconstruction by a plastic surgeon.
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**Burns**
* **Chemical burns** can result when caustic agents contact the oral mucosa. Chemical burns may appear as thick, rough hyperkeratotic plaques with a corrugated or cratered surface and/or areas of ulceration.
* Patients may misuse acidic medications, such as aspirin tablets or powders that contain acetylsalicylic acid.
* Aspirin may cause a significant burn if placed adjacent to or over a painful tooth, rather than being swallowed.
* Patients may use strong agents, such as hypochlorite (bleach), to clean or disinfect
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**CLINICAL REPORT**
Australian Dental Journal 2000;45:(4):257-269
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Safety issues relating to the use of hydrogen peroxide
in dentistry
Laurence J. Walsh*
Abstract
Hydrogen peroxide is used widely in professionally
and self-administered products. Hydrogen peroxide
is a highly reactive substance which can damage
oral soft tissues and hard tissues when present in
high concentrations and with exposures of
prolonged duration. This report provides an
overview of health issues relating to the use of
hydrogen peroxide, with an emphasis on safety
with prolonged exposure to low concentrations of
peroxide products. There is good evidence for the
safety of hydrogen peroxide when used at low
concentrations on a daily basis over extended
periods of time, in self-administered oral health
care products such as dentifrices and mouthrinses.
These low concentrations neither damage oral hard
or soft tissues, nor do they they pose a significant risk of
adverse long-term effects. Caution should be
exercised with the increasingly higher concentration
peroxide products used for 'walking' or 'power'
bleaching due to the possibility of chemical irritation
of oral soft tissues with injudicious use. The
volumes of material and application times should
be controlled carefully. Thorough education of
patients is particularly important with self-applied
gels because of the lack of professional supervision
with such products. Such education is part of the
duty of care of the dentist who supplies bleaching
gels for at-home use.
**Key Words:** Dentifrice, bleaching, peroxide, toxicity.
applied bleaching agents which either contain or
generate hydrogen peroxide, by both the dental
profession and the general public. The most
common ingredient used is carbamide peroxide,
which when present at a concentration of 10 per
cent releases 3.5 per cent hydrogen peroxide.
While hydrogen peroxide can be toxic in high
concentrations and with exposures of prolonged
duration, concentrated (30-35 per cent) hydrogen
peroxide solutions have been used for in-office
bleaching treatments with no serious adverse soft
and hard tissue effects observed clinically, other than
the relatively common but self-limiting post-treat-
ment sensitivity. Nevertheless, there have been
occasions when accidental ingestion of hydrogen
peroxide products in the home has led to
hospitalization and adverse health outcomes, and
this should be kept in mind when assessing the
relative safety of hydrogen peroxide-containing
products for home (unsupervised) use.
Much of the recent dental literature on the safety
of hydrogen peroxide has focused on dentist-
prescribed home bleaching, in which the teeth and
oral soft tissues can be in contact with peroxide-type
agents for extended periods of time. This provides a
very different situation from either in-office bleaching
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**Nicotinic stomatitis**
* Nicotine stomatitis occurs in smokers and results from exposure of the palate to the smoke and heat of burning tobacco products.
* It generally appears as a thick, white plaque of the hard and soft palate, containing scattered, tiny, raised red (erythematous) dots. The erythematous dots represent irritated minor salivary gland ducts.
* Nicotine stomatitis persists as long as the individual continues smoking. The lesion itself is benign and will regress upon smoking cessation.
Histological image of glandular skin structures with dermal and epidermal layers.
**Pyogenic granuloma**
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• *Pyogenic granulomas* are exophytic
lesions composed of an exuberant
overgrowth of granulation tissue in
response to minor chronic irritation.
• The name is inaccurate because it is
not due to pyogenic (pus-producing)
bacteria and is not granulomas.
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**Traumatic fibroma**
* Traumatic (irritation) fibromas are benign lesions with dense, highly fibrous connective tissue, like a scar.
* They are more appropriately called *focal fibrous hyperplasia* to denote a reactive rather than neoplastic origin.
* They occur anywhere that persistent chronic tissue irritation occurs, most often along the line of occlusion, where repetitive trauma from biting may occur.
* They may be sessile or pedunculated with a pink smooth surface
# **Drug-induced gingival hyperplasia**
* Drug-induced gingival overgrowth is considered a reactive phenomenon seen in patients taking medications that stimulate collagen growth or prevent its breakdown.
* It is well documented that phenytoin (Dilantin), cyclosporine, nifedipine, and other calcium channel blockers may lead to gingival overgrowth.
* Clinically, the lesions are similar and do not differ based on type of drug.
**JOURNAL OF**
**ORAL PATHOLOGY & MEDICINE**
<img src="image1.jpg" width="41" height="15" alt="Full Access checkbox"/> Full Access
**On the mechanism of drug-induced gingival hyperplasia**
Ronald S. Brown, William T. Beaver, William K. Bottomley
First published: May 1991 | https://doi.org/10.1111/j.1600-0714.1991.tb00419.x | Citations: 83
Find It@UWA
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**Volume 20, Issue 5**
**May 1991**
**Pages 201-209**
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References
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**Abstract**
Proposed mechanisms of the side effect of drug-induced gingival hyperplasia are
reviewed. Hypotheses with regard to inflammation from bacterial plaque, increased
sulfated glycosaminoglycans, immunoglobulins, gingival fibroblast phenotype population
differences, epithelial growth factor, pharmacokinetics and tissue binding, collagenase
activation, disruption of fibroblast cellular sodium/calcium flux, folic acid and a
combination hypothesis are evaluated.
**Recommended**
The effect of a plaque control program on
the development of phenytoin-induced
gingival overgrowth
Göran Dahllöt, Thomas Modéer
**Journal of Clinical Periodontology**
Prevalence and risk of gingival
overgrowth in patients treated with
diltiazem or verapamil
Jaume Miranda, Lluís Brunet, Pere Roset,
Leonardo Borini, Marí Farré
43
```markdown
**Flowchart: Management of Suspected Reactive Lesion**
1. Lesion suspected to be reactive
↓
2. Look for source of irritation
↓
├──> Suspected source identified and removed or relieved
│ ↓
│ Patient returns in 2–3 weeks
│ ↓
│ ├──> Lesion gone: continue observation
│ └──> Lesion still present: try again to remove suspected source
│ ↓
│ Patient returns in another 2–3 weeks: lesion still present
│ ↓
│ → Biopsy
↓
└──> No source identified or suspected: source cannot be removed or relieved
↓
→ Biopsy
```
References
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• Odell E. 2018. Cawson's Essentials of Oral Pathology and Oral
Medicine
• Woo SB. 2023. Oral Pathology. A Comprehensive Atlas and Text
• Sapp JP, Eversole LR, Wysocki GP. 2004. Contemporary oral and
maxillofacial pathology.
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**Quiz**
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**Questions**
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YOU HAVE ACUTE
GINGIVITIS.
THANK
YOU!
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