Ebook Textbook of oral pathology (2/E): Part 2

(BQ) Part 2 book “Textbook of oral pathology” has contents: Acquired immunodeficiency syndrome, odontogenic infection and pulp pathology, tongue disorders, temporomandibular joint pathology, chemical and physical injuries, blood pathology, skin disorders,… and other contents.

Acquired Immunodeficiency Syndrome

 Recurrent herpes labialis

 Oral human papilloma virus lesions

21

and HTLV-II) that are capable of oncogenic transformation and are usually associated with leukemia or lymphoma

The case of AIDS was detected in June 1981 when

5 young homosexuals men came with the suffering from rare lung infection due to microorganism called

Pneumocystis carinii In India, the first description of

AIDS came in Madras where 6 women out of 125 who were screened were HIV positive in high-risk group of prostitutes

The AIDS appear to be endemic in central and equatorial Africa and it may be old disease of Africa that has gone unrecognized The HIV-1 infection has also become the primary emphasis of effort at controlling

Acquired immunodeficiency syndrome (AIDS) is a

devastating fatal disease, which is in epidemic form

throughout the world It is an incurable viral STD caused

by human immunodeficiency virus (HIV) It stands for:

∙ A: Acquired, i.e contagious not inherited

∙ I: Immune, i.e power to receive disease

∙ D: Deficiency

∙ S: Syndrome, i.e number of signs and complains

indicative of particular disease

Four identified etiological agents are of substantially

lenti virus (HIV-I an HIV-II) that cause slow infection in

which sign and symptoms only appear after many months or

years of infection and two member of oncovirus (HTLV-I

 Herpes zoster

 HIV associated salivary gland diseases

 Idiopathic thrombocytopenic purpura

 Screening test for AIDS

 Enzyme-linked immunosorbant assay

 The Western Blot method

 Viral culture and polymerase chain reaction

 Surrogate marker for progression of HIV-I infection

 Management

Anil Govindrao Ghom, Shubhangi Mhaske (Jedhe)

∙ Invasive cervical cancer

∙ Disseminated or extrapulmonary coccidioidomycosis, extrapulmonary cryptococcosis

∙ Chronic intestinal cryptosporidiosis more than 1 month duration

∙ Cytomegalovirus retinitis with loss of vision

∙ HIV related encephalopathy

∙ Herpes simplex bronchitis, pneumonitis and esophagitis

∙ Kaposi sarcoma, Burkitt’s lymphoma and immunoblastic lymphoma

∙ Mycobacterium tuberculosis infection at any pulmonary

or extrapulmonary sites

∙ Pneumocystic carinii pneumonia and recurrent

pneumonia

∙ Progressive multifocal leukoencephalopathy

∙ Toxoplasmosis of brain and wasting syndrome

∙ Recurrent Salmonella septicemia

CD4 + T-cell categories A

Asymptomatic, acute HIV and PGL

B Symptomatic, not A or C conditions

C AIDS indicator condition

Category A: In adolescent less than 13 years with

documented HIV infection:

∙ Persistence generalized lymphadenopathy

∙ Active condition

Category B: Condition is attributed to HIV infection or

indicative of defect in the cell-mediated immunity

∙ Bacillary angiomatosis

∙ Oropharyngeal and vulvovaginal candidiasis

∙ Cervical carcinoma in situ

∙ Constitutional symptoms like fever (38.5˚C) and

diarrhea

∙ Oral hairy leukoplakia and herpes zoster

∙ Idiopathic thrombocytopenic purpura

Category C: AIDS indicative condition

∙ Candidiasis of bronchi, trachea or lung and esophageal

candidiasis

sexually transmitted diseases (STDs) Moreover, the

knowledge gain about sexual and other behavior associated

with transmission of HIV, as well as strategies that have

been effective in modifying those behaviors, is transferable

to other sexually transmittable and bloodborne infections

and has revolutionized standard approaches to the control

of these infections

Oral and perioral lesions are common presenting

features in patient with human immunodeficiency virus

and may have deterioration of general health and a poor

Absence of all known underlying causes of cellular immune deficiency (other than HIV infection) and absence

of all other causes of reduced resistance reported to be associated with at least one of those opportunistic diseases

CLASSIFICATION

1st Classification (given in 1993) by Center for Disease Control (CDC)

2nd Classification by USPHS-CDC

∙ Group I: Acute infection

∙ Group II: Asymptomatic infection

∙ Group III: Persistence generalized lymphadenopathy

∙ Group IV: Other disease

– Subgroup A: Constitutional diseases

– Subgroup B: Neurological diseases

– Subgroup C: Secondary infectious diseases

- C1: Specified secondary infectious diseases listed in CDC surveillance definition for AIDS

- C2: Other specified secondary infectious stages

– Subgroup D: Secondary cancer

– Subgroup E: Other conditions.

AIDS RELATED COMPLEX

For clinical and research studies, persons exhibiting

complex clinical problems and immunological or

hematological abnormalities on the laboratory tests, have

been classified as having AIDS related complex (ARC)

The ARC requires any two or more symptoms and two or

more abnormal laboratory findings It must be present for

at least 3 months

PREVALENCE

It is more common in Western countries particularly

in the United State Largest population of AIDS is in homosexuals, intravenous drug users and, heterosexuals with sexual contact with AIDS patient Patients who received transfusion of blood or blood pigments donated by the person with risk factors Ninety-two percent of victims are males, 6.5 percent female with 1 percent children It is common at the age of 25 to 49 years

Etiology

T lymphocytes: There is quantitative and qualitative

deficiency of T4 helper cells in AIDS patients, which lead

to certain investigators to focus their efforts on determining

if etiologic agent was a virus that manifested a particular tropism for T4 helper lymphocytes

HTLV-III virus: Dr Robent C Galleo determined

that type C retrovirus was tropic for T4 lymphocytes in adult T-cell leukemia/lymphoma He named the virus, Humans T-cell leukemia/lymphoma virus (HTLV–I) So

it is considered to be etiological agent for AIDS But as

it causes lymphoproliferation in T-cell leukemia, where as AIDS is a disease of lymphodepletion The answer came in the discovery of type D retrovirus of HTLV family that has been termed as HTLV-III

LAV virus: On the other hand, virus called

lymphadeno-pathy associated virus (LAV), was being isolated from the AIDS patient in Europe

HTLV-III and LAV is closely related members of same class of virus Finally, it is proved that HTLV and LAV are cytopathic human T–lymphocytotropic viruses that manifested selective infectivity for the helper/inducer subset of T-cells that as phenotypically designated reactivity with monoclonal antibody T4 or Leu3

HIV: In order to avoid different nomenclatures

retrovirus responsible for the AIDS are named ‘Human immunodeficiency virus’ which belong to family of retroviruses

Risk person: Six groups are at risk of developing AIDS

These are homosexuals or bisexuals—71.4 percent, intravenous drug users—18.4 percent, hemophilia, recipient of multiple blood transfusion, infant born of parents belonging to first three high-risk groups and heterosexual contacts of high-risk group

Symptoms Laboratory findings

• Decreased ratio of T helper cells to T suppressor cells

• Anemia or leukopenia

or thrombocytopenia or lymphopenia

• Increased serum globulin level

• Decreased blastogenic response of lymphocytes to mitogen

• Increased level of circulating immune complex

• Cutaneous anergy to multiple the skin test antigens

CHARACTERISTIC OF HIV VIRUS

The HIV is a spherical enveloped virus, about 90 to

120 nm in size (Fig 21.1) The nucleocapsid has an outer

icosahedral shell and inner cone shaped core, enclosing the

ribonucleoproteins The genome is diploid, composed of

two identical single stranded, positive sense RNA copies

Inside the envelope is a protein core, which contain enzymes

reverse transcriptase, intregrase, protease, etc all essential for

viral replication and maturation When the virus infects a cell,

the viral RNA is transcribed by the enzymes, first into single

stranded DNA and then to double stranded DNA (provirus),

which is integrated into the host cell chromosomes The virus

is extremely sensitive to heat, thus boiling and autoclaving are

very effective measure of inactivating the virus

Mechanism of Action

The HIV attacks the immune system of the body Due

to that an individual is not able to protect himself from

potentially harmful organism

Normal mechanism: Pathogenic viruses → identified

by macrophage → it activates T lymphocytes → it get

differentiated into effecter cell like T helper cell or T4

and T suppresser cell or T8 → T4 cells secrete various

lymphokines which induce lymphocyte to differentiated

into plasma cell → it secrete specific antibodies against

viral antigen → it destroy the virus

Mechanism in AIDS: HIV virus is lymphotropic virus

→ its primary target is T4 cell → when the virus enters the

bloodstream, it integrates into gene into DNA of some primary

T4 lymphocyte → this viral DNA then becomes integrated into the host chromosomes → the chromosomal integration

is prerequisite for replication of retroviruses, but also for the latency → once the viral genes are integrated into cells of own DNA, they can apparently remain dormant for an indefinite period of time, without causing its affects This is called

‘incubation period’ → once the viral gene is activated, virus particles convert T4 lymphocytes into AIDS virus factory →when the number of T4 lymphocyte is severely depleted, the immune system collapses and variety of infections occur → at this stage patient is said to have AIDS

Transmission

Repeated intimate contact: It is in 90 percent of cases

It depends upon number of sexual partners, receptive anal intercourse and presence of other STDs All these are in high-risk group Prostitution is a major heterosexual factor associated with AIDS

Use of contaminated blood products: Intravenous drug

users, HIV contaminated blood transfusion, blood clotting concentrate and organ transplantation

Perinatal transmission: It occurs in 13 percent among

children born to HIV seropositive mother

Other nosocomial routes: Transmission from patient to

patient due to reuse of contaminated and shared needles

Professional hazards: The risk of transmission from HIV

infected patient to health care workers is more than health care workers to patient

CLINICAL FEATURES (FIG 21.2)

Protozoan and helminthes infection: Crypto sporidiosis

(intestinal) causing diarrhea for over one month The

most common opportunistic infection is by Pneumocystis carinii which causes pneumonia CNS infection or other

disseminated infections and toxoplasmosis

Fungal infection: Candidiasis causing esophagitis,

cryptococcosis causing CNS infection, disseminated histoplasmosis and bronchial or pulmonary candidiasis

Bacterial infections: Mycobacterium avium intra cellulare

causing infection disseminated beyond lung and lymph

node Mycobacterium tuberculosis will cause tuberculosis

Viral infections: Cytomegalovirus causing infection in the

internal organs other than liver, spleen and lymph nodes Herpes simplex virus, causing chronic mucocutaneous infection with ulcers persisting more than one month

Figure 21.1 HIV virus

Malignancy: Kaposi’s sarcoma and squamous cell

carcinoma Lymphoma limited to bronchi and non-

Hodgkin’s lymphoma

AIDS dementia complex: This occur in patient with HIV

infection and causes progressive encephalopathy

ORAL MANIFESTATIONS

Oral manifestations of HIV disease are common and

include oral lesions and novel presentations of previously

known opportunistic diseases

Careful history taking and detailed examination

of the patient’s oral cavity are important parts of the

physical examination and diagnosis requires appropriate

investigative techniques

Early recognition, diagnosis and treatment of

HIV-associated oral lesions may reduce morbidity The

presence of these lesions may be an early diagnostic

indicator of immunodeficiency and HIV infection may

change the classification of the stage of HIV infection and

is a predictor of the progression of HIV disease Around 95

percent of AIDS patients have head and neck lesions and

about 55 percent have important oral manifestation They

are described below

Oral Disorders in HIV Disease

∙ FungalMore common – Candidiasis Less common – Aspergillosis – Histoplasmosis – Cryptococcus neoformans

– Geotrichosis

∙ Bacterial More common– HIV gingivitis – HIV periodontitis– Necrotizing gingivitis Less common

– Mycobacterium avium intracellulare

Figure 21.2 Features of HIV infection

– Recurrent apthous ulceration

– Progressive necrotizing ulceration

– Lichenoid and other drug reaction

EC-Clearinghouse Classification of Oral

∙ Periodontal disease (linear gingival erythema,

necrotizing gingivitis and necrotizing periodontitis)

Group II—less commonly associated with HIV infection

∙ Bacterial infection (Mycobacterium)

∙ Melanotic hyperpigmentation

∙ Necrotizing ulcerative stomatitis

∙ Salivary gland disease

∙ Thrombocytopenia purpura

∙ Oral ulceration NOS (not otherwise specified)

∙ Viral infections like herpes simplex, zoster, papillomavirus

Group III—seen in HIV infection

∙ Bacterial infection (Actinomyces israelii, E coli, Klebsiella pneumonia)

∙ Cat scratch disease

∙ Epithelioid angiomatosis

∙ Drug reaction

∙ Fungal infection other than candidiasis

∙ Neurologic disturbance

∙ Recurrent aphthous stomatitis

∙ Viral infection like cytomegalovirus, molluscum contagiosum

Candidiasis

Oral candidiasis is most commonly associated with Candida albicans, although other species, such as C glabrata and

C tropicalis, are frequently part of the normal oral flora

A number of factors predispose patients to develop

can-didiasis: infancy, old age, antibiotic therapy, steroid and

oth-er immunosuppressive drugs, xoth-erostomia, anemia, endocrine disorders and primary and acquired immunodeficiency

Candidiasis is a common finding in people with HIV infection Reports describe oral candidiasis during the acute stage of HIV infection, but it occurs most commonly

with falling CD4+ T-cell count in middle and late stages of

HIV disease

Several reports indicate that most persons with HIV

infection carry a single strain of Candida during clinically

apparent candidiasis and when candidiasis is quiescent

Clinical Features

Location: Patient with a HIV usually has lesion of hard palate and soft palate

Appearance: The clinical appearances of oral

candi-diasis vary The most common presentations include

pseudomembranous, hyperplastic, angular, and

erythe-matous candidiasis, which are equally predictive of the

development of AIDS and angular cheilitis (Fig 21.3)

Symptoms: These lesions may be associated with a variety

of symptoms, including a burning mouth, problems in

eating spicy food and changes in taste All three of these

common forms may appear in one individual

Pseudomembranous candidiasis (Thrush):

Charac-teristic creamy white, removable plaques on the oral

mucosa are caused by overgrowth of fungal hyphae mixed

with desquamated epithelium and inflammatory cells The

mucosa may appear red when the plaque is removed This

type of candidiasis may involve any part of the mouth or

pharynx

Erythematous candidiasis: Erythematous candidiasis

appears as flat, red patches of varying size It commonly

occurs on the palate and the dorsal surface of the tongue

Erythematous candidiasis is frequently subtle in appearance

and clinicians may easily overlook lesions, which may

persist for several weeks if untreated

Angular cheilitis: Angular cheilitis appears clinically

as redness, ulceration and fissuring, either unilaterally or

bilaterally at the corners of the mouth It can appear alone

or in conjunction with another form of candidiasis

Histopathological Features

Candida is a commensal organism in the oral cavity

Candidiasis is diagnosed by its clinical appearance and

by detection of organisms on smears Smears taken from

clinical lesions are examined using potassium hydroxide (KOH), PAS, or Gram’s stain

Smear shows candidal organism embedded in superficial keratin

Management Topical clotrimazole is treatment option in case of

candidiasis associated with HIV infection

Systemic fluconazole is given if the CD4+ count is below

50 cell/mm3 In some patient itraconazole and intravenous amphotorecin B are given to combat severe infection

Points to Remember

C glabrata and C tropicalis, falling CD4+ T-cell count,

pseudomembranous, hyperplastic, angular, and matous candidiasis, burning mouth, smears, embedded

erythe-in superficial keraterythe-in, topical clotrimazole, systemic conazole, itraconazole and intravenous amphotorecin B

flu-Kaposi’s Sarcoma

It is also called angioreticulo-endothelioma It is the most

common tumor associated with AIDS and occurs in 1/3rd

of AIDS patients

Etiology

There is higher incidence of Kaposi’s sarcoma is in homosexual men with AIDS as compared to heterosexuals with AIDS It has been suggested that there is transmissible agent prevalence in homosexual population, which stimulate certain factor such as angiogenesis protein that may be critical in the pathogenesis of neoplasm

The patient with AIDS often shows clustered lesion

in the oral cavity, which suggests direct inoculation of

mucosa with sexually transmitted agent

Some theories suggests role of cytomegalovirus in

the pathogenesis of Kaposi’s sarcoma, but studies on prevalence of antibodies to cytomegalovirus in patient with classic and epidemic Kaposi’s sarcoma have failed to demonstrate role of cytomegalovirus

Nowadays, it has been stated that Kaposi’s sarcoma is

associated with human herpes virus (HHV 8) The HHV 8

is detected in oral epithelial cells and in oropharynx

Types

• Classic

• African (cutaneous variant)

• African (lymphadenopathy variant)

• Kaposi’s sarcoma associated with AIDS

Figure 21.3 Candidiasis in AIDS patient

Epidemiology and Form

Kaposi’s sarcoma appears in various forms like classic,

African (cutaneous variant), African (lymphadenopathy

variant) and Kaposi’s sarcoma associated with AIDS

Classic type is a rare neoplasm and occurs in the older

man Usually, it appears as blue-black macule on the lower

extremities It is slow growing and rarely involves the

lymph nodes and visceral organs

African Kaposi’s sarcoma is considered an endemic

disease and affects children, 10-year-old or younger

patients, more common in men than women It appears as

exophytic growth located in legs and arms This form is

locally aggressive and lymph nodes involvement is rare

The lymphadenopathic form occurs in children of 10 years

age and younger with same frequency in men and women

The visceral and massive nodal involvement is common

Kaposi’s sarcoma is observed in patients with kidney

transplantation and in patients who receive the

immuno-suppressive drugs for variety of diseases Drugs such as

prednisolone, cyclosporine and cyclophosphamide have

been associated with development of Kaposi’s sarcoma

It usually affects legs, arms, lymph nodes and visceral

organs

Clinical Features

Age and sex distribution: It is more common in male as

compared to female in ratio of 20:1 It can occur at any age

but most common in 5th, 6th, 7th decade except in Africa

where it more common in children

Site: Commonly affects skin, oral and visceral organs It

occurs commonly in head and neck region Tip of nose is

peculiar and frequent location of it It can involve lymph

nodes, soft tissue, extremities, GIT, lung, liver, pancreas,

spleen and adrenal gland

Appearance: It begins as multinucleated neoplastic

process that manifests as multiple red or purple macules

and in more advanced stage, a nodule occurring on the skin

or mucosal surface

Sign: Size of it ranges from a few millimeters to a centimeter

or more in diameter and are usually tender on palpation It

is slow growing but can behave as a very aggressive lesion

with rapid visceral involvement

Oral Manifestations

Location: It has tendency to involve the oral cavity, with

hard palate as the most common site But lesions may occur

on any part of the oral mucosa including the gingiva, soft palate, buccal mucosa and in the oropharynx It can involve either alone or in association with skin and disseminated lesions It may be the first symptom of AIDS

Appearance: It can appear as a red, blue, or purplish lesion

It may be flat or raised solitary or multiple Occasionally, yellowish mucosa surrounds the lesion The lesions may enlarge, ulcerate and become infected Good oral hygiene

is essential to minimize these complications

Sign: It may vary in size from few millimeter to a centimeter

or more in diameter and are tender and painful

Histopathological Features

It consists of interweaving band of spindle shaped and

or plump endothelial cell and atypical vascular channels,

enmeshed in reticular or collagen fibers

It consists of numerous, small capillary type blood vessels, which may or may not contain blood Inflammatory cell infiltration is common (Fig 21.4)

In late stage, lesion consists of well defined nodules or lesions with diffuse involvement of the lamina propria

Histopathological Stages

• Patch stage (macular): In this proliferation of

miniature vessels

• Plaque stage: It shows further proliferation of

vascular channels with development of spindle cells

• Nodular stage: Spindle cell increase to form nodular

tumor like mass

Figure 21.4 Capillary blood cell seen in Kaposi’s sarcoma

Management

Treatment is determined on the basis of the number, size

and location of the oral lesions The choice of therapy

depends on the effect of treatment on the adjacent mucosa,

pain associated with treatment, interference with eating

and speaking and the patient’s preference

It is important to perform thorough dental prophylaxis

before initiating therapy for lesions involving the gingiva

Response to therapy is improved if all local plaque and

calculus are removed Local application of sclerosing

agents may reduce the size of oral lesions

Local treatment is appropriate for large oral lesions that

interfere with eating and talking Oral lesion can be treated

surgically or with localized intralesional chemotherapy

Intralesional vinblastine, radiation therapy,

intra-venously interferon alpha and sclerotherapy with 3 percent

sodium tetradecyl sulfate

Points to Remember

Angioreticulo-endothelioma, affects skin,

multinucle-ated neoplastic process that manifests as multiple red or

purple macules, hard palate, most common site, red, blue,

or purplish lesion, yellowish mucosa surrounds the lesion,

spindle shaped and or plump endothelial cell, numerous,

small capillary type blood vessels, Inflammatory cell

infiltration, thorough dental prophylaxis, intralesional

vinblastine, radiation therapy, intravenously

Hairy Leukoplakia

Oral hairy leukoplakia, which presents as a non-movable,

corrugated or “hairy” white lesion on the lateral margins

of the tongue occurs in all risk groups for HIV infections,

although less commonly in children than in adults

It occurs in about 20 percent of persons with

asymptomatic HIV infection and becomes more common

as the CD4+ T-cell count falls

Etiology

Exact etiology is not known but Epstein-Barr virus has

identified in these lesions

One hypothesis is that basal epithelial cells of lateral

margin of tongue normally harbors EBV in majority of

adult population, who are EBV sero-positive and carrier of

that disease

It is found primarily in homosexual male Direct

infection of Langerhans cell due to HIV induced loss of

factor essential for their integrity and function, permit

reactivation of EBV with frequent epithelial hyperplasia

Clinical Features

Location: It is unique and significant lesion which

primarily occurs unilaterally or bilaterally on the lateral border of tongue It can also occur on dorsum of the tongue, buccal mucosa, floor of mouth, retromolar area and soft palate Many time lesion start on lateral border and spread

to entire dorsum of tongue

Appearance: There is characteristic corrugated and

white appearance It does not rub off and may resemble the keratotic lesion The surface is irregular and may have prominent folds or projections, sometimes markedly resembling hairs Occasionally, however, some areas may

be smooth and flat (Fig 21.5)

Pseudo hairy leukoplakia: Sometimes, the white lesion

satisfies many criteria for diagnosis of hairy leukoplakia, but if EBV not present this is called ‘pseudo hairy leukoplakia’ Presence of hairy leukoplakia is fairly indicator of HIV pro-sensitivity and is predictor of deficiency immunocompetence

Histopathological Features Histologically lesion shows hyperkeratosis, acanthosis,

contain Epstein-Barr virus and no or minimum mmation

infla-Balloon cells: The epithelial exhibits band-like zone of

lightly stained cells with abundant cytoplasm in the upper spinous layer

Nuclear beading: There is presence of scattered cells with

nuclear clearing with pattern of peripheral margination of

Figure 21.5 Hairy leukoplakia showing characteristic

corrugated appearance

chromatin on superficial epithelium This is called nuclear

beading

Immunochemistry tissue in situ hybridization,

non-invasive tissue in situ hybridization, or electron microscopy

does demonstrate of Epstein-Barr virus The lesion of

leukoplakia consists of Langerhans cells.

Management

Hairy leukoplakia usually is asymptomatic and does not

require treatment Hairy leukoplakia is almost always a

manifestation of HIV infection and clinicians should arrange

evaluation of HIV disease and appropriate treatment for

patients with hairy leukoplakia

Hairy leukoplakia has disappeared in patients receiving

high-dose acyclovir for herpes zoster, presumably because

of the anti-EBV activity of acyclovir Doses of acyclovir

(2.5–3 mg per day for 2–3 weeks) usually eliminate HL, but

the lesion usually recurs with cessation of treatment

Elimination or almost complete clinical resolution of

the lesion has occurred in patients treated with agents such

as desciclovir (an analog of acyclovir), phosphonoformate,

Retin A and podophyllin resin, although lesions tend to

recur within few months Occasionally, Candida albicans

may be found in HL lesions

Antifungal medications like topical clotrimazole,

topical nystatin 10000 unit/g 5 times a day can be given

Systemic agent like ketoconazole 200 mg BD a day,

acyclovir, azidothymidine and retinoid acid podophyllin

resin can also be given

Points to Remember

Nonmovable, corrugated or hairy white lesion on the

lateral margins of the tongue, Epstein-Barr virus, does

not rub off, pseudo hairy leukoplakia, hyperkeratosis,

acanthosis, balloon cells, nuclear beading, demonstrate

of Epstein-Barr virus, Langerhans cells, high-dose

acyclovir, desciclovir, phosphonoformate, Retin A,

podophyllin resin, antifungal medications like topical

clotrimazole, topical nystatin 10000

Periodontal Disease Associated with HIV

Periodontal disease is a fairly common problem in both

asymptomatic and symptomatic HIV-infected patients

Form

• Linear gingival erythema

• Necrotizing ulcerative gingivitis

• Necrotizing ulcerative periodontitis

Clinical Features

Site: It often occur in clean mouths, where there is very

little plaque or calculus to account for the gingivitis

Sign: The onset is often sudden, with rapid loss of bone and

soft tissue Patients sometimes complain of spontaneous bleeding

Linear gingival erythema: In this condition gingiva may

be reddened involving the free gingival margin There is linear band of erythema which can extend 3 mm apically The diagnosis of this should be done if gingivitis does not respond to improved plaque control (Fig 21.6)

Necrotizing ulcerative gingivitis: In these ulcers

occurs at the tips of the interdental papilla and along the gingival margins and often elicits complaints of severe pain The ulcers heal, leaving the gingival papillae with a characteristic cratered appearance

Necrotizing ulcerative periodontitis may present as

rapid loss of supporting bone and soft tissue Typically, these losses occur simultaneously with no formation of gingival pockets, sometimes involving only isolated areas

of the mouth Teeth may loosen and eventually fall out, but uninvolved sites can appear healthy There is loss of more than 6 mm attachment

Necrotizing stomatitis may develop and areas of

necrotic bone may appear along the gingival margin The bone may eventually sequestrate Patients with necrotizing ulcerative periodontitis and necrotizing stomatitis frequently complain of extreme pain and spontaneous bleeding

Figure 21.6 Linear gingival erythema

Management

Clinicians should refer patients to a periodontist or dentist

for management

The following protocol has achieved reasonable

success: plaque removal, local debridement, irrigation

with povidine-iodine, scaling and root planning and

maintenance with a chlorhexidine mouth rinse once or

twice daily

The use of systemic antibiotics like metronidazole has

been given in patient which has got extensive involvement

Points to Remember

Linear gingival erythema, necrotizing ulcerative

gingivitis, necrotizing ulcerative periodontitis,

necro-tizing stomatitis, plaque removal, local debridement,

irrigation with povidine-iodine, scaling and root

planning, metronidazole

Non-Hodgkin Lymphoma

This is the second most common malignancy in HIV

infection It may cause by EBV virus infection and HHV 8.

Clinical Features

Site: It is seen in extranodal location CNS is the most

common site of involvement Intraorally, it can be seen on

gingiva, palate, tongue, tonsil, and maxillary sinus

Sign: There is loss of periodontal attachment and loosening

of teeth

Appearance: There is erythematous and soft tissue

enlargement seen in oral cavity

Management

Combination of chemotherapy and radiotherapy is

effective

Points to Remember

EBV virus infection and HHV 8, CNS involvement,

gingiva, loss of periodontal attachment, erythematous and

soft tissue enlargement, chemotherapy, radiotherapy

UNCOMMON ORAL MANIFESTATION

OF HIV

Recurrent Herpes Labialis

Recurrent herpes labialis mainly appears as herpes labialis

and recurrent intraoral herpes It is cause by HSV

Appearance: Herpes labialis occurs as characteristic lip

lesion consisting of vesicles on an erythematous base that

heals within 7 to 10 days The recurrent herpes labialis (RHL) are small, shallow, irregular and erosive-like lesion that may coalesce and seen to occur only on keratinized epithelium like that of gingiva, hard palate or dorsal surface

HSV, vesicles on an erythematous base, antiviral drugs

Oral Human Papilloma Virus Lesions

It is cause by human papilloma virus Oral warts, papillomas, skin warts and genital warts are associated

with the human papilloma virus (HPV) lesions Because the HPV types found in oral lesions in HIV-infected persons are different from the HPV types associated with anogenital warts, clinicians should probably not use the term condyloma acuminate to describe oral HPV lesions

Location: Lesions caused by HPV are common on the skin

and mucous membranes of persons with HIV disease Anal warts have frequently been reported among homosexual men It can be found on any mucosal surface and are contagious to both host and sex partner

Appearance: HPV lesions in the oral cavity may appear

as solitary or multiple nodules They may be sessile or pedunculated and appear as multiple, smooth-surfaced

raised masses resembling focal epithelial hyperplasia or as multiple, small papilliferous or cauliflower-like projections Histopathologically lesion is sessile or papillary which is covered by acanthotic or hyperplastic stratified squamous epithelium Affected epithelium demonstrated

vacuolization of numerous epithelial cells which is called

Herpes Zoster

It occurs more frequently in HIV infected patients and

carries poor prognosis

The occurrence of unilateral vesicles that break and

scab is characteristic of this infection They are

self-limiting When herpes zoster infection involvements occur

intraorally, it will lead to sequestration of bone with loss of

teeth.

Main complication is neuropathy after inflammation

Diagnosis is made by cytological smear and finding of

multinucleated giant cells

Management

Systemic acyclovir 800 mg orally or 15 to 30 mg/kg/day

IV 8 hourly for 10 to 15 days

Points to Remember

Occurrence of unilateral vesicles, sequestration of bone,

loss of teeth, neuropathy, systemic acyclovir

HIV Associated Salivary Gland Diseases

Salivary gland disease associated with HIV infection

(HIV-SGD) can present as xerostomia with or without salivary

gland enlargement Reports describe salivary gland

enlargement in children and adults with HIV infection

usually involving the parotid gland

The etiology of HIV-SGD is as yet unknown It has

been postulated that cytomegalovirus infection has got

predilection for salivary glands Cytomegalovirus infection

produces inflammation which causes reduced salivary

production

Sign: The enlarged salivary glands are soft but not

fluctuant, but the enlarged parotid glands can be a source

of annoyance and discomfort

Xerostomia is sometimes seen in individuals with

HIV-SGD HIV-infected patients may also experience dry

mouth

Diffuse infiltrative lymphocytosis syndrome: It is seen

in HIV infected salivary gland disease There is salivary

gland enlargement The glandular involve ments result from

infiltration of CD8 lymphocytes

Management

Antiretroviral therapy is useful in this case Removal of

the enlarged parotid glands is rarely recommended For

individuals with xerostomia, the use of salivary stimulants such as sugarless gum or sugarless candies may provide relief Candies that are acidic should be avoided as frequent use may lead to loss of tooth enamel The use

of salivary substitutes may also be helpful An increase

in caries can occur, so fluoride rinses (that can be bought over the counter) should be used daily and visits to the dentist should occur two to three times per year

Points to Remember

Xerostomia, parotid gland, cytomegalovirus infection, enlarged salivary glands, diffuse infiltrative lymphocytosis syndrome, antiretroviral therapy

Idiopathic Thrombocytopenic Purpura

Reports have described idiopathic thrombocytopenic purpura (ITP) in HIV-infected patients It can be cause by

direct infection by HIV, immune dysfunction, alteration of platelet production and drug reaction

Oral lesions may be the first manifestation of this

condition Petechiae, ecchymosis and hematoma can occur

anywhere on the oral mucosa

Spontaneous bleeding from the gingiva can occur and

patients may report finding blood in their mouth on waking

Management

HAART has reduced the prevalence of thrombocytopenia Other approach like splenectomy, intravenous immuno-globulin, platelet transfusion is given

Points to Remember

Infection by HIV, immune dysfunction, alteration of platelet production, petechiae, ecchymosis and hematoma, spontaneous bleeding

Diagnosis: It is difficult as maximum cases do respond

to tuberculin skin test Confirmative diagnosis is done by AFB stained section of biopsy material

Management

Triple drug regimen is used It includes rifampicin,

isoniazid, and pyrazinamide with ethambutol

There is increase melanin pigmentation occur in basal

layer of affected epithelium

In some cases, adrenocortical destruction occur due to

HIV resulting in addisonian pattern of pigmentation

Histoplasmosis

It is cause by Histoplasma capsulatum It is most common

type of fungal infection seen in patient with HIV other than

candidiasis

Sign: There is fever, splenomegaly and pulmonary

infiltrate

Appearance: Orally, it is presented as indurated mucosal

ulceration with raised border

Histopathologically, fungal organism are visible within

the cytoplasm of histiocytes and multinucleated giant cells

Management

Intravenous amphotericin B is useful in this case

Recurrent Aphthous Stomatitis

In HIV infection all three forms of aphthous ulceration like

minor, major and herptiform is seen

There is well defined ulceration seen in the oral cavity

Management

It is done with the help of topical and intralesional

corticosteroids

Molluscum Contagiosum

It is infection of skin cause by pox virus

Location: It is seen on genital, trunk and facial region

Appearance: Lesion are small, waxy, dome-shaped

papules with center depressed crater In HIV infection, this

are hundred in number

Histopathologically surface epithelium forms several

hyperplastic down growth There is presence of molluscum bodies which are large intracytoplasmic inclusion

Management

There is resolution of lesion after giving HAART therapy

Oral Squamous Cell Carcinoma

Squamous cell carcinoma of oral cavity, pharynx, and larynx has been seen in the HIV infected patients The HIV infection accelerated the development of squamous cell carcinoma due to impaired immune surveillance

To ensure accurate differential diagnosis and

appro-priate treatment of the oral lesions those are associated with development of AIDS

To assess the risk to dental health care worker (HCW)

after needle stick or other injury from contaminated once

by contact with patients blood and saliva

To convey with communicable disease control (CDC)

guideline that all HCW engaging in invasive dental practice should be aware of HIV antibody status

SCREENING TEST FOR AIDS Enzyme-linked Immunosorbent Assay (Fig 21.7)

Enzyme-linked immunosorbent assay (ELISA) is a color reaction test in which prepared whole HTLV III virus

particle which acts as antigen, will bind with antibodies to HTLV III in an infected human serum

Then this complex is added to goat antihuman antibody

labeled with chemical enzymes, which gives color reaction

with particular chemicals e.g orange color with peroxides labeled goat antihuman antibody.

ELISA test is simple and convenient to perform; it is very sensitive for small amount of HTLV III antibodies and in initial screening tests

It is not 100 percent reliable because it is not completely

specific only for HTLV II antibodies and reacts with other

related viral antibodies and other nonspecific chemicals

giving false positive result of about 5 to 25 per 1000

patients

In case of positive test, there is strong indication of past

exposure and infection with virus but this does not show

whether the patient is infectious because it does not show

whether virus is still active or has been destroyed

The Western Blot Method

The prepared HTLV III virus particles consists of specific

HTLV III specific proteins separated by a process called

electrophoresis and subsequent transfer of nine protein

bands to nitrocellulose membrane strip, which are reacted

with patient’s serum followed by an enzyme linked

antihuman antibody and enzyme substance

Positive test is indicated when the treated, i.e

HTLV-III specific nitrocellulose strip are exposed to infected

human serum and a goat antihuman antibody strip display

the characteristic band detected for each of three (env, pol

and gag) group of viral protein on exposure to X-ray film

Those that react with only one of these three groups

of antigens are termed indeterminate and those react with

only non viral proteins are negative

It is more specific for HTLV III antibodies and is used

to eliminate false positive result

Viral Culture and Polymerase Chain Reaction

Cultivation of HIV from blood and other body fluids and

tissues with detection of the increased filter by either HIV

antigen or reverse transcriptase assay provide method that specifically demonstrates the presence of virus in given patient or specimen

The variable amount of virus present in peripheral blood monocytes at different stage of infection and degree

of immunosuppression both influence the extent HIV-I viremia

Polymerase chain reaction technique has provided

an opportunity for detection of very small amount of an infectious agent like HIV-I based on reported cycle of enzymatic duplication of number of copies of either DNA

or RNA specific for microorganism

Surrogate Marker for Progression of HIV-I Infection

The absolute CD4+ T-cell lymphocyte count correlate best with progression of HIV-I related immune dysfunction Other serum neoprotein beta-2-microreceptor HIV P24antigen interleukin-2 receptor IgA and impaired delayed type of sensitivity are also used

MANAGEMENT

Various drugs are used for immunotherapy are as follows:

Interferon: It is a useful therapeutic agent in this

syndrome of infection and neoplasms in view of their antiviral antiproliferative and immunomodulater activity The interferon is a glycoprotein produced by a number of different types cells Type I interferon (alpha and beta) are produced by leukocytes and fibroblasts Type II interferon (gamma) is produced by lymphocytes and monocytes Low doses of interferon enhance the antibody formation and lymphocyte blastogenesis They also prolong cell cycle and cause inhibition of intracellular enzyme system (antineoplastic effect) The gamma interferon stimulate macrophage oxidative metabolism and have antimicrobial effect

Thymic replacement therapy: The thymic epithelium

plays an important role in transformation of blood borne precursor cell into mature T-cells Thymic hormones or factor mediates this effect, since the immune system in AIDS is characterized by numerical and functional defects

of T-cell lymphocytes, it will correct the immune defect Transplant of fetal thymus of cultural thymic epithelium and injection of thymic hormone have been successfully utilized in treatment of AIDS

Figure 21.7 ELISA kit for detection of AIDS

Lymphokines and cytokines: Lymphokines are materials

produced by lymphocyte Interleukin-I is macrophage

product In in vitro system interleukin-I enhance plague

forming cells responses and the generation of cytotoxic

T-cell alloantigen In the presence of macrophage,

interleukin-1 stimulates the production of interleukin-2,

which stimulates and maintains the growth of T-cell

activated by antigens Various studies have conformed

that purified interleukin-2 (which stimulate and maintain

growth of T-cell activated by antigen), preparation in

in vitro system can normalize lymphocyte reaction

in high percentage of individuals with unexplained

lymphadenopathy and immunologic abnormalities, but the

result are not significant in patients with AIDS

Bone marrow transplantation: Syngeneic (identical

twin) allogenic (HLA/NHC matched) bone marrow

transplantation has been successful in reconstituting

immune function in the patients with severe congenital

immune defects If this could be therapeutic in patient with

AIDS that have appropriate marrow donor

Monoclonal antibodies therapy: In this, antibodies are

directed against T-cell differentiation antigens as a result

of that number of circulating leukemic cells are decreased

in patients with adult T-cell active lymphoblastic

leukemia

Pharmacological immunomodulation: Amitidine,

isoprinosine and retinoid are also used but results are

insignificant

Intravenous immunoglobulin therapy: It reduces

incidence of bacterial and viral infection Infusion of

hyperimmune gamma globulin enriched for neutralizing

antibodies for LAV/HTLV-III could prove beneficial

for individuals with AIDS or ARC who have inadequate

specific antibodies

Antiviral drug HPA–23: It is an oraganometallic

compound of tungsten and antimony, azidothymidine It is

analogs of thymidine It appears to inhibit multiplication

of HTLV-III virus and cyclosporine It shows marked

increase in T lymphocyte population

HAART therapy—nowadays introduction of highly

active antiretroviral therapy (HAART) results in long

survival of the patient The HAART includes two

nucleoside analog reverse transcriptase inhibitor, at least

one protease inhibitor and/or one non-nucleoside analog

reverse transcriptase inhibitor Nucleoside analogue

reverse transcriptase inhibitors, which are used are abacavir, didanosine, emtricitabine, lamivudine, stavudine Non-nucleosides used are capravirine, delavirdine, efavirenz and nevirapine Protease inhibitor used is amprenavir, darunavi, indianvir, tipranvir

PREVENTION

∙ Educational counseling of general public

∙ Avoid sexual contact with suspect and in high-risk group

∙ Use of disposable syringes and needles

∙ Blood donor should be properly screened

∙ Avoid multiple sex partners, intimate kissing and oral contact

∙ Educate healthcare workers on safety measures

BIBLIOGRAPHY

1 Baccaglini L, Atkinson JC, Patton LL, et al Management

of oral lesion in HIV positive patients: Oral Surg Oral Med Oral Pathol Oral Radiol 2007;103(Supp 1);S50.e1-23

2 EC:Clearinghouse on oral problems related to HIV infection and WHO collaborating center on oral manifestation of immunodeficiency virus: classification and diagnostic criteria for oral lesion in HIV infection J Oral Pahtol Med; 1993;22:289-91

3 Epstein JB, Cabay RJ, Glick M Oral malignancies in HIV disease: change in disease presentation, increasing understanding of molecular pathogenesis and current management Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2005;100:571-8

4 Frezzini C, Leao JC, Porter S Current trends in HIV disease

of mouth J Oral Pathol Med 2005;34:513-31

5 Greenspan D, Greenspan JS Significance of oral hairy leukoplakia: Oral Surg Oral Med Oral Pathol 1992;73:151-4

6 Holmstrup P, Westergaard J HIV infection and periodontal disease: periodontal 1998;18:37-46

7 Lager I, Altini M, Coleman H Oral Kaposi’s sarcoma: a clinicopatholgoic study from south Africa Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2003;96:701-10

8 Miziara ID, Weber R Oral candiadisis and oral hairy leukoplakia as predictor of HAAAT failure in Brazilian HIV infected patients Oral Dis 2006;12:402-7

9 Neville BW, Damm DD, Allen CM, Bouquot JE Oral and maxillofacial pathology, 3rd edn, Saunder Elsevier; 2009

10 Piluso S, Ficarra G, Lucatorto FM, et al Cause of oral ulcer

in HIV infected patients: a study on 19 cases Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1996;82:166-72

MULTIPLE CHOICE QUESTIONS

5 Causative organism for hairy leukoplakia is:

c Rota virus d None of the above

6 ELISA is a:

a Color reaction test b Electrophoresis test

7 Balloon cells and nuclear beading are seen in:

a Hairy leukoplakia

b Pseudo hairy leukoplakia

c Non-Hodgkin’s lymphoma

d All of the above

8 The following are the histopathological stages of Kaposi’s sarcoma except:

a Patch stage b Plaque stage

c Nodular stage d Bullous stage

d None of the above

3 Most common fungal oral manifestation of HIV is:

a Kaposi’s sarcoma b Candidiasis

4 Most common tumor associated with AIDS is:

a Squamous cell carcinoma

b Hodgkin’s lymphoma

c Non-Hodgkin’s lymphoma

d Kaposi’s sarcoma

Odontogenic Infection and Pulp Pathology

 Acute suppurative osteomyelitis

 Chronic suppurative osteomyelitis

life-Infection is a clinicopathological entity involving invasion

of the body by pathogenic microorganisms and reaction of

the tissues to microorganisms and their toxins

Soft tissue infections of head and neck are commonly

encountered in routine practice in dentistry These

infections may be odontogenic or nonodontogenic in

origin Once the infection extends past the apex of the

tooth the pathophysiology of the infectious process

can vary, depending upon the number and virulence of

 Infantile osteomyelitis

 Diffuse sclerosing osteomyelitis

 Primary chronic osteomyelitis

 Chronic tendoperiostitis

 SAPHO syndrome

 CRMO

 Focal sclerosing osteomyelitis (condensing osteitis)

 Osteomyelitis with proliferative periostitis

• Cavernous sinus thrombosis

• Odontogenic infection of orbit

occur due to neutralization of host defence There is fever, endotoxic shock and intravascular coagulation The pathogen or its products, in certain situations, may combine with antibodies or sensitized mononuclear leukocytes to produce harmful immunologic effects called

hypersensitivity reaction.

Compromised host: It is a person whose defense

mechanisms have been lowered as a result of diabetes, tuberculosis, rheumatic fever, malignancy, radiation therapy, use of therapeutic immunosuppressive drug or antibiotics, extensive skin burns, genetic deficiency of immune system and malnutrition

in nearly all patients with infection

Redness (rubor) is seen when the infection is close

to the tissue surface, which is secondary to the intense hyperemia caused by increased vasodilation of arterioles

Calor or heat is due to inflow of relatively warm blood

from deeper tissues, increased velocity of blood flow and increased rate of metabolism

Dolor or pain results from pressure on sensory nerve

endings, from distension of tissues caused by edema or spread of infection Release of substance like kinins, histamines or bradykinin is also responsible for pain It is the most universal sign of infection

Swelling accompanies infection, unless the infection

is confined to bone which cannot swell It is due to the accumulation of fluid, exudate or pus

Loss of function is another sign of infection A patient

immobilizes the painful part in the most comfortable position he can find Hence, when the masticatory muscles are involved, there is limitation of jaw movement

Fever occurs in some cases, which reflect a

non-specific physiologic response of host to tissue injury This injury results in increase of substance called pyrogen from endogenous (injured tissue) and exogenous source (infecting agent) In clinical fever, it appears that the hypothalamic regulating center is stimulated by endogenous

complications The key to successful management is sound

surgical principles

The relationship between the host and microbes is a

dynamic one Usually, host resistance is the dominant

factor On the other hand, when the host resistance is

lowered, microbes predominate and clinical infection

occurs In establishing the presence of infection there is

interaction between three viz factors host, environment and

microbes

A compromised patient is more likely to have infection

and this infection can rapidly acquire a serious form Hence,

patient history is more important so as to recognize the

patient ability to defend himself against the infection The

adverse relationship between the host and the infectious

microorganism can be best understood by imagining a

balance on which the pathologic attribute of microbes are

weighed against the protective mechanisms of the host

Body defends against the microbial invasion by three

major defenses local defense, cellular defense and humoral

defense The microorganisms on the other hand use

two weapons in this battle, i.e virulence and number of

EFFECT OF INFECTION ON HOST

Infectious agents initiate, in the host, a series of reactions

that are collectively called inflammatory reaction This

response results in generation and release of mediators,

microvascular changes and mobilization and activation

of leukocytes, all designed to eliminate the infectious

pathogens and repair tissue injury Therefore, these

reactions are protective in nature

Direct injury to the host cells, enhancement of the

parasite’s invasiveness and amplification of these effects

pyrogen, which is activated by bacterial endotoxin release

from granulocytes, monocytes and macrophages

Cardinal Sign of Inflammation

The pulp is the formative organ of the tooth It builds

primary dentin during the development of the tooth,

secondary dentin after tooth eruption and reparative dentin

in response to stimulation as long as the odontoblasts

remain intact The pulp has been described as both a

highly resistant organ and as an organ with little resistance

or recuperating ability It is a delicate connective tissue

liberally interspersed with tiny blood vessels, lymphatics,

myelinated and unmyelinated nerves, and undifferentiated

connective tissue cells

– Abnormally responsive to cold

– Abnormally responsive to heat

• Focal or subtotal or partial pulpitis: In it

inflammatory process is confined to a portion of the pulp, usually a portion of the coronal pulp

• Total or generalized pulpitis: In it most of the pulp is

• Pulpitis aperta (open pulpitis): In it pulp is

communicated with the oral cavity

• Pulpitis clausa (closed pulpitis): No communication

exists

PULPITIS

The initial response to injury to pulp is same as that of other tissue, but the end results is different due to rigid dentinal wall of pulp chamber

Pathogenesis

Some stimuli of short duration, such as cutting dentin may cause short-term vasodilation and a reversible increase in

vessel wall permeability

More severe stimuli and a greater degree of cell

damage cause more marked vasodilatation and the

movement of polymorphonuclear leukocytes into the injured tissues

These acute inflammatory reactions are usually limited

to the odontoblast and subodontoblastic regions adjacent to the dentinal tubules involved

Odontoblastic nuclei may be displaced into the tubules,

due to either increased local tissue pressure or dentinal fluid during the injury It is reversible, if the etiological factors are removed Repair involves the return to normal tissue fluid dynamics, exit of polymorphonuclear leukocytes from the area and the re-differentiation of odontoblasts

if they have damaged The pulpal tissue after repair is usually less vascular, more fibrous and less cellular than before and may be less able to withstand a subsequent insult

If stimuli are not removed, pulpal damage can

overwhelm the system and spread progressively to apical

portion of pulp This will result in pulpal necrosis

Causes

Mechanical cause: It includes traumatic accident,

iatrogenic damage for dental procedure, attrition, abrasion

Thermal cause: It may cause through uninsulated metallic

restoration, during cavity preparation, polishing

Chemical cause: It arises from erosion or inappropriate

use of acidic dental material

Bacterial cause: It can damage the pulp through the toxins

secreted by bacteria from caries

Clinical Features

Reversible Pulpitis

It is a mild-to-moderate inflammatory condition of the pulp

caused by noxious stimuli in which the pulp is capable of

returning to un-inflamed state following removal of the

stimuli

Pulp hyperemia: It is the earliest form which is sometimes

known as pulp hyperemia There is excessive accumulation

of the blood within the pulp tissue leading to vascular

congestion

Symptoms: It is characterized by sharp pain lasting for a

moment It is more often brought on by cold than hot food or

beverages and by cold air It does not occur spontaneously

and does not continue when the cause has been removed

Tooth responds to electric pulp testing at lower current

Irreversible Pulpitis

It is a persistent inflammatory condition of the pulp, which

may be symptomatic or asymptomatic and is caused by a

noxious stimulus

Symptoms: In early stages of irreversible pulpitis, a

paroxysm of pain may be caused by the following: sudden

temperature changes like cold, sweet and acid foodstuffs

The pain often continues when the cause has been removed

and it may come and go spontaneously

Nature of pain: Pain is sharp, piercing or shooting and

is generally severe It may be intermittent or continuous,

depending on the degree of pulpal involvement and

depending on whether it is related to an external stimulus

The patient may also state that bending over or lying down

i.e change of position, exacerbates the pain which is due to change in intrapulpal pressure

Referred pain: Patient may complain of pain referred to adjacent teeth to the temporal region or sinuses when an upper posterior tooth is involved, or to the angle, when lower posterior tooth is affected

In later stages, pain is more severe and is generally described as boring, gnawing or throbbing or as if tooth is

under constant pressure Patient is often awake at night due

to pain Pain is increased by heat and is sometimes relieved

by cold, although continued cold may intensify the pain

Chronic Hyperplastic Pulpitis

It is also called pulp polyp or pulpitis aperta It is essentially

an excessive, exuberant proliferation of chronically inflamed dental pulp tissue It occurs due to long standing low grade infection Mechanical irritation from chewing and bacterial infection often provides the stimuli

Teeth involved: Teeth most commonly involved are

deciduous molars and first permanent molars as they have

an excellent blood supply because of a large root opening, and this coupled with high tissue resistance and reactivity

in young person’s accounts for unusual proliferative properties of the pulp tissue It is asymptomatic and it is seen only in teeth of children and young adults

Appearance: Polypoid tissue appears as a fleshy, reddish pulpal mass filling most of the pulp chamber or cavity

or even extending beyond the confines of the tooth (Fig 22.1) Sometimes, mass if large enough interferes with

Figure 22.1 Chronic hyperplastic candidiasis showing reddish

pulpal mass

comfortable closure of teeth Polypoid tissue is less

sensitive than normal pulp tissue and more sensitive than

the gingival tissue

Signs and symptoms: It may cause discomfort during

mastication, due to pressure of food bolus This tissue

bleeds easily because of rich network of blood vessels

The tooth may respond feebly or not at all to the thermal

test There is presence of squamous covering as a result

of grafting of exfoliated epithelial cells from adjacent oral

mucosa

Histopathological Features (Figs 22.2 to 22.4)

It may range from hyperemia to mild-to-moderate

inflammatory changes to the area of the involved dentinal

tubules such as dentinal caries

Microscopically one sees involved reparative dentin,

disruption of the odontoblastic layer, dilated blood

vessels, extravasation of fluid (edema) and the presence

of immunological response Chronic inflammatory cells

predominate In some cases acute inflammatory cells can

also be seen

In irreversible pulpitis the postcapillary venules

become congested and affect the circulation within the

pulp, causing pathologic changes such as necrosis These

necrotic areas attract polymorphonuclear leukocytes by

chemotaxis and start an acute inflammatory reaction

After phagocytosis, the polymorpho-nuclear leukocytes,

which have a short life span, die and release lysosomal

enzymes The lysosomal enzymes lyse some of the pulpal

stroma and together with the cellular debris of the dead

polymorphonuclear leukocytes form purulent exudates

(pus)

The inflammatory reaction produces micro-abscess

(acute pulpitis) The pulp trying to protect itself walls off

the areas of the micro-abscess with fibrous connective

tissue The surrounding pulp tissue exhibits fibrosis and

mixture of plasma cells, lymphocytes and histiocytes

In some cases within a few days, the acute inflammation

spreads to involve most of the pulp so that neutrophilic

leukocytes fill the pulp The entire odontoblastic layer

degenerates As pulp is closed, there is rise in pressure

and the entire pulp tissue undergoes rapid disintegration,

forming numerous small abscesses Eventually the entire

pulp undergoes liquefaction and necrosis which is called

acute suppurative pulpitis.

Figure 22.4 Pulp hyperemia showing many dilated blood

vessels and necrotic area in the center

Figure 22.2 Necrosis of pulp in pulpitis

Figure 22.3 Pulp hyperemia showing cellular infiltrate and

inflammatory cells

In chronic hyperplastic pulpitis the surface of the

pulp polyp is covered by stratified squamous epithelium

Such epithelium may be derived from gingiva or freshly

desquamate epithelial cells of the oral mucosa or tongue

The tissue in the pulp chamber is often transformed into

granulation tissue which projects from the pulp into the

carious lesion

The granulation tissue is a young vascular tissue

containing polymorphonuclear neutrophils, lymphocytes

and plasma cells The granulation tissue may become

epithelized as a result of implantation of epithelial

cells on its surface Granulation tissue is made up of

delicate connective tissue fibers interspersed with a

variable number of small capillaries Inflammatory cell

infiltration chiefly lymphocytes and plasma cells are also

seen

Clinical Differences between Reversible and

Irreversible Pulpitis

The pain of irreversible pulpitis is more severe and

lasts longer In reversible pulpitis, the cause of pain is

generally traceable to a stimulus such as cold water or

air whereas in irreversible pulpitis, the pain may come

without any apparent stimulus

Management

Prevention is the best management for it It is done by

periodic care, early insertion of a filling if a cavity has

developed Removal of noxious stimuli should be done.

In early stages pulpotomy (removal of the coronal

pulp) and placing material that favors calcification such as

calcium hydroxide over the entrance of root canals Root

canal filling with inert material like gutta percha should be

done

Complete removal of the pulp or pulpectomy and

placement of an intracanal medicament to act as a

disinfectant or obtundent such a cresatin, eugenol or

formacresol is carried out in irreversible pulpitis

In case of hyperplastic pulpitis elimination of

polypoid tissue, followed by extirpation of the pulp is

done After removing the hyperplastic tissue bleeding

can be controlled by pressure Extraction of tooth can

also be done

Points to Remember

Stimuli of short duration, mechanical cause, thermal cause, chemical cause, bacterial cause:

• Reversible pulpitis: Mild noxious stimuli, pulp

hyperemia, sharp pain lasting for a moment, brought

on by cold

• Irreversible pulpitis: Paroxysm of pain, sudden

temperature changes like cold, pain often continues cause has been removed and it may come and pain

is sharp, piercing or shooting, referred pain, later stages, pain is more severe, patient is often awake at night due to pain

• Chronic hyperplastic pulpitis: Pulp polyp, pulpitis

aperta, polypoid tissue appears as a fleshy, reddish pulpal mass filling most of the pulp chamber, discomfort during mastication

• Histopathological features: Hyperemia,

mild-to-moderate inflammatory changes, disruption

of the odontoblastic layer, dilated blood vessels, extravasation of fluid (edema), chronic inflammatory cells predominate, polymorphonuclear leukocytes by chemotaxis, lysosomal enzyme, microabscess, chronic hyperplastic pulpitis, stratified squamous epithelium, delicate connective tissue fibers interspersed with a variable number of small capillaries

• Management: Removal of noxious stimuli, pulpotomy,

pulpectomy, elimination of polypoid tissue

PULP DEGENERATION

Degeneration is usually present in older aged people It

is a result of persistent, mild irritation in teeth of younger people

Clinical Features

In early stages, there are no symptoms and no clinical findings As degeneration progresses, the tooth may become discolored and the pulp within does not respond

to stimuli

Types

Calcific degeneration: A part of pulp tissue is replaced

by calcific material that is pulp stones and denticles are formed The calcific material has a laminated structure like

the skin of an onion and lies unattached within the body of

pulp In another type of calcification the calcified material

is attached to the wall of the pulp cavity and is an integral

part of it which is called diffuse calcification

Atrophic degeneration: It is observed in older people

The pulp tissue is less sensitive than normal

Fibrous degeneration: It is characterized by replacement

of the cellular element by fibrous connective tissue On

removal from the root canal, the pulp has the characteristic

appearance of a leathery fiber (Fig 22.5)

Pulp artifacts: Vacuolization of the odontoblasts was once

thought to be a type of pulp degeneration characterized by

empty spaces formally occupied by odontoblasts It is an

artefact caused by poor fixation of the tissue specimen

Tumor metastasis: It is rare except possibly in the terminal

stages It may occur due to direct local extension from the

jaw

Points to Remember

No symptoms, no clinical findings, calcific degeneration,

atrophic degeneration, fibrous degeneration, pulp

artifacts, tumor metastasis

PULP CALCIFICATIONS

Various forms of pulp calcifications are found within the

pulp which may be located in the pulp chamber or in the

root canals It can occur in any sex and in any teeth in the

dental arch

Etiology

There is no clear-cut etiology There is strong association between chronic pulpitis and presence of pulpal calcification But pulp calcification can be found in unerupted teeth

Extremely high percentage of pulp stones yield pure growth of streptococci on culture but often the affected teeth are normal

Sundell Schematic Presentation

Local metabolic dysfunction = trauma = hyalinization of injured cells = vascular damage = thrombosis = vessels wall damage = fibrosis = minerlization (nidus formation)

= growth = pulp stone

Classification of Pulp Stone

• Denticle

• Pulp stones – True

- Free

- Attached – False

- Free

- Attached

• Interstitial

Classification

There are of following types:

Denticle: It occur due to epitheliomesenchymal interaction

within developing pulp They develop during the formation and root and form before completion of primary dentin So denticle will become attached to or embedded in the dentin

Pulp stone: Also called pulp nodules It is of following

types:

∙ True: They are made of localized masses of calcified

tissue that resembles dentin due to their tubular structure Tubules are irregular and few in number It is more common in pulp chamber than root canals They are subdivided into:

– Free: It lies entirely within pulp tissue and is not attached to the dentinal wall

– Attached: These are continuous with the dentinal wall

∙ False: It is composed of localized mass of calcified

material and they do not exhibit dentinal tubules Nodule appears to be made up of concentric layers

Figure 22.5 Fibrosis of pulp seen as replacement of cellular

element by fibrous connective tissue

or lamellae deposited around a central nidus It is

composed of cells around which laid down is a layer

of reticular fibers that subsequently calcifies They are

again classified as free or attached They are larger

than true denticles and they may fill nearly the entire

pulp chamber

∙ Interstitial: As the concentric deposition of calcified

material continues it approximates and finally is in

apposition with the dentinal wall where it may be

surrounded by secondary dentin then it is called an

interstitial pulp stone

Diffuse linear calcification: It is also called calcific

degeneration It is amorphous unorganized linear strands

or columns parallel with blood vessels and nerves of pulp

It contains fine fibrillar irregular calcification

Clinical and Radiographic Significance

As such they have very little clinical significance Usually

it is discovered on the radiograph only as radiopacity

Sometimes, it may cause pain from mild pulpal

neuralgia to severe excruciating pain resembling that of tic

douloureux as the denticle can impinge on the nerve of the

pulp

Difficulty may be encountered in extirpating the pulp

during root canal therapy

In some cases pulp calcification may become large

enough to interfere with root formation which may lead to

periodontal destruction and tooth loss

In some condition like dentin dysplasia (type II),

tumoral calcinosis, calcinosis universalis and Ehlers

Danlos syndrome you may observe calcification

Radiographic features: It is radiopaque on the resultant

radiograph It can be seen hanging in pulp chamber or it is

attached to wall of pulp chamber (Fig 22.6)

Histopathological Features (Figs 22.7 to 22.9)

Denticle consists of tubular dentin which surround central

nest of epithelium After some time it degenerated and

tubules undergo necrosis

Pulp stone shows central amorphous mass of

calcification which is surrounded by concentric lamellar

rings In some cases fibrillar irregular calcified material

can be seen at the periphery of pulp stone

Diffuse calcification consists of fine fibrillar and

irregular calcification which developed in pulp chamber

and canals This is deposited in linear fashion

Management

No treatment is necessary as tooth is asymptomatic Care should be taken while undergoing root canal therapy for tooth having pulp stone

Points to Remember

Discovered on the radiograph, difficulty during root canal therapy, periodontal destruction, radiopaque on the resultant radiograph, denticle consists of tubular dentin, pulp stone, central amorphous mass of calcification, diffuse calcification consists of fine fibrillar and irregular calcification

Figure 22.6 Radiopaque pulp stone seen in the pulp chamber

Figure 22.7 Pulp calcification

Liquefaction necrosis: It results when proteolytic enzymes

convert the tissue into softened mass, liquid or amorphous debris

Clinical Features

It causes no painful symptoms

Sign: Discoloration of the tooth is the first indication that the pulp is dead (Fig 22.10) The tooth with partial necrosis can respond to thermal changes owing to presence

of vital nerve fibers passing through the adjacent inflamed tissue

History of severe pain lasting from a few minutes to a

few hours, followed by complete and sudden cessation of pain

Histopathological Features

Necrotic pulp tissue, cellular debris and microorganisms

may be seen in the pulp cavity

The periapical tissue may be normal or slight evidence

of inflammation of the apical periodontal ligament may be seen

Management

Preparation and obturation of root canals should be carried out

Points to Remember

Discoloration of the tooth, history of severe pain, necrotic pulp tissue, cellular debris, microorganisms, obturation of root canals

Figure 22.9 Diffuse calcification presented as linear strands

Figure 22.8 Pulp calcification (Courtesy: Dr Sangamesh

Halawar, Reader, Department of Oral Pathology, VPDC and

H, Kavalapur, Sangli, Maharashtra, India)

NECROSIS OF PULP

It is the death of pulp It may be partial or total depending

on whether a part or the entire pulp is involved

It is sequelae of inflammation and can also occur

following trauma, in which the pulp is destroyed before an

inflammatory reaction

Types

Coagulation necrosis: The soluble portion of tissue is

precipitated or is converted into a solid material Caseation

is a form of coagulation necrosis in which the tissue

is converted into a cheesy mass consisting chiefly of

coagulated proteins, fats, and water Figure 22.10 Necrotic pulp showing discoloration of tooth

CRACKED TOOTH SYNDROME

The term cracked tooth syndrome (CTS) refers to an

incomplete fracture of a vital posterior tooth that involves

the dentine and occasionally extends into the pulp

Parafunctional habits such as bruxism are also

associated with the development of this condition

Clinical Features

Age: The condition presents mainly in patients aged

between 30 and 50 years

Location: Mandibular second molars, followed by

mandibular first molars and maxillary premolars

Symptoms: Patient complains of pain ranging from

mild to excruciating, at the initiation or release of the

biting pressure It can mimic the condition as severe

as trigeminal neuralgia A crack may involve enamel

and dentine only or it may also involve the pulp and

symptoms will vary accordingly (Fig 22.11) Pain

occurs due to fluid movement within the dentinal tubules

causing stimulation of sub-odontoblastic nerve fibers

The fluid movements are induced by pressure changes

when biting with the offending cusp

Sign: If the crack involves dental pulp, direct bacterial

invasion will occur with predictable pulpal inflammation

and resultant pulpitic pain

Fiberoptic examination:Close examination of the crown

of the tooth may disclose a crack in enamel, which may be

better visualized by using a dye or by trans-illuminating

the tooth with fiberoptic light.

Bite test: Crack can be confirmed by selective biting pressure using a cotton roll or a small wooden stick to

Points to Remember

Mandibular second molars, pain ranging from mild to excruciating, fluid movements are induced by pressure change, fiberoptic examination, bite test, splinting of the offending cusp

PERIAPICAL ABSCESS

An abscess is a localized collection of pus, surrounded

by an area of inflamed tissue in which hyperemia and infiltration of leukocytes is marked

Bacteriology

Staphylococci are frequently associated with abscess

formation They produce the enzyme called coagulase which causes fibrin deposition and thus helps in walling

off the lesion Coagulase promotes virulence by inhibiting

phagocytosis

Small pockets of necrotic tissue are formed within

cellulites, which coalesce and enlarge, compressing the surrounding fibrous connective tissue Thus an abscess

is generated, which is a collection of pus surrounded by a wall of fibrous connective tissue

Types

∙ Acute periapical abscess: It is also called acute

alveolar abscess

∙ Chronic alveolar abscess: It is a long standing, low

grade infection of the periradicular tissues

But as this acute and chronic process both have acute inflammatory reaction so this term may be wrong to used Instead it should be used as symptomatic and asymptomatic

Etiopathogenesis

It may be result of trauma or chemical or mechanical

irritation The immediate cause is the bacterial invasion of

Figure 22.11 Cracked tooth syndrome

dead pulp When inflammatory response may extend into

adjacent periapical alveolar bone, it will initiate necrosis

of periapical tissue and diffuse rarefaction of bone, leading

to formation of periapical abscess with symptoms of acute

inflammation

Primary or necrotic abscess are pulpo-periapical

inflammatory conditions associated with teeth, which

have not developed apparent periapical radiolucent lesion;

usually described as acute apical periodontitis or acute

periapical abscess

The surrounding tissue attempt to localize the pyogenic

infection by forming enclosure of granulation tissue; this in

turn is surrounded by fibrous connective tissue; this results

in well circumscribed lesion containing necrotic tissue

Well circumscribed lesion may form sinus due to

inability of the body to completely contain or localized

the causative organisms, increase in number of causative

organisms, lowering of patient’s general resistance and

trauma or surgical intervention

Enlarging dentoalveolar abscess contains purulent

material that is under pressure due to the production of pus—

the purulent material travels along path of least resistance,

until it reaches the surface, where due to limitation of

periosteal layer, it temporally forms subperiosteal abscess

Eventually, it erodes through the periosteum and

penetrates the soft tissue, again, following the path of least

resistance Path of least resistance is determined by the

location of breakthrough in the bone and the anatomy of

muscles and fascia plane in the area

Clinical and Radiological Features

Symptoms: Pain is severe and of throbbing type Periapical

abscess may confine to osseous structures and during the

early period of abscess formation, may cause excruciating

pain without observable swelling The patient may appear

pale, irritable and weak from pain, loss of sleep as well

as from absorption of septic products He may have slight

fever (99 to 100°F)

Sign: Patients experience sensitivity or pressure in the

affected area Ice relives the pain and heat intensifies it

aspiration yield yellowish pus The tooth becomes more

painful, appears elongated and mobile In acute periapical

infection, tooth is sensitive to percussion and movement

There is also painful lymphadenopathy After some period

the affected pulp is necrotic and does not respond to electric

current or to application of cold Swelling is usually seen in

adjacent tissues adjacent to the affected tooth

The tissues at the surface of swelling appear taut and

inflamed The surface of tissue become distended from the pressure of underlying pus and finally ruptures due

to pressure and lack of resistance caused by continued liquefaction

When the maxillary anterior teeth are involved,

swelling of upper lip may extend to one or both eyelids When the maxillary teeth are involved, the cheek may swell to an immense size, distorting the patient’s face It may results in buccal space infection (Fig 22.12)

When the maxillary posterior teeth are involved, there

is possibility of maxillary sinus to involvement When the mandibular posterior teeth are involved, swelling of the cheek may extend to ear

Sudden decrease in pain signals the formation of sinus Tooth is tender, vitality test is negative Draining fistulas

are also commonly associated with chronic alveolar abscess Majority opens on labial and buccal aspect of alveolus, as apices of both maxillary and mandibular teeth are located nearer to the buccal than the lingual cortical plate In maxilla, roots of lateral incisors and molars are close to palatal cortical plate, so sinus appear there (Fig 22.13) Most root tips lie below the mylohyoid muscle, so pus drains into the submandibular space

Sinus opening appears as a small ulcer At the opening

of sinus mass of inflamed granulation tissue is found, it is

called parulis or gum boil

Occasionally, after temporary emphysema, sinus heals and form slightly raised pale papule As the pus accumulates, another signs formation may take place eventually

Figure 22.12 Periapical infection from tooth which involve

buccal space

polymorphonuclear leukocytes, surrounded by inflamed

connective tissue wall of varying thickness

Acute abscess contain necrotic and unidentical soft

tissues There is an empty space, where suppuration has

occurred The root canal appears to be devoid of tissue and

instead, microorganism and debris may be observed

In case of chronic condition macrophages and

granulation tissue are present Lymphocytes and plasma

cells are found at the periphery of the abscessed area

Fibroblast may start to form capsule at the periphery

Sinus tract are generally lined by granulation tissue In addition, chronic inflammatory cells are also present

Management

Establish drainage immediately, if possible: It may be

done by opening the pulp chamber and passing file through the canal into the periapical region Trephination opening through mucosa and bore to the abscess at apex Through and through drain is placed in the abscess and irrigated with 1:1 mix of 3 percent H2O2 and normal saline solution

Antibiotics like Penicillin 500 mg, QID, for 5 days and analgesics should be given In 24 to 48 hours, it can be determined if the tooth can be treated endodontically or extraction is necessary

Warm saline mouth rinse often aid in localizing the

infection and maintaining adequate drainage, before endodontic treatment or extraction

If there is need of retention of offending tooth, necrotic pulp should be opened and tooth should be treated endodontically

PERIODONTAL ABSCESS

It is usually culmination of a long period of chronic periodontitis

Causes

Many cases of periodontitis arise in the patients who are

going periodontal therapy due to incomplete removal deep of calculus There is also microbial penetration of

surrounding tissue

Other factors which can cause periodontal abscess are

diabetes, trauma, enamel pearls

Figure 22.13 Intraoral swelling seen on palatal side in patient

Figure 22.14 Periapical loss of bone due to periapical

abscess

Pathogenesis

It usually occurs in pre-existing periodontal pocket When

such pocket reaches sufficient depth of about 5 to 8 mm, the

soft tissues, around the neck of the tooth may approximate

the tooth so tightly that orifice of the pocket is occluded

Bacteria multiply in the depth of pocket and cause sufficient

irritation to form an acute abscess, with exudation of pus

into this area It results in sufficient swelling to destroy the

cortical plates of bone

Clinical and Radiological Features

It starts at the gingival crevice and extends down on one or

more surface of the root, frequently as far as apical region

Symptoms: Acute episode usually has sudden onset with

extreme pain There is also distension and discomfort

Signs: They are associated with swelling of the soft tissues

overlying the surface of the involved root (Fig 22.15)

Tooth is tender and mobile Pus usually exudes from the

gingival crevice

Other features includes lymphadenopathy, fever,

leukocytosis, foul taste.

Radiographic features: There is bone loss associated

with affected teeth In some cases infection can spread to

periapical region causing periodontal-endodontic lesion

Histopathological Features

It consist of a central cavity filled with pus walled off on

one side by the root and on the other side by connective

tissue, as the epithelial lining of the crevice has been destroyed by the inflammatory process

There is also large colonies of microorganism can also

be present

Management

Incision and drainage: Primary treatment for relief of

acute symptoms is incision of the fluctuant abscess, from

the depth of the abscess cavity to the gingiva The incision should extend into the soft tissues of the root surface If the surrounding tissue is normal, the tooth may be retained and debridement of the root surface by removal of granulation tissue should be done

Treatment for new attachment and new tissue regeneration should be performed However, if the roots

are denuded beyond the apical thirds of the root, the tooth should be extracted and curettage should be carried out to remove the granulation tissue from the socket

Antibiotics: Antibiotics of choice is penicillin

Points to Remember

Incomplete removal deep of calculus, sudden onset with extreme pain, soft tissues overlying the surface of the involved root, lymphadenopathy, fever, leukocytosis, foul taste, bone loss associated with affected teeth, central cavity filled with pus walled off on one side by the root, large colonies of microorganism, incision and drainage, new attachment and new tissue regeneration, antibiotics

ACUTE EXACERBATION OF A CHRONIC LESION

It is an acute inflammatory reaction superimposed on an existing chronic lesion, such as on cyst or granuloma It is

also called phoenix abscess due to mythical bird that would

die only arise again from its own ashes

Causes

The peri-radicular area may react to noxious stimuli form a diseased pulp with chronic peri-radicular disease At times, because of an influx of necrotic product from a diseased pulp or because of bacteria and there toxins, this apparently dormant lesion may react and cause an acute inflammatory response

Figure 22.15 Swelling in soft tissue due to periodontal

abscess

Clinical Features

Symptoms: At the onset, tooth may be tender to touch

Patients complain of intense pain, local swelling and

possibly associated cellulitis

Signs: Mucosa over the radicular area may be sensitive

to palpation and may appear red and swollen The patient

has history of traumatic accident that turned the tooth dark

after a period of time or of postoperative pain in a tooth that

had subsided until the present episode of pain

Lack of response to vitality test points to diagnosis

necrotic pulp

Radiological features: There is radiolucency seen at the

apex of tooth (Fig 22.16)

Histopathological Features

Area of liquefaction necrosis with disintegrating

polymor-phonuclear neutrophils and cellular debris is seen

These are surrounded by infiltration of macrophages

and some lymphocytes These abscesses can maintain soft

tissue component

Management

Drainage, either via the root canal or by incision, if there

is localized swelling

Antibiotics and analgesic: Appropriated antibiotics

and analgesic should be given

Points to Remember

Phoenix abscess, tooth may be tender to touch, mucosa over the radicular area may be sensitive to palpation, lack of response to vitality test, radiolucency seen at the apex of tooth, area of liquefaction necrosis, disintegrating polymorphonuclear neutrophils, drainage, antibiotics and analgesic

PERIAPICAL GRANULOMA

It is the most common type of pathologic radiolucency

encountered in dentistry It is a growth of granulation tissue continuous with the periodontal ligament resulting from the death of the pulp and diffusion of bacteria and bacterial toxins from the root canals into the surrounding

periradicular tissues through the apical and lateral foramina

Etiopathogenesis

It occurs as a response to intense and prolonged irritation from infected root canals producing extension of chronic apical periodontitis beyond the periodontal ligament The expanding inflammation and increased vascular pressure result in abscess formation and resorption of the bone in the affected area, which in cause of time is replaced by granulation tissue It is the result of a successful attempt by the periapical tissues to neutralize and confine the irritating toxic product that is escaping from the root canal

But continuous discharge into the periapical tissues induces a vascular inflammatory response Insult from diseased pulp represents broad spectrum of inflammatory mediations like prostaglandins, kinin and endotoxins Elevated level of IgG in pulpoperiapical lesion

Clinical and Radiological Features

The tooth is nonvital, i.e it does not respond to thermal and

electric pulp test

Symptoms: Mild pain can be occasionally experienced

while biting or chewing on solid foods Sensitivity occurs due to hyperemia, edema and inflammation of the apical periodontal ligament

Sign: Tooth may be darker in color, because of the blood

pigments that diffuse into the dentinal tubules There is, seldom, swelling or expansion of the overlying cortical bone Tooth may feel to be slightly elongated in the socket

Figure 22.16 Phoenix abscess seen as radiolucency in

relation to first molar

Radiological features: The lesion is radiolucent well

circumscribed less than 1.5 cm in diameter Margin are

well defined usually but in some cases it can be ill defined

Histopathological Features (Fig 22.18)

It consists of proliferating endothelial cells capillaries,

young fibroblasts minimum amount of collagen and

occasionally, nests of odontogenic epithelium, Russell’s bodies (scattered eosinophilic globules of gamma globulin), pyronine bodies (cluster of lightly basophilic particles), foam cells and cholesterol clefts New capillaries are lined

by swollen endothelial cells

There is more inflammation in the center with fibrosis at

the periphery Connective tissue is more prominent on the periphery and the bundles of collagen become condensed there, apparently as a result of the slow expansion of the soft tissue mass, resulting in formation of a continuous capsule separating the granulation tissue from the bone

Epithelial rest of Malassez may be seen with granulation

tissue Lymphocytes, plasma cells, macrophages and

foreign body multinucleated giant cells may also be

present Occasionally, cholesterol clefts may form the

major portion; then it is called as cholesterol granuloma of

in the center, epithelial rest of Malassez, multinucleated giant cells, cholesterol granuloma

Periapical Scar

It is a possible end point of healing It is composed of

dense fibrous tissue and is situated at the periapex of pulp

Figure 22.17 Periapical granuloma showing well defined

radiolucency less than 1.5 cm in diameter

Figure 22.18 Periapical granuloma

less tooth, in which usually, the roots canal have been

successfully filled

Formation of Scar

Irritant substance confined in the periapical area It leads

to accumulation of chronic inflammatory cells Young

fibroblasts, endothelial cells and capillaries proliferate, which

lead to granuloma formation After endodontic treatment,

the granuloma resolves, but in some cases, granulation tissue

gets slowly organized with the production of more and more

collagen fibers, which in turn leads to scar formation

Clinical Features

It occurs usually after endodontic treatment and in patients

treated by periapical curettage or root resection

It is more common in anterior region of maxilla Tooth

is nonvital and the patient is asymptomatic

Radiologically periapical radiolucency is seen (Fig

22.19)

Histopathological Features

It will show spindle shaped fibroblast scattered throughout

the dense collagen bundles, which show advanced degree

It may be defined as an inflammatory condition of the bone that begins as an infection of medullary cavity and the haversian system and extends to involve the periosteum of the affected area

Predisposing Factors

Certain predisposing factors play an important role in the onset and severity of the osteomyelitis, in addition to the virulence of microorganism

Conditions affecting host resistance: Diabetes mellitus, tuberculosis, severe anemia, leukemia, agranulocytosis, acute illness such as influenza, scarlet fever, typhoid and exanthematous fever, sickle cell anemia, malnutrition and chronic alcoholism

Conditions affecting jaw vascularity: Metastasis from

remote area of infection such as another bony site, skin and kidneys, radiation, osteoporosis, osteopetrosis, fibrous dysplasia, bone malignancy and peripheral vascular disease

Odontogenic infections which can be periapical or

periodontal infection, pericoronal infection and infection from infected dental cyst

Compound fractures of the jaws: Generally, these

fractures are compound through the tooth socket into the mouth and rarely, to the skin

Figure 22.19 Periapical scar seen as radiolucency at the apex

of central incisor (Courtesy: Dr RN Modi, Professor and Head,

Department of Oral Medicine and Radiology, Hitkarini Dental

College, Jabalpur, Madhya Pradesh, India)

Traumatic injury: Local traumatic injury of the gingiva

leads to periostitis, in patients with low resistance to

infection and later to osteomyelitis

Middle ear infection and respiratory infection: Via

hematogenous route, either from middle ear infection or

from infection of the upper respiratory tract

Furunculosis of chin: Furunculosis of chin, i.e spread

through lymphatic channel via infected lymph nodes

Peritonsillar abscess: Peritonsillar abscess has also

been reported to cause osteomyelitis of the ramus of

of bone = penetration of periosteum = involucrum =

sequestra = cloacae = systemic spread of infection =

necrosis of bone

Pathogenesis

Compromised blood supply is a critical factor in the

establishment of osteomyelitis The virulent

micro-organisms get entry in the medullary cavity via many

routes like odontogenic infections, compound fractures,

periostitis, hematogenous route and lymphatic channel

Inflammatory reaction: These microorganisms cause

intense inflammatory reaction within the marrow of the

bone Pain is a feature of this stage

Localization of infection: Most of the odontogenic

infections, like periapical and periodontal infections, are

localized by pyogenic membrane or soft tissue abscess

walls

Disorganization of clot: However, disorganization of this

pyogenic membrane occurs by virulent microorganism or

by chronic movement of the unreduced fractures of jaws

Mechanical trauma: Mechanical trauma, due to chronic

movement of unreduced fractures, burnishes the bone and

causes ischemia, thereby introducing the microorganisms

deep into the underlying tissues

Accumulation of pus: When this protective barrier

breaks, the pus accumulated in the medullary cavity gives

rise to increased intra-medullary pressure, which results

in compression of vasculature, vascular collapse, venous stasis and ischemia

Elevation of periosteum: Pus travels through the Haversian and Volkmann’s canals and accumulates beneath the periosteum, elevating it from the cortex, thereby further reducing the blood supply

Necrosis of bone: The reduced blood supply leads to slow

necrosis of the bone

Penetration of periosteum: If the pus continues to

accumulate the periosteum is penetrated and mucosal and cutaneous fistulae develop and thereby discharging the purulent pus

After therapy: As the therapy begins to be effective and

the host resistance increases, the process become chronic Inflammation regresses, granulation tissue forms and new blood vessels are formed which cause lysis of bone; thus causing fragments of necrotic bone from the viable bone

Involucrum: Small sections of necrotic bone may be

completely lysed, while large one get localized and get separated from the shell of the new bone by a bed of granulation tissue This dead bone surrounded by viable bone is called involucrum

Sequestra: Small pieces of necrotic bone are called

as sequestra, which are avascular and which harbor microorganisms These sequestra need to be removed, otherwise they continue to be chronically infected and infect the surrounding granulation tissue and cause further sequestration, which weakens the bone and may cause pathologic fracture

Cloacae: An involucrum contains one or more holes on

the surface which lead into channels, which can be traced

to end in the depth of the bone at the site of an area of bone destruction around the sequestrum These orifices are termed ‘cloacae’ Pus finds its way from the depth of the bone to the surface, through the cloacae The presence of cloacae indicates that there is a dead bone or a foreign body

at the deep end

Systemic spread of infection: Besides the pathogenic

activity of the virulent microorganisms, these organisms precipitate thrombi formation by virtue of their destructive lysosomal packages The coagulum

provides the host medium for further pathogenic

proliferation as well as an isolating barrier from the

host immune response It also allows systemic spread

of infection

Necrosis of bone: The necrosis of bone is brought about by

thrombosis of the vessels or compression of the vasculature

The necrosis of bone, with superadded infection forms a

base line pathogenesis of the osteomyelitis Compression

of neurovascular bundles can result in osteomyelitis

mediated anesthesia

Occurrence

It is more common in men, than women It occurs in

mandible in premolar area because cortical plate of

the bone in mandible is dense it takes longer for sinus

formation and release and hence, the infection gets directs

into spongiosa and spreads Other reason for occurrence

in mandible are removal of posterior mandibular teeth

attended by more damage to the bone, mandible is less

vascular than maxilla and thin cortical plates and relative

paucity of medullary tissue in the maxilla precludes

confinement of infection within the bone and permits

dissipation of edema and pus into the soft tissues and

paranasal sinuses

Infantile osteomyelitis is more common in maxilla than

mandible, as it spreads by hematogenous route and maxilla

has more blood supply than mandible

Microbiology of Osteomyelitis

Staphylococcus aureus and Staphylococcus albus,

hemolytic streptococci, gram negative organisms

like Klebsiella, Pseudomonas, Proteus, E coli

Anaerobic microorganisms like pepto-streptococci,

Bacteroides and fusobacteria Some specific forms like

Mycobacterium tuberculosis, Treponema pallidum and

– SecondaryInfantile osteomyelitis

Nonsuppurative

• Chronic nonsuppurative – Focal sclerosing – Diffuse sclerosing

• Radiation osteomyelitis

• Garre’s sclerosing osteomyelitis

• Osteomyelitis due to specific infection:

– Actinomycosis – Tuberculosis – Syphilis

Clinical Staging of Osteomyelitis

• Initial stage: Spontaneous pain (localized)

• Acute stage (Suppurative stage): In this stage, there

is severe pain, soreness and looseness of the involved teeth

– Early acute stage: In reference to the involved tooth, progressive sensitivity of the adjacent teeth

to percussion and pain of the involved side – Late acute stage: Paresthesia or anesthesia of the lip region supplied by the mental nerve Other systemic symptoms can occur

• Osteonecrotic stage: Diminished spontaneous pain,

abscess formation and pus discharge

• Sequestrum stage: Lack of symptoms sequestrum

formation visible on the radiograph

ACUTE SUPPURATIVE OSTEOMYELITIS

It is serious sequelae of periapical infection there is often

a diffuse spread of infection throughout the medullary

spaces, with subsequent necrosis of variable amount of

bone There is insufficient time for body to react to the

presence of inflammatory infiltrate This process is of less

than one month of duration

Clinical Features

In early acute suppurative osteomyelitis: It has rapid

onset and course, severe pain, paresthesia or anesthesia of

the mental nerve At this stage the process is truly

intra-medullary, therefore swelling is absent, teeth are not

mobile and fistulae are not present

In established suppurative osteomyelitis: In this type

there is deep intense pain, anorexia, fetid oral odor malaise

and fever, regional lymphadenopathy There is also soreness

of involved teeth which become loose within 10 to 14 days

Pus exudes around the gingival sulcus or through

mucosal and cutaneous fistula There is firm cellulitis

of cheek and abscess formation with localized warmth

and tenderness on palpation The patient feels toxic and

dehydrated

Radiological features: The radiograph shows ill defined

radiolucency In some cases periosteal new bone formation

can be seen Sequestration can be seen as radiopaque

structure in the radiolucency

Histopathological Features

It usually consists of necrotic bone The medullary spaces

are filled with inflammatory exudate that may or may not

progress to the actual formation of pus (Figs 22.20 and

22.21)

The inflammatory cells are chiefly neutrophilic

polymorphonuclear leukocytes, but may show occasional

lymphocytes and plasma cells

The osteoblastic rimming of the bony trabeculae is

generally destroyed Depending upon the duration or the

process, the trabeculae may loose their viability and begin

to undergo slow resorption

The periphery of the bone and haversian canals

contains necrotic debris with acute inflammatory infiltrate

Management

Antibiotics therapy: If abscess formation is seen

antibiotics medication like aqueous penicillin, clindamycin,

cephalexin, cefotaxime, tobramycin and gentamicin

Incision and drainage: When early diagnosis is made,

drainage of the fluctuant areas should be carried out under

Figure 22.20 Necrotic bone seen in case of osteomyelitis

Figure 22.21 Acute suppurative osteomyelitis showing

inflammatory infiltrate (Courtesy: Dr Sangamesh Halawar,

Reader, Department of Oral Pathology, VPDC and H, Kavalapur, Sangli, Maharashtra, India)

antibiotic cover After pus is evacuated, drains are placed The consistency, color and odor of the pus may provide important clues to the diagnosis and initial treatment

Points to Remember

Rapid onset and course, paresthesia or anesthesia of the mental nerve, deep intense pain, anorexia, fetid oral odor, pus exudes around the gingival sulcus, cellulitis

of cheek, ill defined radiolucency, necrotic bone, inflammatory exudate, neutrophilic polymorphonuclear leukocytes, lymphocytes, plasma cells, trabeculae may loose their viability, haversian canals contains necrotic debris, antibiotics therapy, incision and drainage

CHRONIC SUPPURATIVE

OSTEOMYELITIS

Chronic osteomyelitis develops without initial acute stage,

if the virulence is of low grade

Chronic osteomyelitis is persistent abscess of the

bone that is characterized by usual complex inflammatory

process including necrosis of mineralized and marrow

tissues, suppuration, resorption sclerosis and hyperplasia

It occurs as defensive response lead to production of

granulation tissue which forms dense scar tissue to wall of

infection

Clinical Features

Virulence of the microorganism is low and the host

resistance is high This type is not preceded by an episode

of acute symptoms

Symptoms: It has insidious onset with slight pain, slow

increase in jaw size and a gradual development of sequestra

without fistula

Signs: Local tenderness and swelling develop over the

bone in the area of abscess

Intraorally and extraorally sinus develops intermittently

and drains small amount of pus and then gradually heals

Sinus extends from medullary bone, through cortical plate,

to mucus membrane or skin Sinus may be at a considerable

distance from the offending infection It is painless unless

there is an acute or sub-acute exacerbation (Figs 22.22 and

22.23)

Involvement is single feeder vessels may lead to

necrosis of entire quadrant of jaw in long standing chronic

osteomyelitis

Radiographic features: It shows patchy, ragged and

ill-defined radiolucency which contain central radiopaque sequestra Surrounding bone show increase radiodensity (Fig 22.24)

Histopathological Features

There is significant soft tissue component which consist

of inflamed fibrous connective tissue in areas of

Figure 22.22 Exposed bone seen clinically as sequestra

Figure 22.24 Sequestra seen as radiopaque structure in

osteomyelitis

Figure 22.23 Extraoral discharging sinus in osteomyelitis

Antibiotics: These are similar to used in case acute

osteomyelitis

Irrigation and debridement of the necrotic areas—

thorough debridement of the affected areas should be

carried out Debride any foreign bodies, necrotic tissue

or sequestra These areas may be irrigated with hydrogen

peroxide and saline

Extraction of offending tooth: Extraction of carious teeth

with periapical infection, should be done It should be

carried out to remove the source of infection from the oral

cavity

Supportive therapy: Patients is suffering from osteomyelitis required adequate rehydration in the form of fluids Rich nutritional diet should be given Multivitamin supplements should be given

Sequestrectomy: It is the removal of sequestra which are

small pieces of necrotic bone that are avascular and harbor microorganisms

Saucerization: It means excision of the margins of necrotic

bone, overlying the focus of osteomyelitis which allows better visualization of sequestra and excision of margins of the affected bone

Decortication: Decortication of mandible refers to removal

of the chronically infected and inferior cortical plates, 1

to 2 cm beyond the area of involvement Thus, access is provided to the medullary cavity

Hyperbaric oxygen therapy: In this patient is placed in

multiplace/monoplace chamber and a concentration of 100 percent O2 is given Duration of treatment is of 1.5 to 2 hours for 5 to 6 days in a week, for a total of 60 treatments

Points to Remember

Slight pain, slow increase in jaw size, local tenderness, intraorally and extraorally sinus, shows patchy, ragged and ill defined radiolucency, soft tissue component which consist of inflamed fibrous connective, scattered sequestra, pockets of abscess formation, antibiotics, irrigation and debridement of the necrotic areas, extraction of offending tooth, supportive therapy, seq-uestrectomy, saucerization, decortications, hyperbaric oxygen therapy

INFANTILE OSTEOMYELITIS

It is a rare type of osteomyelitis seen in infants few weeks after the birth It usually involves the maxilla

Route of Infection

Hematogenous route: Infantile osteomyelitis is usually

transferred through the hematogenous route

Trauma: Prenatal trauma of oral mucosa from obstetrician’s finger

Infection: Infection from mucous bulb used to clear the

airway immediately after birth

Infected nipple: Infected human or artificial nipple

Figure 22.25 Suppurative osteomyelitis showing

inflammatory cells

Figure 22.26 Chronic suppurative osteomyelitis seen as

scattered sequestra and pockets of abscess formation

Clinical Features

Location: It is more common in maxilla due to

hematogenous route The infection is thought to arise in

maxillary antrum or lacrimal sac It appears to center in the

region of first deciduous molars and the adjacent portion

of maxilla, although it may involve the inferior aspect of

the orbit

Symptoms: There is fever, anorexia and dehydration In

some cases, convulsions and vomiting may occur

Signs: There is redness and edema of eyelids, alveolar

bone and palate of the affected side Intracanthal swelling,

palpebral edema, conjunctivitis and proptosis may result

Maxilla on affected side is swollen both buccally and

palatally, especially in the molar region Sinus develops

and discharges pus intraorally and extraorally

Complications may occur like TMJ infection and

devitalization of adjacent tooth germs may occur

Points to Remember

Hematogenous route, common in maxilla, fever, anorexia

and dehydration, redness and edema of eyelids, alveolar

bone, intracanthal swelling, complications may occur

like TMJ infection

Diffuse Sclerosing Osteomyelitis

Reactive proliferation of bone is the primary response in

diffuse sclerosing osteomyelitis due to a balance between

the virulence of infection and resistance of host It is

analogous to focal form of the disease It occurs due to low

grade infection

This term should be used when an obvious infectious

process directly responsible for sclerosis of bone In this

chronic bacterial infection of intraosseous nature creates

mass of chronically granulation tissue which incites

sclerosis of bone

Clinical and Radiological Features

Age and sex distribution: It can occur at any age but most

common in older persons It has got no sex predilection

Location: It is common especially in mandibular jaw in an

edentulous area

Symptoms are very mild to absent During the period of

growth the patient complains of pain and tenderness Pain

persists for few weeks to months to even years

Signs: Jaws may be slightly enlarged on the affected side.

Radiographic features: Increase radiodensity seen around

sites of chronic infection This area can be multifocal involving the entire quadrant

Histopathological Features

It shows dense irregular trabeculae of bone, some of which are bordered by an active layer of osteoblasts The bone, in some

lesions, shows a pronounced ‘mosaic’ pattern, indicative of

repeated periods of resorption followed by repair

The haversian canals are scattered with little marrow

spaces The soft tissue between the individual trabeculae is

fibrous and show proliferative fibroblasts and occasional small capillaries focal collections of lymphocytes and

plasma cells

Polymorphonuclear leukocytes may be present, if the

lesion is undergoing an acute phase

Necrotic bone surrounded by inflamed granulation tissue

Points to Remember

Reactive proliferation of bone, mandibular jaw, complains of pain and tenderness, jaws may be slightly enlarged, increase radiodensity, mosaic pattern, haversian canals are scattered, proliferative fibroblasts, capillaries focal collections of lymphocytes, polymorphonuclear leukocytes, resolution of infection

Primary Chronic Osteomyelitis

It gets often confused with chronic suppurative myelitis In this case association with bacterial infection is not so obvious and suppuration and sequestration is absent This condition does not respond long term antibiotics therapy

osteo-Clinical and Radiological Features

Location: It is isolated process seen in the mandible

Age: It is seen in two peaks one seen in adolescence and

other in adults after 5th decade

Symptoms: Recurrent pain, swelling, local induration and

limited mouth opening is present

Sign: Regional lymphadenopathy and reduce sensation in

the distribution of inferior alveolar nerve can be seen

Fascial asymmetry: It is seen and takes year to resolve

secondary to slow remodeling

Radiographic features: It demonstrated areas of

radiolucent osteolysis mixed with zone of sclerosis

Osteolytic area are not continuous and alternate with zones

of sclerosis Bone is thickened with periosteal reaction

which is more solid as compared to laminated proliferate

periostitis of inflammatory origin

Histopathological Features

In the areas of sclerosis irregular trabecular of pagetoid

bone are present with prominent reversal line, osteoblastic

rimming and focal areas of osteoclastic activity

Intra-trabecular fibrosis with scattered lymphocytes

and plasma cells is present

Other features include microabscess formation,

hyalinization around small blood vessels and subperiosteal

bone formation also occurs

Management

Elimination of infection should be carried out

Surgical decortication: It should be done and it will help

decrease the intensity and frequency of symptoms

IV bisphosphonates: IV bisphosphonates like alendronate,

disodium clodronate and pamidronate can results in

complete disappearance of pain and dramatic suppression

bone turnover

Other drugs like corticosteroids, NSAIDs and calcitonin

can also help in relieving the symptoms

Points to Remember

Recurrent pain, swelling local induration, regional

lymphadenopathy, Fascial asymmetry, radiolucent

osteolysis mixed with zone of sclerosis, trabecular of

pagetoid bone, intra-trabecular fibrosis, microabscess

formation, hyalinization around small blood vessels,

subperiosteal bone formation, surgical decortications,

IV bisphosphonates

Chronic Tendoperiostitis

Clinical presentation of chronic tendoperiostitis is similar

that of primary chronic osteomyelitis

It occur due to reactive alternation in bone occur due

to parafunctional habits There is overuse of masticatory

muscle mainly masseter and digastric Many people believe

that this is variation of primary chronic osteomyelitis in which parafunctional habits exacerbate

Microbiological culture is negative in chronic tendoperiostitis

Clinical and Radiological Features

Age: It is more commonly seen in 3rd and 4th decade of life

Symptoms: Recurrent pain, swelling of cheek and trismus

are present

Radiological features: Sclerosis is usually found on the

anterior region of mandibular angle and posterior portion

of mandibular body These are the area where attachment

of masseter and digastric muscle occur In the area of sclerosis radiolucent zone appear There is erosion of inferior border of mandible occur

Histopathological Features There is sclerosis and remodeling of the cortical and subcortical bone with increase in bone volume

Management

Treatment should be done to resolution of muscle overuse

It should be done by muscle relaxation, rotation exercise, occlusal splint therapy, myofeedback and muscle relaxant drug like diazepam and mefenoxalon should be used

Points to Remember

Reactive alternation in bone, overuse of masticatory muscle, recurrent pain, swelling of cheek and trismus, sclerosis, sclerosis and remodeling of the cortical and subcortical bone with increase in bone volume, muscle relaxation, rotation exercise, occlusal splint therapy, myofeedback

SYNOVITIS, ACNE, PUSTULOSIS, HYPEROSTOSIS AND OSTEOMYELITIS SYNDROME

It consists of synovitis, acne, pustulosis, hyperostosis and osteomyelitis

This syndrome occurs usually younger than 60 years of

age Osteolytic area are scattered randomly within areas of

sclerotic bone

Bones involved are anterior chest wall, clavicles, ribs,

spine, pelvis, and long bone

Periosteal new bone formation is also present which

leads to enlargement of affected bone After some days

bone become more sclerotic with less periosteal apposition

resulting in decrease in size of the bone External bone

resorption and deformity of the mandible are characteristic

of these syndrome

Points to Remember

Synovitis, acne, pustulosis, hyperostosis, osteomyelitis,

osteolytic area are scattered randomly, periosteal new

bone formation, external bone resorption and deformity

of the mandible

CHRONIC RECURRENT MULTIFOCAL

OSTEOMYELITIS

It is chronic recurrent multifocal osteomyelitis In this

there is involvement of multiple bones and it is widespread

variant primary chronic osteomyelitis

There is metachronous involvement of multiple bone

like clavicle, humerus, radius, femur, or tibia Mandibular

involvement in CRMO occur in less than 10 percent of

cases

Focal Sclerosing Osteomyelitis

(Condensing Osteitis)

It is nonsuppurative inflammatory condition often seen in

dentulous jaw When the resistance of the alveolar bone

to odontogenic infection is high or the virulence of the

organisms is low, a chronic condition characterized by the

formation of focal areas of sclerosis around the roots of

the teeth can possibly result There is deposition of new

bone along the existing trabeculae, a process known as

appositional bone deposition

Clinical and Radiological Features

Age: It occurs almost in young person before the age of

20 years

Location: The tooth commonly affected is mandibular

first molar with a large carious lesion It is associated

with nonvital teeth or in teeth undergoing the process of

degeneration

Symptoms: Tooth is usually asymptomatic But in some

cases, patient may report pain or tenderness on percussion

or palpation

Radiological features: There is uniform zone of increase

radiodensity in the periapical area of tooth (Fig 22.27) There is also widening of periodontal ligament space

Histopathological Features

It appears as an area of dense bone with trabeculae borders

lined by osteoblasts Chronic inflammatory cells, plasma cells and lymphocytes are seen in the scanty bone marrow Management

Endodontic therapy: Endodontic therapy should be carried out

Points to Remember

Formation of focal areas of sclerosis around the roots of the teeth, mandibular first molar with a large carious lesion, asymptomatic, uniform zone of increase radiodensity, osteoblasts, chronic inflammatory cells, plasma cells, lymphocyte, endodontic therapy

Osteomyelitis with Proliferative Periostitis

It is also called periostitis ossificans There is bone

formation within periosteal reaction It is characterized by formation of hard bony swelling at the periphery of the jaw

It is essentially a periosteal osteosclerosis analogous to the

endosteal sclerosis of chronic, focal and diffuse sclerosing osteomyelitis

Figure 22.27 Condensing osteitis seen as increase

radiodensity