 Fetal development during the first 3 months of

M5F - Introduction
pregnancy is a complex process of organogenesis –
the fetus is then especially at risk from
developmental defects.

to Dental Changes during pregnancy

Management of 1. endocrine changes: causes the most systemic

alterations, there is an increase in production of
maternal and placental hormones

Pregnant Patients 2. neurologic findings:

1st trimester: fatigue, hyperemesis (nausea and vomiting)

Pregnancy syncope and postural hypotension

3rd trimester: increasing fatigue, mild

 Pregnancy is a sequence of events that
begins with fertilization; proceeds to
implantation, embryonic development, and
fetal development; and ideally ends with
birth about 38 weeks later, or 40 weeks
after the last menstrual period
depression
3. cardiovascular changes: slight increase in blood
pressure
> blood volume increases approx. 45-50%

> cardiac output increases 20-30%

Topic 1: Stages of Pregnancy
> tachycardia and heart murmurs
Topic 2: Common medical problems and oral
manifestations associated with pregnancy > dyspnea at rest aggravated by a supine position

*Supine hypotensive syndrome or vena cava

Topic 3: Risk factors in Drug Administration syndrome- manifested by abrupt fall in BP and a
during pregnancy sudden loss of consciousness when patient is in supine
position.
Topic 4: Dental Management Guidelines

M5F - Graphic Common medical problems during pregnancy

Organizer
 Anemia- inadequate level of hemoglobin, iron
deficiency and inadequate supply of folic acid
 fatigue, breathlessness, fainting, palpitations
 pale skin
 Back pain
 Constipation
 Edema
 Eclampsia- triad of elevated BP, proteinuria and
edema, seizures
 Heartburn
 Hemorrhoids
 Morning sickness
 Sleeping problems
 Varicose veins

M5F - Lesson 1-2 Chloasma gravidarum, pigmented lesion of the skin and
mucosa

M5F Lesson 1 2.pdf download

Common oral Manifestations during pregnancy
 Pregnancy gingivitis and pyogenic granuloma start
around the 2nd month and continues until after
parturition and regresses.
 Halitosis and enamel erosion are not uncommon,
due to hypersensitive gag reflex and acid
regurgitation from the stomach
M5F - Lesson 3-4
M5F Lesson 3 4.pdf download
Risk Assessment
 During the first trimester the only safe
course of action is to protect the patient as
far as possible from infections and to avoid
the use of radiography and drugs,
particularly general anesthetics
 In the second and third trimesters the fetus
is growing and maturing but can still be
affected by infections, drugs such as
tetracyclines, and possibly other factors
Teratogens
 any agent or influence that causes
developmental defects in the embryo
 Chemicals and Drugs
 viruses
 Smoking
 Irradiation
Drug use
 Drugs may be teratogenic and should be
avoided.
 Penicillin is the drug of choice to treat oral
infections
 Aspirin and other NSAIDs - cause closure
of the ductus arteriosus in utero, and fetal
pulmonary hypertension, as well as
delaying or prolonging labour
 Aspirin and other NSAIDs- cause a platelet
defect and are best avoided throughout
pregnancy
 Use of analgesics should be minimised
during the 1st trimester; if necessary,
paracetamol/acetaminophen is
recommended
 Dental treatment, if required, is best carried
out during the second trimester; advanced
restorative procedures are probably best
postponed until the periodontal state
improves after parturition and prolonged
sessions of treatment are better tolerated
 In the third trimester the supine hypotension
syndrome may result if the patient is laid flat
– if this occurs, the patient should be placed
on one side to allow venous return to
recover
 In the last month of pregnancy, elective
dental care is best avoided as it is
uncomfortable for the patient. Moreover,
premature labour or even abortion may also
be ascribed, without justification, to dental
treatment.
Dental Treatments
1st trimester 2nd trimester 3rd trimester
Plaque control Plaque control Plaque control
Oral hygiene oral hygiene Oral hygiene
instruction instruction instruction
Scaling/polishi Scaling/polishi Scaling/polishi
ng/curettage ng/curettage ng/curettage
Emergency Routine dental Emergency
care only care care only
No elective
treatment
Local anesthetics
 LA with adrenaline are relatively safe with
required amount even though they cross
the placental barrier. Lidocaine and
prilocaine are safer than bupivacaine which
causes fetal bradycardia
Radiographs
 Exposing the patient to radiation should be
avoided during pregnancy because of the
stochastic effects especially during the 1st
 Under unavoidable circumstances exposing
pt to dental radiographs is considered safe
provided precautionary measures in
minimizing radiation are established. (use
of lead aprons, F speed films)
Dental Management Guidelines
 Anxiety reduction.
 Detailed medical history and consultation
with pt’s obstetrician and physician
M5G - Lesson 1
 Monitoring vital signs. HIV Infections
 Left lateral positioning of the patient to
prevent supine hypotensive syndrome
during 3rd trimester HIV
 Preventive program to develop healthy oral
 HIV infects cells in the immune system and
environment
the central nervous system
 Elimination of periodontal irritants  One of the main type of cells that HIV
infects is the T helper lymphocyte
o These cells play a crucial role in the
M5G - Learning immune system, by coordinating the
actions of other immune system cells
Outcomes o A large reduction in the number of T
helper cells seriously weakens the
immune system
At the end of this module, students will be able  HIV infects the T helper cell because it has
to: the protein CD4 on its surface, which HIV
uses to attach itself to the cell before
1. Assess the medical condition by discussing gaining entry
the etiologies and signs and symptoms.  This is why the T helper cell is sometimes
2. Interpret the diagnostic tests results referred to as a CD4+ lymphocyte. Once it
required for each condition. has found its way into a cell, HIV produces
new copies of itself, which can then go on

M5G - Graphic 
to infect other cells
Over time, HIV infection leads to a severe
reduction in the number of T helper cells
Organizer available to help fight disease. The number
of T helper cells is measured by having
a CD4 testand is referred to as the CD4
count
 It can take several years before the CD4
count declines to the point that an individual
is said to have progressed to AIDS
 HIV infection can generally be broken down
into four distinct stages: primary infection,
clinically asymptomatic stage, symptomatic
HIV infection, and progression from HIV to
AIDS
o STAGE 1 : Primary HIV infection
 This stage of infection lasts for a few
weeks and is often accompanied by
a short flu-like illness
 In up to about 20% of people the
HIV symptomsare serious enough to
consult a doctor, but the diagnosis of
HIV infection is frequently missed
 During this stage there is a large
amount of HIV in the peripheral
blood and the immune system
begins to respond to the virus by
producing HIV antibodies and
cytotoxic lymphocytes
 This process is known as
seroconversion
 If an HIV antibody testis done
before seroconversion is
complete then it may not be
positive
o STAGE 2 : Clinically asymptomatic
stage
 This stage lasts for an average of
ten years and, as its name suggests,
is free from major symptoms,
although there may be swollen
glands
 The level of HIV in the peripheral
blood drops to very low levels but
people remain infectious and HIV
antibodies are detectable in the
blood, so antibody tests will show a
positive result
 Research has shown that HIV is not
dormant during this stage, but is
very active in the lymph nodes
 A test is available to measure the
small amount of HIV that escapes
the lymph nodes
 This test which measures HIV
RNA (HIV genetic material) is
referred to as the viral load test,
and it has an important role in
the treatment of HIV infection
o STAGE 3 : Symptomatic HIV infection
 Over time the immune system
becomes severely damaged by HIV
 This is thought to happen for three
main reasons:
 The lymph nodes and tissues
become damaged or 'burnt out'
because of the years of activity;
 HIV mutates and becomes more
pathogenic, in other words
stronger and more varied,
leading to more T helper cell
destruction;
 The body fails to keep up with
replacing the T helper cells that
are lost
 As the immune system fails,
symptoms develop. Initially many of
the symptoms are mild, but as the
immune system deteriorates the
symptoms worsen
 Symptomatic HIV infection is mainly
caused by the emergence of
certain opportunistic infections that
the immune system would normally
prevent
 This stage of HIV infection is often
characterised by multi-system
disease and infections can occur in
almost all body systems
 Treatment for the specific infection is
often carried out, but the underlying
cause is the action of HIV as it
erodes the immune system
 Unless HIV itself can be slowed
down the symptoms of immune
suppression will continue to worsen
o STAGE 4 : Progression from HIV to
AIDS
 As the immune system becomes
more and more damaged the
individual may develop increasingly
severe opportunistic infections and
cancers, leading eventually to an
AIDS diagnosis
 A clinical criteria is used by WHO to
diagnose the progression to AIDS,
this differs slightly between adults
and children under five
 In adults and children (5+) the
progression to AIDS is diagnosed
when any condition listed in clinical
stage 3 or stage 4 is diagnosed
and/or the CD4 count is less that
350 cells/mm3
  In children younger than five, an
AIDS diagnosis is based on having
any stage 3 or stage 4 condition
and/or a CD4 count of less than
between 20 cells/mm3and 30
cells/mm3 depending on the child's
age in months
 The criteria for diagnosing AIDS
may differ depending on individual
country guidelines
 Examples of opportunistic infections
and cancers
 The table below shows examples
of common opportunistic
infections and cancers and the
body systems that they occur in
M5G - Lesson 1
HIV Infections
HIV
 HIV infects cells in the immune system and
the central nervous system
 One of the main type of cells that HIV
infects is the T helper lymphocyte
o These cells play a crucial role in the
immune system, by coordinating the
actions of other immune system cells
o A large reduction in the number of T
helper cells seriously weakens the
immune system
 HIV infects the T helper cell because it has
the protein CD4 on its surface, which HIV
uses to attach itself to the cell before
gaining entry
 This is why the T helper cell is sometimes
referred to as a CD4+ lymphocyte. Once it
has found its way into a cell, HIV produces
new copies of itself, which can then go on
to infect other cells
 Over time, HIV infection leads to a severe
reduction in the number of T helper cells
available to help fight disease. The number
of T helper cells is measured by having
a CD4 testand is referred to as the CD4
count
 It can take several years before the CD4
count declines to the point that an individual
is said to have progressed to AIDS
 HIV infection can generally be broken down
into four distinct stages: primary infection,
clinically asymptomatic stage, symptomatic
HIV infection, and progression from HIV to
AIDS
o STAGE 1 : Primary HIV infection
 This stage of infection lasts for a few
weeks and is often accompanied by
a short flu-like illness
 In up to about 20% of people the
HIV symptomsare serious enough to
consult a doctor, but the diagnosis of
HIV infection is frequently missed
 During this stage there is a large
amount of HIV in the peripheral
blood and the immune system
begins to respond to the virus by
producing HIV antibodies and
cytotoxic lymphocytes
 This process is known as
seroconversion
 If an HIV antibody testis done
before seroconversion is
complete then it may not be
positive
o STAGE 2 : Clinically asymptomatic
stage
 This stage lasts for an average of
ten years and, as its name suggests,
is free from major symptoms,
although there may be swollen
glands
 The level of HIV in the peripheral
blood drops to very low levels but
people remain infectious and HIV
antibodies are detectable in the
blood, so antibody tests will show a
positive result
 Research has shown that HIV is not
dormant during this stage, but is
very active in the lymph nodes
 A test is available to measure the
small amount of HIV that escapes
the lymph nodes
 This test which measures HIV
RNA (HIV genetic material) is
referred to as the viral load test,
and it has an important role in
the treatment of HIV infection
o STAGE 3 : Symptomatic HIV infection stage 3 or stage 4 is diagnosed
 Over time the immune system and/or the CD4 count is less that
becomes severely damaged by HIV 350 cells/mm3
 This is thought to happen for three  In children younger than five, an
main reasons: AIDS diagnosis is based on having
 The lymph nodes and tissues any stage 3 or stage 4 condition
become damaged or 'burnt out' and/or a CD4 count of less than
because of the years of activity; between 20 cells/mm3and 30
 HIV mutates and becomes more cells/mm3 depending on the child's
pathogenic, in other words age in months
stronger and more varied,  The criteria for diagnosing AIDS
leading to more T helper cell may differ depending on individual
destruction; country guidelines
 The body fails to keep up with  Examples of opportunistic infections
replacing the T helper cells that and cancers
are lost  The table below shows examples
 As the immune system fails, of common opportunistic
symptoms develop. Initially many of infections and cancers and the
the symptoms are mild, but as the body systems that they occur in
immune system deteriorates the
symptoms worsen
 Symptomatic HIV infection is mainly
caused by the emergence of
certain opportunistic infections that
the immune system would normally
prevent
 This stage of HIV infection is often
characterised by multi-system
disease and infections can occur in
almost all body systems
 Treatment for the specific infection is
often carried out, but the underlying
cause is the action of HIV as it
erodes the immune system
 Unless HIV itself can be slowed
down the symptoms of immune
suppression will continue to worsen
o STAGE 4 : Progression from HIV to
AIDS
 As the immune system becomes
more and more damaged the
individual may develop increasingly
severe opportunistic infections and
cancers, leading eventually to an
AIDS diagnosis
 A clinical criteria is used by WHO to
diagnose the progression to AIDS,
this differs slightly between adults
and children under five
 In adults and children (5+) the
progression to AIDS is diagnosed
when any condition listed in clinical
System Examples of Infection/Cancer

Pneumocystis jirovecii Pneumonia (PCP)

Respiratory system Tuberculosis (TB)
Kaposi's Sarcoma (KS)

Cryptosporidiosis
Candida
Gastro-intestinal system Cytomegolavirus (CMV)
Isosporiasis
Kaposi's Sarcoma

Cytomegolavirus
Toxoplasmosis
Cryptococcosis
Central/peripheral Nervous system
Non Hodgkin's lymphoma
Varicella Zoster
Herpes simplex

Herpes simplex
Skin Kaposi's sarcoma
Varicella Zoster

 Asymptomatic

M5G - Lesson 2 
 Persistent generalized
lymphadenopathy
Clinical Stage II:
WHO clinical staging of HIV disease in  Moderate unexplained* weight
adults and adolescents (2006 revision) loss (under 10% of presumed or
measured body weight)**
  Recurrent respiratory tract
o In resource-poor communities, medical infections (sinusitis, tonsillitis,
facilities are sometimes poorly otitis media, pharyngitis)
equipped, and it is not possible to use  Herpes zoster
CD4 and viral load test results to  Angular chelitis
determine the right time to begin  Recurrent oral ulceration
antiretroviral treatment  Papular pruritic eruptions
o The World Health Organisation (WHO)  Seborrhoeic dermatitis
has therefore developed a staging  Fungal nail infections
system for HIV disease based on  Clinical Stage III:
clinical symptoms, which may be used  Unexplained* severe weight loss
to guide medical decision making. (over 10% of presumed or
 Clinical Stage I: measured body weight)**
  Unexplained* chronic diarrhoea  Recurrent septicaemia (including
for longer than one month non-typhoidal Salmonella)
 Unexplained* persistent fever  Lymphoma (cerebral or B cell
(intermittent or constant for non-Hodgkin
longer than one month)  Invasive cervical carcinoma
 Persistent oral candidiasis  Atypical disseminated
 Oral hairy leukoplakia leishmaniasis
 Pulmonary tuberculosis  Symptomatic HIV-associated
 Severe bacterial infections (e.g. nephropathy or HIV-associated
pneumonia, empyema, cardiomyopathy
pyomyositis, bone or joint
infection, meningitis,
bacteraemia)
 Acute necrotizing ulcerative
M5H - Introduction
stomatitis, gingivitis or
periodontitis to Dental
 Unexplained* anaemia (below 8
g/dl), neutropenia (below 0.5
billion/l) and/or chronic
Management of
thrombocytopenia (below 50
billion/l) Cancer Patients
 Clinical Stage IV:***
 HIV wasting syndrome Introduction
 Pneumocystis pneumonia
Dentists play an important role in the
 Recurrent severe bacterial
management of cancer patients, particularly in
pneumonia
early detection and diagnosis of the disease.
 Chronic herpes simplex infection
This necessitates proper knowledge and
(orolabial, genital or anorectal of
training in ascertaining pertinent medical
more than one month’s duration
history and clinical information from a patient.
or visceral at any site)
 Oesophageal candidiasis (or Topic 1: Oral Cancers, clinical features and
candidiasis of trachea, bronchi or etiology
lungs)
 Extrapulmonary tuberculosis Topic 2: Diagnosis and Treatment Modalities
 Kaposi sarcoma for Oral Cancers
 Cytomegalovirus infection
Topic 3: TNM Staging
(retinitis or infection of other
organs) Topic 4: Surgery, Chemotherapy, Radiotherapy
 Central nervous system and their effects to Oral Health
toxoplasmosis

M5H - Lesson 1-2

 HIV encephalopathy
 Extrapulmonary cryptococcosis
including meningitis
 Disseminated non-tuberculous
mycobacteria infection M5H Lesson 1 2.pdf download
 Progressive multifocal
leukoencephalopathy Cancer is characterized by uncontrolled growth
 Chronic cryptosporidiosis of aberrant neoplastic cells.4 Cancerous cells
 Chronic isosporiasis kill by destructive invasion of tissues—that is,
 Disseminated mycosis direct extension and spread to distant sites by
(extrapulmonary histoplasmosis, metastasis through blood, lymph, or serosal
coccidiomycosis) surfaces.
Oral cancer includes a variety of malignant
neoplasms that occur within the mouth. More
than 90%
of cases are attributed to SCC. About 9% are
carcinomas that arise from salivary gland
tissues and other tissue types such as
sarcomas and lymphomas. The remaining 1%
or so are metastatic from elsewhere in the Histopathologic
body, most commonly from lung, breast, appearance
prostate, and kidney.
Squamous Cell Carcinoma (SCCA) is the
most frequent malignant neoplasm affecting
structures of the oral lining

 Accounts for more than 90% of all

malignant lesions in the mouth
 More frequent in male, 5th decade of life
Clinical Presentation:
Early SCCA often presents as a white
patch(leukoplakia), red patch(erythroplakia) or
a mixed white and red patch.
 Ulceration of the mucosal surface
 Exophytic (verrucous or papillary)
 Enlargement of lymph node
Etiologic Agent/ Risk Factors
 Tobacco smoking/chewing
 Alcohol
 Betel nut chewing
 Dietary factors
 Microorganisms, HPV,
 UV light
 Chronic Irritation/ poor oral hygiene
 Genetic susceptibility
Pathogenesis
2 Important Biologic Stages in Oral Cancer:
1. Loss of cell cycle control thru increased
proliferation and apoptosis
2. increased neoplastic cell mobility, leading to
invasion and metastasis.
Common sites of lesion:
 Tongue- 25- 40% of oral cancer
 Floor of the mouth- 15-20%
 SCCA of gingiva/buccal mucosa- approx.
15%
 Lip, (Vermillion border)- 25-30%
 Palate 10-20%
Gingival SCCA
 Frequently involves mandible than maxilla
 Mainly observed in female than male older
than 50 yrs old.
 Gingival SCCA does not show a strong
association with classical risk factors
(tobacco use, alcohol)

Normal Histologic Appearance of Oral Histologic Subtypes of SCCA

mucosa
Classification of SCCA (based on degree of
differentiation of the neoplastic proliferating
cells)
Grade 1- Well differentiated- cells are generally
large and show distinct cell membrane,
individual cell keratinization, keratin pearls of
varying size
Grade 2- moderately differentiated- tumor cells
less differentiated, have less resemblance to
squamous cell epithelium
Grade 3- poorly differentiated- proliferation of
anaplastic cells, highly invasive with poor
prognosis, high mitotic figures
Other Variants of SCCA
Verrucous Carcinoma- usually found in buccal
mucosa or vestibule, slow growing, well
differentiated, growth pattern is more expansile
than invasive
Spindle Cell- arises from surface epithelium,
usually of the lips, appears as a proliferation of
spindle cells that may be mistaken as sarcoma
Papillary Squamous Cell Ca- resembles
verrucous Ca but is less differentiated and has
poorer prognosis
Basaloid Squamous Ca- has predilection to
tongue and pharynx
Diagnosis
Routine practice:
> brush biopsy
> tissue biopsy M5H - Lesson 3-4
> imaging modalities(radiographs, MRI,
ultrasonography, CT) M5H Lesson 3 4.pdf download
Brush Biopsy
obtain a complete transepithelial biopsy Management
specimen with cellular representation from
each of the three layers of the lesion: the basal, There are 3 recognized treatment modalities
intermediate, and superficial layers for managing head and neck cancers:

Metastasis
 Most frequently develop in the ipsilateral
cervical lymph nodes
 Tumors from the lower lip and floor of the
mouth may initially involve submental
nodes
 Involved nodes are usually enlarged, firm
and nontender to palpation
>Surgery
>Chemotherapy
>Radiotherapy
Stage I and Stage II cancers can be managed
either by surgery or radiotherapy
Stage III and IV cancers are managed using
combination of radiation therapy and surgery
Surgical Management  alopecia
 bone marrow suppression (risk to infection
Surgical treatment aims at complete removal of and bleeding tendencies)
the primary lesion as well as the metastatic  mucositis
nodes.  nausea and vomiting
The extent of resection of lesion depends upon  reproductive function suppression
the size and the adjacent structures that may
have been infiltrated. Common Oral Findings During and After
Chemotherapy
> Neck Dissection (Cervical
lymphadenectomy).  mucositis
 infections
> Commando surgery- Combined mandibular  bleeding
and neck dissection operation  xerostomia
 craniofacial maldevelopment

Prognosis and Survival Rate Risk assessment

Tongue Ca, if localized(no lymph node
 Dental screening should be undertaken
involvement), 5-yr survival is >50%. Localized
prior to commencement of chemotherapy
Ca of floor of the mouth, survival is >65%.
and the patient’s oral health stabilised.
Lymph Node metastasis decreases survival
 During chemotherapy, only emergency
rate by about 50%.
dental treatment should be performed
Lower lip lesions, 5 yr survival rate is 90%.
If surgery is not done immediately after
diagnosis, survival rate of 5 yrs decrease to
months to 1 yr.

Chemotherapy
Cytotoxic chemotherapy drugs act mainly by
interaction with the cancer cell DNA or RNA, to
inhibit cell division and/or protein
synthesis.
Chemotherapeutic drugs can:  Directly lifted from: Little and Falaces Dental Management of
Medically Compromised patients 8th edition

 impair mitosis, or prevent cell division, as in

Dental Management: Treatment modifications
the case of cytotoxic drugs
 target the cancer cells' food source, which
 Dental treatment preferably should be
consists of the enzymes and hormones
carried out in the day(s) before starting a
they need to grow
new cytotoxic treatment cycle
 trigger the suicide of cancer cells, known
medically as apoptosis
Preventive Dentistry
 stop the growth of new blood vessels that
supply a tumor (Links to an external site.) in
 strict attention to oral hygiene before,
order to starve it
during and after chemo
 caries prevention, dietary control, sealant
Complications/Side Effects
and Fl application

Radiotherapy
 Radiotherapy is the treatment of disease
with ionising radiation
 Radiation dose or exposure is measured in
units of absorbed radiation per unit of
tissue.
 The Gray (Gy) represents 1J/kg of tissue
 External beam radiotherapy (RTP or DXR)
is often used to treat head and neck, and
oral
 EBRT is now commonly delivered via a
medical linear accelerator or Cobalt-60 unit.
These units deposit the maximum dose
beneath the surface, therefore reducing the
dose to the skin
 All patients undergoing head and neck
irradiation are immobilized with a neck rest
and mask immobilization or with bite block
devices.
 Oral Findings
Complications of RT often involves the
salivary glands and the mouth
o radiation induced mucositis
o xerostomia
o radiation caries
o infections
o loss of taste
o ORN
o craniofacial defects
o trismus
 Treatment Modifications
1. Prior to RT
o Teeth with poor prognosis should be
removed PRIOR to RT.
o An interval of at least 10 days to 2
weeks between extracting the teeth and
starting RT is ideal
o No bone should be left exposed in the
mouth when RT begins since, once the
blood supply is damaged by RT, wound
healing is jeopardised.
o Meticulous oral hygiene should be
implemented and preventive oral health
care instituted
2. On-Going RT
 During RT, mucosal and salivary
gland protection is critical:
 amifostine can minimise mucositis
and xerostomia
 chlorhexidine mouthwash, 0.2%,
helps maintain oral hygiene
 antifungal drugs such as nystatin
suspension q4
3. Post RT
 If extractions become unavoidable:
 trauma should be kept to a
minimum, sharp bone edges
removed, and suture carefully
 prophylactic antibiotics from 24–48
hours preop are indicated and
continued for at least 4 weeks;
clindamycin 300mg q6h is an
appropriate antibiotic since it
penetrates bone well
 HBO may be indicated.
 oral hygiene and preventive dental
care should be continued
 radiation caries and dental
hypersensitivity can be controlled
with a non-cariogenic diet, and daily
topical fluoride applications (sodium
fluoride mouthwash, stannous
fluoride gel or acidulated fluoride
phosphate gel)
 salivary substitutes and sialogogues
are usually required.