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Elizan, Trixia Mae A. SAS 11
Elizan, Trixia Mae A. SAS 11
Text
Name: ____________________________________________________________ Class number: _______
Section: ____________
D1 Schedule: _____________________________________ Date: _______________
PRODUCTIVITY TIP:
Good day! You are about to start your module. Do short stretching and breathing exercises. After you are
done, sit down, be comfortable and say a short prayer. You are now ready to start your work. Enjoy and
learn!
A. LESSON PREVIEW/REVIEW
Introduction (2 minutes)
Welcome to Periodontics 1! In the previous module you learned that destruction in the periodontium is not
solely due to the presence of microorganisms but mostly due to the host response to its presence. Now, you
move forward to gingival pathology. This topic is quite huge hence three modules are allocated for this.
Knowledge of the various gingival diseases will help you in making a diagnosis of future patients.
Activity 1: What I Know Chart, part 1 :Think on the questions found in the second column of the chart.
Write your answers in the first column. Leave the third column blank at this time.
B. MAIN LESSON
An experimental study has been made by Page and Schroeder wherein a group of people were made to not
brush their teeth for a certain period of time. In the study, they found 4 stages of inflammation that occurs
around the periodontium in the presence of the accumulation of dental plaque.
Gingival Inflammation
Stage 1 –Initial Stage Fig.6.1A Diagrammatic presentation of Stage 1
gingival inflammation of Page and Schroeder: The
Initial Phase or Subclinical Phase Clinically, this
initial response to bacterial plaque is not apparent
and therefore referred to as subclinical gingivitis.
‰ It is the first manifestation of gingival
inflammation.
Histologically:
Fig.6.1
Stage III –The Established Gingivitis Fig.6.3 Stage III of Gingival Inflammation by Page and
(Subgingival Plaque Phase) Schroeder: The Established Gingivitis (Subgingival
Plaque Phase)
This lesion is predominated by plasma cells and B
lymphocytes.
‰ B lymphocytes are mainly of immunoglobulin G1
(IgG1) and G3 (IgG3) subclasses.
‰ This stage occurs around 2–3 weeks of plaque
accumulation.
‰ There is presence of localised gingival anoxemia
which is due to engorged and congested blood vessels,
impaired venous return and sluggish blood flow.
‰ Anoxemia leads to bluish hue on the reddened gingiva.
‰ Colour of the gingiva can deepen due to extravasation
of erythrocytes and into the connective tissue and break
down of haemoglobin into its component pigments.
‰ Collagenase is an enzyme which is normally present in
gingival tissue it is produced by PMNs and also by some
bacteria.
‰ The activity of this collagenase is increased in inflamed
gingival tissue which causes destruction of the gingival
connective tissue.
‰ In the chronically inflamed gingiva there is also
increased levels of acid phosphatase, alkaline
phosphatase, b-glucuronidase, b-glucosidase, b-
galactosidase, esterases, aminopeptidase and
cytochrome oxidase. Histologically:
‰ There is presence of a chronic inflammatory reaction.
‰ There is increase in the number of plasma cells and B
lymphocytes.
‰ Intercellular spaces within the Junctional epithelium
widens.
‰ Intercellular spaces are filled with granular debris,
along with lysosomes derived from disrupted neutrophils,
lymphocytes and monocytes.
‰ Tissue components can be destroyed, because of acid
hydrolases released by lysosomes.
‰ Rete ridges can be seen in the Junctional epithelium
Fig.6.3 that protrude into the connective tissue.
‰ Collagen fibres are also destroyed within the
connective tissue, around, the infiltrate disrupted plasma
cells, neutrophils, lymphocytes, monocytes and mast
cells.
Fig. 6.4
Clinical features of gingivitis are as follows: A. Color changes in the gingiva. B. Changes in gingival contour
C. Changes in surface texture of gingiva. D. Changes in consistency of gingiva. E. Changes in position of the
gingiva. F. A. Gingival bleeding on probing
Fig.6.8
D.Changes in Consistency
‰ Both the acute and chronic form of gingiva produce changes in the consistency of gingiva. ‰ In chronic
gingivitis, both the forms, i.e. destructive which is oedematous and reparative which is fibrotic, coexists and the
form which is predominated, will define the consistency of gingiva.
Normal position of gingiva is usually at cementoenamel junction (CEJ) ‰ In cases of inflammation the gingiva
can be above CEJ, due to increase in the size of gingiva ‰ Also in cases of gingival enlargement, the gingiva
will be above CEJ, most of the times covering the clinical crowns as well
again • Bleeding on probing is a sign of active tissue destruction . Injury can lead to active episodes of gingival
inflammation • Injury could be laceration of gingiva during tooth brushing or by sharp pieces of hard food,
gingival burns from hot foods or chemicals • Spontaneous bleeding is also seen in acute necrotising ulcerative
gingivitis as the inflamed connective tissue consists of engaged blood vessels, which get enrobed by ulceration
due to necrotic surface epithelium. ‰
>Systemic factors causing bleeding: • Certain conditions have common feature of a haemostatic mechanism
failure which result in abnormal bleeding in the skin, internal organ and other tissues including oral mucosa. •
In such condition, the bleeding is spontaneous. • Haemorrhagic disorders, in which there is abnormal gingival
bleeding is seen are as follows: Vascular abnormalities like vitamin C deficiency or allergy like Schonlein-
Henoch purpura, platelet disorders like thrombocytopenic purpura, hypoprothrombinemia like vitamin K
deficiency, other coagulation defects such as haemophilia, leukaemia or Christmas disease, deficient platelet
thromboplastic factor (PF3) resulting from uraemia, multiple myeloma and post rubella purpura. There are
certain other. They can be effects of hormonal replacement therapy, oral contraceptives, pregnancy and the
menstrual cycle. • Fluctuation in certain hormones such as androgonic hormones have been associated in
modifying gingivitis, especially during puberty. • Certain medications also alter the gingivitis like,
anticonvulsants antihypertensive calcium-channel blockers and the immunosuppressant drugs, cause gingival
enlargements, which cause gingival bleeding, secondarily.
>In diseased tissue, the sulcus lining becomes ulcerated and the blood vessels become engorged
>When the gingival tissues are disturbed by probing or instrumentation, they can bleed easily
>Severity of bleeding and ease of its provocation depend on the intensity of the inflammation
2.Extent of Inflammation
>localized gingivitis-confined to the gingiva of a single tooth or group of teeth
>generalized gingivitis-involves the entire mouth
3.Distribution of Inflammation
>marginal gingivitis-involves the gingival margin and may include a portion of the contiguous attached
gingiva
>papillary gingivitis-involves the interdental papillae and often extends into the adjacent portion of the
gingival margin
>diffuse gingivitis-affects the gingival margin,the attached gingiva,and the interdental papillae
I. Identify the particular change of the gingival tissue as seen here in the pictures. Describe.
1. 2.
There are changes in the interdental papilla which is the size Receded marginal line caused by gingivitis
and color and shape
3. 4.
.
the contour is in the wrong position. Receded and exposure of neck part of the tooth
5.In your answer to no.4, what could be its clinical significance? Can cause hypersensitivity to the patient
A. Stage I Gingivitis
B. Stage II Gingivitis
C. Stage III Gingivitis
_______1. The blood vessel becomes engorged and congested, venous return is impaired and the blood flow
becomes sluggish.
_______2. Page and Schroeder termed this stage as advanced lesion.
_______3. The predominant cell type are plasma cells.
_______4. The initial response is dilatation of the blood vessels and clinically this stage is not apparent.
_______5. The color of the gingiva in this stage is bluish red as a result of localized anoxemia.
_______6. Seventy percent of collagen in this stage is destroyed.
_______7. The junctional epithelium becomes densely infiltrated with neutrophils as does the gingival sulcus
and the junctional epithelium may begin to show development of rete pegs or ridges.
_______8. This stage will take place 4 days to one week after plaque has been allowed to accumulate.
_______9. Subclinical type of gingivitis.
_______10. Erythema,bleeding on probing are its clinical findings.
3.A papilla that is enlarged and appears to bulge out of the interproximal space is called:
a. scooped b. cratered
c. bulbous d. blunted
4.The earliest signs of gingival inflammation that precede established localized gingivitis include which of the
following?
a. increased gingival crevicular fluid production
b. bleeding from the gingival sulcus on gentle probing
c. suppuration on gentle probing
d. A and B only
e. all of the above
• Stop and check your answers against the Key to Corrections found at the end of this Activity Sheet.
Write your score/s on your paper.
C. LESSON WRAP-UP
Activity 6: Thinking about Learning (5 minutes)
A. Work Tracker
You are done with this session! Let’s track your progress. Shade the session number you just
completed.
1) Please rate your activity today by placing a check mark (/) before a choice. Please explain your
choice on the blank space beside the table:
1. Boring
2. Not informative
3. Challenging
4. Fair
5. Fun
2) “What details in the content and/or activities were not clear to you?”
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2.Aside from removing plaque and debris from the teeth, what other advantages does one get from
toothbrushing?
Answer: There are various effects of tooth brushing on the consistency of gingiva such as: ‰ It promotes
keratinisation of oral epithelium. ‰ Capillary gingival circulation is enhanced
KEY TO CORRECTIONS:
Activity #3:
Test I. Answers:
1.A change in the size and shape of the interdental papilla, from thin knife-edge and pyramidal in shape in a
healthy gingiva. In the diseased, it has become bulbous and enlarged.
2.There is a change in the shape and contour of the interdental papilla. In this picture, the interdental papilla
has become cratered.
3.The change is on the contour of the interdental papilla. It has become blunted. Gingiva does not fill up the
embrasures.
4. There is a change in the position of the marginal gingiva. There is recession or apical movement of the
gingival margin.
5.The clinical significance of gingival recession is the exposure of the cementum or dentin in the area which
can cause hypersensitivity.