4. There are no nutritional diffeciences that by
themselves can cause gigivitis or periodontitis but it
can affect the condition of the priodontium &
aggrevate the injurious effect of local factors.
Physical character of the diet :
in experimental animals it was found that:
1- Soft diet ( nutritionally adequate ) plaque and
calculus formation.
2- Hard fibrous food surface cleaning action and
stimulation less plaque and calculus even if
nutritionally inadequate .
5. In humans effect of nutrition ort oral M.O.:
Dietry intake, influence the oral, bacteria as it form
the source of nutrition for bacteria . So, it influence:
Relative distribution of types of organisms.
Metabilic activity of the organisms.
Pathogenicity of organisms.
7. A ) fat soluble Vit.
(1) Vit. A Diffeciency
Function:
maintain the health of epithelial cells of the skin and
m.m.
responsible for re-epitheliazation as epithelial tissues
provide a protective barrier against invading micro-
organisms
Vitamin A diffeciency result in:
dermatologic , mucosal and accular manifestations .
degenerative changes in epithelial tissues
resulting in keratinizing metaplasia .
8. (2) Vit. D “calciferol”
Function:
absorption of calcium from GIT .
maintainer of calcium phosphorus balance
Vitamin D diffeciency result in:
Inexperimaental animals there will be :
1. Osteoprosis of alveolar bone .
2. Sever alveolar bone resorption Proliferation of
fibroblast that replace the bone and marrow New
bone formation around the remnant unresobed bony
trabiculae .
3. Radiographically :
• absence of lamina dura .
• decrease density of supporting bone
• loss of trabeculae.
9. (2) Vit. D "calciferol”
Function:
absorption of calcium from GIT .
maintainer of calcium phosphorus balance
10. (2) Vit. E
Function:
anticxiddant to limit the free radical reaction .
protect cells from peroxidation .
Effect of vit. E diffeciency
no relationship demonstrated between vit.E and oral
disease in humans .
11. B) Water soluble
Vitamins
(1 ) vit, B complex:
Thiamin.
Riboflavin.
Niacin.
Pyridoxine (B6).
Biotin.
Folic acid.
Cobalamin (B12).
12. oral diseases rarely accure due to diffeciency in one
component but diffeciency is generally multiple
Thamin Riboflwin Niacin Folic acid
Diffeciency Diffeciency Diffeciency Diffeciency
1- Beriberi: 1) Glossitis 1) Pellegra : • Macrocytic anemia
• paralysis. • Magenta discoloration •Dermatitis. with megaloplastic
• C.V. symptoms. and atrophy of tongue •GIT disturb. erythropiosis
• Edema . papillae. •Mental disturb.
• Loss of appetite • In mild cases there is •Glossitis. • Diarhea and GIT
patshy atrophy with •Gingivitis. malabsorption
2) orally : engorged fungi form •Stomatitis
• hypersensitwity of papillae. • In luimans :
oral mucosa • In severe cases the a. generalized
• Minute viscles on dorsum tongue is flat, dry stomatitis
• The B. mucosa, and fissured. b. ulcerated glossitis
under the tongue or c. cheihtis
on the palate. 2) Seborrheic
• Errosion of the oral • Dermatits
mucosa
3) Dangular cbeilitis
• Which is inflammation at
the lip commisures.
14. Ariboflavinosis, angular In folate deficiency angular
cheilitis, erythema, and cheilitis may be marked.
atrophy of tongue papillae.
15. (2) Vit. C
Vit. C deficiency lead to :
Scurvy which characterized by :
Haemorrhage lesion into the ms. Of extremities,
joints.
Petechial haemorrhage.
Increase susceptibility to infection around hair follicle
and delayed wound healing .
Bleeding and swollen gingiva.
Loosening of teeth
16. Relationship between vit. C & P. diseases :
Decrease vit. C deficiency influence the metabolism
of collagen in the P. tissues decrease ability of the
tissues to regenerate and repair themselves.
Decrease vit. C deficiency interfere with bone
formation due to failure of osteoblasts to form osteod
and decreased calcification o the osteod tissues
deficiency loss of the periodontal bone .
Increase vit. C deficiency enhance the chemotactic
and migratory action of leukocytes without affecting
their phagocyte activity.
Optimal level of vit. C is required to maintain the
integrity of periodontal microvasculature and wound
healing.
17. Vitamin C deficiency
(scurvy) The characteristic Scurvy, swelling and redness
oral change in scurvy is a of the gingiva.
gingivitis, the papillae being
swollen, with a purple tint and
are fragile.
18. II. protein
deficiency
cells and blood components are formed from protein .
19. Protein deficiency will
lead to
Muscular atrophy and weakness.
Weight loss.
Anemia.
Leukemia.
Edema.
Decrease resistance to infection.
Slaw wound healing.
Decrease ability to form hormones and enzyme.
23. insulin dependent diabetes.
Caused by cell mediated autoimmune
distinction of B. cell of the islets of
pancrease.
Type I
Not preceded by obesity.
Great tendency to coma & ketosis.
In young age & treatment by insulin
injection.
24. Non insulin dependent diabetes.
Caused by peripheral resistance to
insulin impaired insulin secretion and
increased glucose production by the
Type II liver.
Preceded by obesity
Coma and ketosis not common
Adult onset and treatment by diet control
or hypoglycemic agents
25. Gestational diabetes : diabetes associated with
pregnancy in 2% - 5% of women but it
disappear after delivery .
Diabetes associated with diseases involve
pancreas and cause destruction of insulin or
pancreateactomy .
26. Xerostomia .
Gingiva:
inflamed.
enlargement either localized or generalized.
sessile or peduncualted gingival p lips.
Gingival color is bright red dark red .
Alveolar bone destruction, deep periodontal pockets and
looseing of the teeth.
Increased susceptibility to infection due to diffceicncy in
Polymorophnuclear leukocytes impaired chemotactic
and phagocytosis.
27. Frequent abscess formation due to :
high glucose level which serve as bacterial substrate.
impaired chemotactic and phagocytosis of neutrophils.
Impaired wound healing due to and collagenitic activity
and decrease synthesis of collagen which is important for-
wound healing .
Alterations in the bacterial pathogenes and oral microbial
flora this is clue to higher glucose content of gingival
fluid and blood which in turn alter the environment of
microflora in ducing qualitivate changes in bacteria that
account for severity of periodontal disease .
28.
29.
30. 2- Hyper
parthyrodism
It will be lead to:
generalized demineralization of the skeleton .
increase osteoclasits with proliferation of C.T. in the
enlarged marrow spaces diffeciency bone cyst and giant
tumors ( osteitis fibrosa cystica )
oral changes include
Malocclusion and tooth mobility.
Widening of P.L. space.
Absence of lamina dura.
Cyst like space in the jaws, diffeciency filled with
fibrous tissues and haemosedrin laden macrophages
and giant cells ( brown tumors ).
32. 3- Sex
hormones
Gingival changes in puberty :
Exaggerated response of the gingiva to local factors.
Pronounced in flammation , bluish red discoloration ,
edema and enlargement .
Increased tendency for bleeding .
Gingival changes with menstrual cycle :
not-accompaneid with notable gingival change .
33. Gingival changes in pregnancy :
pregnancy itself does not cause gingivities.
pregnancy accentuate the gingival response lo plaque.
no notable change occure with absence of local factors.
Enlarged, edematous, discolored gingiva.
increased tooth mobility, pocket depth and gingival
fluids.
marginal and interdental gingiva are edematous, piton
pressure, appear smooth and shiny.
discrete tumor like masses (pregnancy tumor).
due to increase levels of progesterone hormons which
cause:
Dilatation and tortuosity of gingival microvasculary .
Circulatory stasis .
Susceptibility to mechanical irritation.
36. 1.Leukemia
Def. Malignant neoplasias of WBCs.
precursors characterized by :
replacement of the bone marrow with leukaemic cells.
abnormal no. and forms of immature W.B.Cs in the
blood.
wide spread infiltrate in the liver, spleen, L.N. and other
sites throughout the body.
In all types of leukaemia there is : -
decrease in R.B.Cs anemia.
decrease in platelet tlrombocytopenia.
37. Periodontium in leukaemic patients :
leukaemic gingival enlargement.
Bluish red and cyanotic gingiva.
Rounded tens gingival margin .
Bleeding in leukaemic patients:
pctechae, echymosis and spontaneous bleeding
commonly occur due to replacement of the bone marrow
cells by leukaemic cells and inhibition of normal stem
cells function by leukaemic cells or their infiltrate.
38. Oral ulceration and infections in leukaemic
patients:
granulocytopenia resulting from replacement of the
bone marrow by leukaemic cells decrease tissues
resistance to M.O. opportunistic infections
discrete, punched out ulcer penetrate deeply into
submucosa and covered by firmly attached white slough
in the palate or in B. mucosa along the line of occlusion.
Gingiva is bluish red in color, sponge like, friable and
bleed easily.
39. Acute myelomonocytic leukemia, Acute myelocytic leukemia,
severe gingival enlargement. marked gingival enlargement.
Chronic lymphocytic leukemia, Chronic lymphocytic leukemia,
ulcer on the palate. severe gingival enlargement.
40. 2. Anemia
Def. Deficiency in the quantity or quality of the blood
manifested by reduction in no. of erytluocytes and the
amount of haemoglobin.
Types:
1) Pernicious anemia :
Tongue atrophy red , smooth and shiny appearance .
pallor gingiva .
Pernicious anemia, smooth, red,
and shiny dorsum of the tongue.
41. 2) Sickle cell anemia :
generalized osteoprosi.s of the jaw.
pallor and yellowish discoloration of the oral mucosa.
periodontal in fection may precipitate sickle cell crisis.
pallor, jundice, weakness and reumatoid
manifestations.
42. 3) Iron deficiency anemia :
glossitis.
Ulceration of oral mucosa and oropharynx, inducing
dysphagia, (Plummer - Vinson syndrome).
Iron deficiency anemia, smooth Plummer-Vinson syndrome, redness and
dorsal surface of the tongue. atrophy of tongue papillae associated
with angular cheilitis.
43. 4) Aplastie anemia :
occure due to failure of the bone marrow to produce
erythrocytes. As a result of toxic drugs .
• pale discoloration of the oral rnucosa.
• increased susceptibility to infection.
Aplastic anemia, ecchymoses
and ulcers on the tongue.
44. 3. Thrombocytopenia
Etiology:
• Idiopathic.
Effects :
• Spontaneous bleeding in the skin and m.m.
• petechae and haemorrhage vesicles in the palate,
tonsillar pillar and the buccal mucosa.
• the gingiva swollen, soft, friable, bleed easily and
difficult control the bleeding.
Idiopathic thrombo-cytopenic
purpura, petechiae and
ecchymoses of the buccal
mucosa.
46. It affect the oral cavity by :
1) development of habits that are injures to the
periodontium as grinding or clenching the teeth,
nibbing on foreign objects as pencils, nail biting of
excessive use of tobacco gingiaval recession and
periodontal diseases .
2) direct effect to the autonomic nervous system on the
psycologic tissue balance.
48. Leukocyte disorders :
Disorders that affect production or function of
leukocytes severe P. distinction.
Cyclic neutropenia, ulcer
on the labial mucosa
49. Agranulocytosis :
Characters:
reduction in the no. of circulating granulocytes.
Etiology:
occur due to drug idiosyncrasy which occur as acute
disease, but some items it may reappear in cyclic
episodes (Cyclic neutropenia).
Effects :
sever infections including ulcerative necroting lesions
of the oral mucosa skin, GIT and genitourinary tract .
Fever, malaise, general weakness and sore throat .
The mucosa exhibit isolated black to gray necrotic
patches that are sharply demarcated from the adjacent
uninvolved areas .
Gingival hemorrhage, necrosis, increased salivation and
fetid odor.
50. Agranulocytosis, ulcer on Agranulocytosis, severe
the tongue. periodontal destruction.
Agranulocytosis, mild
periodontal destruction.
51. AIDS:
Etiology :
• human Immuno deficiency virus .
Effects:
• Destruction of lymphocytes increase susceptibility to
opportunistic infections including destructive
periodontitis and malignancies .
53. Bismuth intoxication:
It will lead to
GIT disturbances, Nausea, Jaundice.
Lucrative gingivostomatitis with pigmentation.
Metallic taste.
Burning sensation of the mucosa .
Inflamed sore tongue .
Erythromatous eruptions of different types and hyrpes
zoster like eruptions of the skin and m.m.
Narrow bluish black discoloration of the gingiaval
margin due to precipitation of bismuth sulfide
associated with vascular changes in
inflammation of the gingiva .
54. Lead in toxication :
It will lead to :
pallar of face and lips .
GIT disturbances including nausea , vomiting , loss of
apetite and abdominal colic .
Peripheral neuritis, psycologic disorders and
encephalitis .
Excessive salivation .
Coated tongue .
Sweetish taste.
Gingival ulceration and pigmentation (Linear
pigmentation in burtonian line, Steel gray )
55. Mercury in toxication :
It will lead to :
Headache .
Isornnia .
C.V.S. sympioms .
Increase salivation .
Metallic taste .
Giugival pigmentation in liner pattern due to mercuric
sulfide.
Gingival ulceration and destruction of the underlying
bone.
56. Other chemicals :
Include :
Phosphorus .
Arsenic .
Chromium .
It will lead to :
Inflammation and ulceration of the gingiva .
Necrosis of alveolar bone and loosening of teeth .
