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 .
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.
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- organismsVitamin A diffeciency result in: dermatologic , mucosal and accular manifestations . degenerative changes in epithelial tissues resulting in keratinizing metaplasia .
(2) Vit. D “calciferol” Function: absorption of calcium from GIT . maintainer of calcium phosphorus balanceVitamin 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.
(2) Vit. D "calciferol” Function: absorption of calcium from GIT . maintainer of calcium phosphorus balance
(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 .
B) Water soluble Vitamins(1 ) vit, B complex: Thiamin. Riboflavin. Niacin. Pyridoxine (B6). Biotin. Folic acid. Cobalamin (B12).
oral diseases rarely accure due to diffeciency in one component but diffeciency is generally multiple Thamin Riboflwin Niacin Folic acid Diffeciency Diffeciency Diffeciency Diffeciency1- 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. malabsorption2) 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.
Pellagra, typical skinlesions Pellagra, erythema and erosions on the ventral surface of the tongue.
Ariboflavinosis, angular In folate deficiency angularcheilitis, erythema, and cheilitis may be marked.atrophy of tongue papillae.
(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
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.
Vitamin C deficiency(scurvy) The characteristic Scurvy, swelling and redness oral change in scurvy is a of the gingiva. gingivitis, the papillae beingswollen, with a purple tint and are fragile.
II. protein deficiencycells and blood components are formed from protein .
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.
Protein deficiency, redness and atrophy of the dorsal surface of the tongue.
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.
Non insulin dependent diabetes. Caused by peripheral resistance to insulin impaired insulin secretion and increased glucose production by theType II liver. Preceded by obesity Coma and ketosis not common Adult onset and treatment by diet control or hypoglycemic agents
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 .
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.
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 .
2- Hyper parthyrodismIt 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 ).
Primary hyperpara-thyroidism,"brown" giant cell tumor on the palate.
3- Sex hormonesGingival 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 .
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.
1.LeukemiaDef. 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.
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.
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.
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.
2. AnemiaDef. 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.
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.
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.
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.
3. ThrombocytopeniaEtiology:• 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.
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.
Leukocyte disorders : Disorders that affect production or function of leukocytes severe P. distinction. Cyclic neutropenia, ulcer on the labial mucosa
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.
Agranulocytosis, ulcer on Agranulocytosis, severe the tongue. periodontal destruction. Agranulocytosis, mildperiodontal destruction.
AIDS:Etiology :• human Immuno deficiency virus .Effects:• Destruction of lymphocytes increase susceptibility to opportunistic infections including destructive periodontitis and malignancies .
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 .
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 )
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.
Other chemicals :Include : Phosphorus . Arsenic . Chromium .It will lead to : Inflammation and ulceration of the gingiva . Necrosis of alveolar bone and loosening of teeth .