ORAL METABOLIC disorders of body; pptx. 1

details of increase and decrese level of minerals

1. Oral Aspects of Metabolic Diseases

2. INTRODUCTION Metabolism is a complex process that involves a series of chemical reactions in the human body Physio chemical process. Some reactions produce the energy which is stored in the form of ATP while other reactions consume energy to manufacture complex compounds process of metabolism includes 2 types of mechanisms- catabolism and anabolism

3. Catabolism is a process which involves release of energy by breaking complex organic compounds into simple molecules. In this process energy is been produced. Anabolism is a process that requires energy for synthesis of complex compounds from small molecules. In this process energy is been utilized Alterations in these metabolic processes constitute the disturbances of metabolism causing metabolic disorders

4. It is believed that the intraoral production of acids from carbohydrate, arising from incomplete oxidation, is a factor in the production of dental caries, periodontal diseases, oral malodor, bone loss and other associated metabolic diseases

5. DISTURBANCES IN MINERAL METABOLISM

6. widely distributed in the body Normal blood phosphorous level-2.5mg/dL Present in organic and inorganic form RDA- 800mg/day. During pregnancy & lactation-1200mg/dl Essential for formation of bone & teeth. constituent of hydroxyapatite in bone Provides structural support Formation and utilization of high energy compounds - ATP,ADP, Creatine phosphate etc Formation of phospholipid, phosphoprotein, nucleic acids& nucleoproteins. Several enzymes and proteins are activated by phosphorylation

7. HYPOPHOSPHATEMIA Muscle weakness Softening or weakening of bones Altered mental state Seizures Numbness Reflexive weakness Heart failure Muscle pain Muscle cramps Tetany Perioral numbness Tingling Weak bones. Rash. Itchy skin. HYPERPHOSPHATEMIA Oral manifestations Early loss of deciduous teeth Severe dental caries Improperly formed teeth Alveolar bone loss CAUSES Inadequate phosphate intake Increased phosphate excretion Shift from extra cellular phosphate to intracellular CAUSES Chronic renal failure Hypoparathyroidism Metabolic & respiratory acidosis

8. MAGNESIUM Fourth most abundant cation Essential for life and is present as intracellular ion in all living cells and tissues. Participate in every phosphorylating mechanism. Necessary for the activity of certain enzymes- phosphatase and cocarboxylase Normal serum Mg-1-3 mg/dl Functions As a cofactor for enzyme system Activator to a wide spectrum of enzymatic actions. Essential for peptidases, ribonucleases, glycolytic enzymes and cocarboxlylation reactions . RDA 50mg for infants 400mg - teenage males 350mg - pregnancy-& lactation

9. Hypomagnesemia ===Mg <1.46mg/dl Nausea Vomiting Loss of appetite Fatigue Weakness Hypocalcemia Hypokalemia Numbness and tingling in the extremities Cramps and muscle contractions Seizures Personality changes Abnormal heart rhythms Coronary spasms Heart diseases High blood pressure Type 2 diabetes Osteoporosis

10. HYPERMAGNESMIA ( Mg-> 3.6mg/dl) Rare condition Caused by renal failure High dose of Mg containing antacids

11. FLUORIDE Ionic form of fluorine. All foods contain at least traces of fluoride Water- major dietary source. Infants' and young children’s-0.5 to 1 mg of fluoride per day. Older children, adolescents, and adults-1.5 to 2 mg of fluoride per day Fruits, vegetables, and cereals ,sea foods especially fish sardines and salmon

12. Major site of absorption of fluoride – stomach. Teeth and skeleton -highest concentrations of fluoride because of the affinity of fluoride for calcium. Cementum, bone, dentin, and enamel. Fluoride is found in both extracellular and intracellular fluids of soft tissues but at very low concentrations. Fluoride is also found in saliva at about 0.01 ppm

13. Three mechanisms by which fluoride inhibits caries. An increase in the enamel's resistance to acid solubility as a result of a high concentration of fluoride in the outer enamel surface - formation of fluorapatite- more acid resistant , stable and less soluble. The ability of fluoride to remineralize demineralized or hypomineralized enamel Fluoride's antibacterial effects on plaque growth.

14. Excess of fluoride in drinking water or diet is harmful and is considered to be the main cause of the crippling disease known as fluorosis Skeletal Fluorosis Dental Fluorosis

15. Skeletal Fluorosis Prolonged, excessive accumulation of fluoride can cause a debilitating bone and joint disease known as skeletal fluorosis.  It alters the bone metabolism Affecting the entire skeleton. Bones become weaker and more brittle Pain and stiffness in joints increase. Joint immobility Muscle wasting, and neurologic problems can lead to crippling.

16. Fluoride reacts with the calcium in bones to form  calcium fluoride (CaF 2 ). It replaces naturally occurring calcium  hydroxyapatite   Alters the normal bone formation and resorption. leads to bone disorders: Osteomalacia – softening of the bone due to inadequate bone mineralization. Osteoporosis – bone loss makes bones weak and easy to break. Osteoarthritis  - most common form of arthritis affects various joints in body

17. Dental fluorosis Dental fluorosis is caused by taking in too much fluoride over a long period causes changes in the appearance of tooth enamel. Signs of dental fluorosis : Pits or fissures Chalky white appearance White , Yellow or dark brown spots

18. DISTURBANCES IN PROTEIN METABOLISM Complex biologic compounds of high molecular weight containing nitrogen, hydrogen, oxygen, carbon, and small amounts of sulfur. Part of every cell in the body. Helps the body to build and repair cells and tissues. Major component of the skin, muscle, bone, organs, hair, and nails. Required in increased quantity in the last half of pregnancy and during lactation, infancy, childhood, and adolescence

19. Disturbances of protein metabolism Protein energy malnutrition Amyloidosis Porphyria

20. Protein-energy malnutrition The range of conditions arising from lack of calories and proteins in a child below 5 yrs of age  Also called protein-energy undernutrition Due to insufficient intake or absorption of protein, energy, and micronutrients to meet metabolic demand.

21. Classification Of Protein Energy Malnutrition Primary PEM Secondary PEM

22. Primary PEM Found in children. Rarely found in the elders, the main cause being depression. In children-two types: Kwashiorkor Marasmus Secondary PEM It is caused due to disorders in the gastrointestinal tract. It can be caused due to infections, hyperthyroidism, trauma, burns, and other critical illnesses. It decreases appetite and impairs nutrient metabolism

23. Kwashiokar Edematous malnutrition Common in children -1 and 5 years. Due to a protein deficiency which occurs after protein rich foods are discontinued during weaning Symptoms Children appear smaller than their age Children frequently have  digestive problem- diarrhea

24. Skin changes- Pigment loss Red/purple patches Skin sloughing Development of sores Anemia - Main building block of Hb is globulin. - Dec . globulin level- dec.production of RBC. Fatty liver

25. Underdeveloped muscles Pot belly due to abdominal muscle wasting Extreme protein deficiency Decreased liver protein synthesis Osmotic imbalance Edema Abdominal distention

26. Hair changes & nail changes Nails — thin, soft, fissured, and/or ridged nail plate Alternating bands of pale and dark hair along a single strands-indicate alternating periods of good and poor nutrition “flag sign” in the hair of a child with kwashiorkor hair becomes thin and fragile with bands of loss of pigmentation.

27. Moon face Very thin limps Enlarged liver Children looks unhappy

28. Marasmus Seen in infants less than 1 year old. Deficiency of protein carbohydrates and fats. More serious than kwashiorkor. Characterized by muscle wasting and depletion of body fat stores. Symptoms Monkey-like / old man facies with a sunken body Eyes are sunken, cheeks are hollow giving a prematurely is looked Odema is absent

29. Abdomen curve inward. Skin is dry loose and wrinkled due to loss of fat below the skin. Hair may be normal or dry - thin and light-colored. Muscle are waste and have poor tone. Bones are prominent due to absence of fat around them.

30. Oral manifestations Bright reddening of the tongue with a loss of papillae Bilateral angular cheilosis Fissuring of the lips Loss of circumoral pigmentation. Epithelium readily becomes detached from the underlying tissues, leaving a raw, bleeding surface. Oral cytologic smears from his patients-a perinuclear vacuolization or halo around the nucleus

31. Amyloidosis Rare disease Accumulation of inappropriately folded proteins. Misfolded proteins are called amyloids. When proteins that are normally soluble in water- fold to become amyloids, they become insoluble and deposit in organs or tissues, disrupting normal function. Type A and Type B

32. Type A amyloid fibrillar protein of unknown origin seen in prolonged inflammatory diseases, genetic diseases, and syndromes such as familial Mediterranean fever. Type B amyloid immune origin seen in patients with multiple myeloma and macroglobulinemia

33. Any organ may be involved Most commonly affected are the kidneys, heart, gastrointestinal tract, liver, and spleen. Also seen in the respiratory tract, skin, eye, adrenals, and nerves, and may involve bone. Considered to be an irreversible disease.

34. Swelling of ankles and legs Severe fatigue and weakness Shortness of breath with minimal exertion Unable to lie flat in bed due to shortness of breath Numbness, tingling or pain in hands or feet Diarrhoea , possibly with blood, or constipation Unintentional weight loss of more than 10 pounds. An enlarged tongue Skin changes Irregular heartbeat Difficulty swallowing

35. Porphyria Group of rare diseases in which chemical substances called porphyrins accumulate. Porphyrins are essential for the function of hemoglobin Inborn errors of porphyrin metabolism - overproduction of uroporphyrin and related substances Deficiency of the enzymes that transform the various porphyrins into others

36. Erythropoietic Uroporphyria (Congenital porphyria Genetic defects which lead to deficiency of the enzyme uroporphyrinogen III synthase (UROS). The disease is characterised by extreme photosensitivity (abnormal cutaneous reaction to sunlight) which can leave severe scarring, blister formation, and the loss of digits or other features. Damaged skin can become infected, leading to further necrosis and deformities. The face, hands, and arms are the most significantly affected as they are frequently exposed.

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