Oral aspect of metabolic disorder based on shafers textbook of oral pathology

1. ORAL ASPECT OF‌‌
METABOLIC DISEASES‌

2. Outline of the presentation‌‌
1) Introduction‌‌
‌
2) Disturbances in Mineral
Metabolism‌‌
3) Disturbances in Protein
Metabolism‌‌
4) Individual Amino Acids‌‌
5) Lysosomal Storage Diseases‌‌
6) Disturnce in carbohydrates‌‌
‌
metabolism‌‌
‌
7) Hurler Syndrome‌‌
8) Disturbances in Lipid
Metabolism‌‌
9) Avitaminoses‌
‌
10) Disturbance in Hormonal‌‌
‌ Metabolism

3. INTRODUCTION‌‌

4. Duncan's definition of Metabolism‌ ‌( 1959)‌
Duncan described metabolism as “the total sum of tissue activity, considering
the physicochemical changes associated with and regulated by the
availability, utilization, and disposal of proteins, fats, carbohydrates,
vitamins, minerals, water, and the influences exerted by endocrines on these
processes.”
Deviations from these normal metabolic functions are referred to as
metabolic disturbances.
Metabolic Diseases: Conditions that arise when these processes are disrupted,
resulting in various metabolic diseases.
Oral Relevance:Many metabolic disorders first manifest in the oral cavity,
making it crucial for early diagnosis!

6. Disturbance in Mineral
Metabolism

7. Disturbances in Mineral Metabolism
Minerals are vital for both structural and regulatory functions within the body.
Approximately 29 elements account for ~4% of body weight, primarily found in bones.
Essential minerals include:
Macrominerals (daily requirement >100 mg): Sodium, potassium, chloride, calcium,
phosphorus, magnesium, sulfur.
Microminerals/Trace elements (daily requirement <100 mg): Chromium, copper, cobalt,
iron, iodine, manganese, selenium, fluorine, zinc.
Possibly essential trace elements: Cadmium, nickel, silicon, tin, vanadium.
Functions of Minerals:
Contribute to the formation of bone and teeth structure.
Help maintain fluid balance and acid-base equilibrium.
Play a role in hormones and enzymes.
Activate enzymatic reactions.
Are crucial for oxygen transport (e.g., iron in hemoglobin).
An element is considered essential if its deficiency leads to dysfunction that can be reversed
through supplementation.

9. Calcium is the fifth most abundant element in the human body.
The total body calcium content ranges from 100–170 g, with approximately 99% stored in
bones, 0.5% in soft tissues, and 0.1% in extracellular fluid.
The normal serum calcium level is around ~1.1 mg/dL.
Absorption
Calcium is primarily absorbed in the duodenum and the initial segment of the jejunum.
Only 20–40% of dietary calcium is effectively absorbed.
Factors that enhance absorption include:
Vitamin D (essential for effective absorption).
Low pH (for example, citrates produce soluble calcium citrate).
Lactose (which improves intestinal permeability).
High-protein diets (which lead to soluble calcium-amino acid complexes).
Factors that inhibit absorption consist of:
Phytic acid (found in grains, which forms insoluble calcium phytate).
Oxalates (present in spinach, which create calcium oxalate).
Excess fat (which produces insoluble calcium soaps).
Calcium

11. Excretion
Primarily eliminated through feces (unabsorbed calcium) and urine (absorbed calcium).
Normal urinary excretion levels: <250 mg/day for women, <400 mg/day for men.
Increased excretion may result from:
Elevated plasma calcium, excess vitamin D, metabolic acidosis, or hyperthyroidism.
Decreased excretion can be caused by:
Parathyroid hormone, low dietary calcium intake, or during growth/pregnancy.
Functions
1.Formation of bones and teeth (providing structural support).
2.Blood coagulation (crucial for the clotting cascade).
3.Muscle contraction (including the rhythm of the heart).
4.Nerve excitability and conduction.
5.Permeability of cell membranes.
6.Hormonal secretion (as a secondary or tertiary messenger).

12. Calcium Imbalance
Hypocalcemia (serum Ca²⁺ < 1.1 mg/dL):
Causes: Hypoparathyroidism, renal failure, vitamin D deficiency.
Effects: Tetany, muscle spasms, cardiac arrhythmias.
Hypercalcemia (serum Ca²⁺ > 1.1 mg/dL):
Causes: Hyperparathyroidism, malignancy, excessive vitamin D.
Effects: Lethargy, muscle weakness, kidney stones.
Deficiency and Disease
Osteoporosis: Associated with long-term negative calcium balance.
Experimental deficiencies (in animals):
Impaired blood clotting, bone deformities, parathyroid hyperplasia.
Treatment:
Increased calcium intake, strontium/fluoride supplementation (for osteoporosis).
Key Notes
Calcium levels are tightly regulated by parathyroid hormone (PTH) and vitamin D.
Dietary requirements differ:
800 mg/day for adults, 1,200 mg/day for pregnant and lactating women

13. osteoporosis (hypocalcaemia )
Kidney stones (hypercalcaemia )

14. Pathologic Calcification –
Definition & Types
Abnormal accumulation of calcium salts (along with iron,
magnesium, etc.).
Three primary types:
a.Dystrophic calcification – occurs in dead or degenerating
tissues (with normal blood calcium levels).
b.Metastatic calcification – takes place in normal tissues as a
result of elevated blood calcium levels.
c.Calcinosis – involves calcification in or under the skin (which
can be localized or generalized).
Pathologic Calcification

15. Experimental Findings (Animals)
Magnesium deficiency leads to enamel hypoplasia and rickets
(when calcium/phosphorus intake is low).
Excessive magnesium intake can cause rickets (if
calcium/phosphorus intake is low).
Clinical Notes
Relationship between Magnesium and Parathyroid Hormone
(PTH):
Hypomagnesemia results in PTH dysfunction and
hypocalcemia, even with elevated PTH levels.
Some instances exhibit bone resistance to PTH.

16. Dystrophic Calcification
Occurrence:
Found in:
Dead or dying tissues (such as TB necrosis, arteriosclerosis, scars, fatty degeneration).
Oral locations: Gingiva, tongue, cheek, and pulp of teeth (commonly seen in older adults).
Mechanism:
Local alkalinity in damaged tissue leads to calcium precipitation.
Not a result of elevated blood calcium levels.
Pulp Calcifications (Denticles/Pulp Stones):
Nodular type:
Involves calcification of hyalinized connective tissue (perivascular/perineural).
Typically located in coronal pulp, growing through accretion.
Diffuse type:
Found around necrotic cells & corpora amylacea.
Located in the root canal, developing around a central nidus.
Clinical Relevance:
Does not lead to pulp inflammation or dental infection.

17. 2. Metastatic Calcification
Occurs in:
Normal tissues such as kidneys, lungs, gastric mucosa, and blood vessels.
Caused by:
Elevated blood calcium levels (e.g., hyperparathyroidism, hypervitaminosis
D).
Distinguishing from dystrophic calcification:
It can be challenging to differentiate if necrotic tissue also calcifies during
high calcium states.
3. Calcinosis
Calcification of the skin (two types):
a.Calcinosis circumscripta – localized deposits.
b.Calcinosis universalis – widespread deposits (often linked to scleroderma,
dermatomyositis).

18. Feature DYSTROPHIC METASTATIC CALCINOSIS
Tissue State Dead/damaged Normal skin / Subcutaneous
Blood calcium Normal High varies
Common Site Arteries , pulp , scars Kidney,lungs,Vessels Skin(localized/General)
Cause
Local tissue
damage
Hypercalcaemia
(PTH/Vit D)
Connective tissue
disease

19. Dystrophic calcification
(Pulp stone )
Metastatic calcification
in lungs

20. Body Distribution & Blood Levels
Total body phosphorus: 500–800 g
85–90% is found in bones and teeth (with slow turnover)
Approximately 100 g is present in soft tissues (including cell membranes, nucleic acids, etc.)
Blood inorganic phosphate levels:
Adults: 2–4 mg/dl
Children: 3–5 mg/dl
Regulated by PTH, vitamin D, and phosphatase activity (less tightly controlled compared to calcium).
Dietary Requirements & Absorption
Daily intake recommendations:
Infants: 240 mg
Adults: 800 mg
Adolescents, pregnant, and lactating women: 1,200 mg (+50%)
Absorption:
90% of dietary phosphorus is absorbed in the small intestine.
70% is absorbed as orthophosphate post-digestion.
Interference: Excessive calcium, iron, or aluminum can create insoluble phosphates, which may
hinder absorption.
Phosphorus

21. Excretion
Primarily eliminated through urine (regulated by PTH and vitamin D).
Approximately 85% of filtered phosphate is reabsorbed in the proximal tubules.
Fecal excretion: Involves unabsorbed or re-excreted phosphate (as calcium phosphate).
Functions
Bone and teeth formation (in conjunction with calcium).
Energy metabolism:
Contributes to the formation of ATP (the energy storage molecule).
Plays a role in carbohydrate and fat metabolism.
Cell structure and function:
Integral to phospholipids (which compose cell membranes).
Essential for nucleic acids (DNA and RNA).
Serves as coenzymes (e.g., pyridoxal phosphate for amino acid metabolism).

22. Deficiency & Excess
Deficiency (rare in humans, but possible):
Leads to weakness, bone pain, rickets/osteomalacia.
Often observed with long-term antacid use, starvation, or
malabsorption.
Hyperphosphatemia:
Results from hemolysis, excess vitamin D, bone breakdown (e.g.,
cancer), or kidney dysfunction.
Experimental Findings (Rats)
A low phosphorus diet can cause growth retardation and severe rickets
within just one week.

23. Magnesium
General Overview
The fourth most abundant cation found in humans.
Crucial for cellular functions, enzyme activity (such as
phosphatase and cocarboxylase), and phosphorylation
reactions.
Body Distribution
Total body magnesium: approximately 25 g in a 70 kg adult.
More than 50% is stored in bones.
About 25% is located in muscles.
The remainder is distributed in the liver, pancreas,
erythrocytes, serum, and cerebrospinal fluid.

24. Dietary Requirements & Absorption
Daily Intake Recommendations:
Infants: 50 mg
Teenage Males: 400 mg
Pregnancy/Lactation: Additional 150 mg
Absorption:
Occurs mainly in the small intestine.
Competes with calcium (excess calcium can reduce magnesium absorption).
Enhanced by:
Vitamin D
Parathyroid hormone (PTH)
Growth hormone
High protein intake
Neomycin
Impaired by:
Diarrhea
Intestinal damage
High calcium intake

25. Excretion
60% of magnesium is lost through feces, while 40% is excreted via urine.
Sweat loss is approximately 0.75 mEq/day.
Urinary loss ranges from 3–7 mEq/day.
Hypermagnesemia is uncommon since the kidneys effectively excrete excess
magnesium.
Functions
Acts as an enzyme cofactor for processes such as peptidases, ribonucleases, and
glycolysis.
Regulates neuromuscular function (similar to Ca²⁺):
Low magnesium levels lead to tetany (hypomagnesemic tetany).
High magnesium levels can cause sedation, muscle paralysis, and coma.
Contributes to the structure of bones and teeth, with 70% stored as bone apatites.

26. Deficiency (Hypomagnesemia)
Causes:
Inadequate diet, vomiting, malabsorption, IV fluids lacking magnesium.
Symptoms:
Neuromuscular: Tetany, carpopedal spasms, Chvostek’s sign, seizures.
Metabolic: Hypocalcemia, hypokalemia (even with normal intake).
Behavioral: Changes in personality, anorexia, nausea.
Treatment: MgSO₄ injections for rapid relief of symptoms.
Excess (Hypermagnesemia)
Causes:
Renal failure, overuse of magnesium-containing antacids.
Symptoms:
Mild (5 mg/dL): Sedation.
Severe (18–21 mg/dL): Coma, potential death.
Associated Conditions:
Diabetes, adrenal insufficiency, hypothyroidism, renal failure.

28. Sodium
Distribution & Composition
Sodium in the body is primarily found as NaCl and NaHCO₃.
A typical adult male (weighing 70 kg) contains approximately 83–97 grams of sodium.
More than one-third of this is stored in the skeleton (with 65–75% being
unexchangeable).
The majority of the remaining sodium is extracellular, representing 90% of the basic
ions in extracellular fluid and plasma.
Enamel ash includes about 0.3% sodium, though its association with organic/inorganic
fractions or tissue fluid remains unclear.
Requirements & Excretion
Minimal salt requirement: approximately 0.5 grams/day (based on breastfed infants).
Breast milk contains 0.4 grams NaCl/L, while cow’s milk has 1.7 grams NaCl/L.
Maximal intake without edema: 35–40 grams/day.
Average intake in the U.S.: 10–15 grams/day.
Normal blood levels:
160 mg/dl (whole blood)
340 mg/dl plasma (147.8 mEq/L)

29. Functions of Sodium
Maintains acid-base balance and osmotic pressure.
Essential for the sodium-potassium pump, which involves cellular energy use.
Can replace potassium during heart muscle contractions.
Regulates:
Neuromuscular excitability
Blood viscosity
Fluid balance
Hormonal Influence & Clinical Conditions
Deoxycorticosterone, cortisone, hydrocortisone:
Enhance sodium reabsorption.
Reduce potassium reabsorption, increasing the risk of edema and potassium loss.
The kidneys filter approximately 25,000 mmol of sodium daily, yet less than 1% is
excreted due to reabsorption.

30. Sodium Imbalance Disorders
1.Hypernatremia (elevated sodium):
Causes: Dehydration, diabetes insipidus, excessive sodium intake, steroid
usage.
2.Hyponatremia (reduced sodium):
Causes: Diuretics, excessive perspiration, kidney disease, congestive heart
failure, diarrhea.
Addison’s Disease and Sodium Depletion
Leads to rapid loss of sodium and water, resulting in low plasma sodium and
high potassium levels.
Water is shifted intracellularly, leading to sodium and water depletion.
Radioactive sodium (Na²²) studies indicate that bone sodium (approximately
30% of total body sodium) resides on apatite crystal surfaces.

31. Sodium Deficiency
It rarely happens in isolation; it is typically accompanied by
chloride deficiency.
Signs of prolonged low salt intake include:
Weakness, fatigue, apathy, nausea, and muscle cramps.
Anorexia, exhaustion, and peripheral vascular collapse.

32. Potassium
Distribution & Composition
Potassium is the primary intracellular cation.
It is present in body fluids (such as blood and plasma) and tissues (including nerve, muscle, and cells).
The majority of potassium resides within cells, serving as the main cellular base.
Studies involving radioactive potassium (K⁴²) indicate a continuous exchange between intracellular and
extracellular environments.
Cellular membranes limit the free diffusion of potassium outside of cells.
Requirements & Excretion
The average dietary intake is approximately 4 grams per day.
Increased potassium intake is necessary during periods of rapid growth.
About 90% of potassium excretion occurs through urine.
An increase in sodium intake leads to greater potassium excretion.
Aldosterone plays a crucial role in regulating potassium secretion in the kidneys.
The normal plasma level is around 4 mEq/L.
Potassium is also excreted through the GI tract, saliva, and various digestive juices (gastric, bile,
pancreatic, and intestinal).

33. Functions
Collaborates with sodium to:
Support muscle activity (including heart function).
Maintain acid-base balance.
Facilitate neuromuscular excitability & nerve conduction.
Deficiency (Hypokalemia)
Typically not due to dietary insufficiency, but may result from:
Gastrointestinal losses (such as diarrhea and vomiting).
Malnutrition.
Diuretics and ion-exchange resins.
High levels of cortisone/hydrocortisone.
Diabetic acidosis coupled with insulin therapy.
Symptoms:
Muscle weakness, decreased reflexes, and paralysis.
Mental confusion and cardiac arrhythmias.
Gastrointestinal issues.
In severe cases →risk of cardiac/respiratory failure and paralytic ileus (potentially fatal).

34. Excess (Hyperkalemia)
Causes:
Tissue breakdown, adrenal insufficiency, and severe dehydration.
High potassium intake and kidney failure (decreased excretion).
Abrupt release of potassium from cells (due to disease).
Symptoms:
Numbness or tingling, cold skin, and weakness.
Mental confusion and disturbances in cardiac rhythm.
Peripheral vascular collapse.
Clinical Notes
There are no documented direct effects of potassium imbalance on oral
structures.
The kidneys play a vital role in regulating potassium levels.

35. Chlorine
Role in the Body
Closely associated with sodium (Na) and potassium (K) metabolism.
Vital for maintaining water balance and acid-base equilibrium.
Intake & Absorption
Average daily intake: 6–9 grams (primarily as sodium chloride).
Absorption occurs in the small intestine.
Chloride uptake involves an exchange with bicarbonate, whereas sodium exchanges with hydrogen ions.
Distribution & Excretion
A key extracellular mineral (alongside sodium).
Mainly excreted by the kidneys.
Reabsorbed to maintain normal fluid concentrations in the body (acting as a threshold substance).
Functions
Crucial for the production of HCl in gastric juice.
Plays a role in the chloride shift associated with CO₂ transport in the bloodstream.
Activates salivary amylase.
Additional biological functions remain largely unclear.
Deficiency Effects
Rats on low-chloride diets exhibited stunted growth and kidney damage.
In humans:
Pyloric obstruction can result in chloride loss, leading to hyperexcitability, convulsions, and gastric tetany.
Administering chloride can mitigate these symptoms.
No oral deficiency symptoms have been documented.
Normal Blood Levels
Plasma concentration: 550–650 mg/dL (in the form of sodium chloride).

36. Disturbances in Metabolism of
trace element

38. Iodine
Sources:
The best natural source is seafood.
It is also present in vegetables, milk, and the food colorant erythrosine (which is rich in iodine).
Blood Levels:
Whole blood: 8–12 µg/dL (with a range of 3–30 µg/dL).
Protein-bound iodine (PBI): 3–8 µg/dL.
Increased levels may occur during pregnancy and hyperthyroidism.
Decreased levels are associated with hypothyroidism.
Function:
Iodine is essential for the synthesis of thyroid hormones (T3 & T4).
No other known biological function in higher animals.
Deficiency (Goiter):
In humans, iodine deficiency leads to endemic goiter.
In animals, it does not cause colloid goiter.
Prevention can be achieved through the use of iodized salt or water in affected areas.
Distribution:
Approximately one-third of the body’s iodine is stored in the thyroid gland.
It is also concentrated in the ovaries.
Mechanism:
The process of conversion to colloid (thyroglobulin) is not fully understood but is related to tyrosine metabolism.
Oral Effects:
Thyroid dysfunction can impact oral structures (further details can be found in the endocrine section).

39. Goitre

40. COPPER
General Role:
Essential for life, associated with iron metabolism since the planet's oxygenation.
Body Distribution:
Total: 100–150 mg in adults.
Muscles (65 mg), bones (23 mg), liver (18 mg).
The fetal liver contains 10 times more copper than the adult liver.
Daily Requirements:
Infants/children: 0.05 mg/kg/day.
Adults: Approximately 2.5 mg/day.
A typical diet supplies 2.5–5.0 mg/day.
Absorption & Function:
Deficiency in animals: Leads to anemia (less documented in humans).
Crucial for:
Iron absorption (through ceruloplasmin, a ferroxidase).
Erythropoiesis (a lack of copper results in microcytic hypochromic anemia).
Enzyme cofactor for:
Cytochrome c oxidase (involved in cellular respiration).
Superoxide dismutase (serves as an antioxidant).
Tyrosinase (necessary for melanin synthesis).
Lysyl oxidase (important for collagen and elastin cross-linking).
Clinical Disorders:
Wilson’s disease: Characterized by copper overload (hepatolenticular degeneration).
Menkes syndrome: Results from copper deficiency (kinky-hair syndrome, neurological defects).
Therapeutic Use:
Copper supplements (with or without iron) can aid in treating infantile anemias and secondary anemias in adults.

42. 1. General Overview
Iron is an essential trace element, yet deficiency is prevalent, particularly in India.
Total body iron levels:
Adult males: Approximately 3.8 grams
Adult females: Approximately 2.3 grams
Two types of iron:
Functional iron: Utilized in metabolic processes (such as hemoglobin, myoglobin, and enzymes).
Storage iron: Stored as ferritin and hemosiderin.
2. Daily Requirements & Absorption
Daily Requirements:
Adult males: Around 10 mg/day
Adult females: Approximately 20 mg/day (higher due to menstruation)
Lactating mothers: 25–30 mg/day
Children: 10–15 mg/day
Absorption:
Takes place in the duodenum (as ferrous or ferric salts).
Regulated by body iron stores:
Low stores lead to increased absorption.
Adequate stores result in limited absorption.
Minimal excretion (iron is often described as a "one-way substance").
Normal daily loss: Approximately 1 mg/day (through feces, sweat, and urine).
Iron

43. Iron Deficiency Anemia (IDA)
Prevalence: Common among women and children.
Symptoms and Effects:
Plummer-Vinson syndrome: Characterized by esophageal webs, causing difficulty in swallowing.
Koilonychia: Notable for spoon-shaped nails.
Bone marrow changes: Observations include normoblastic arrest.
Blood abnormalities:
Microcytosis: Indicative of smaller red blood cells (RBCs).
Anisocytosis: Presence of uneven sizes in RBCs.
Hypochromia: Indicates pale RBCs.
Oral manifestations:
Sore tongue: Similar in appearance to deficiencies in niacin or riboflavin.
Treatment:
Iron supplementation: Proven effective in correcting anemia.
Differentiation required: It's essential to distinguish from thalassemia to avoid misdiagnosis.
Iron Overload (Excess Iron)
Causes:
Hereditary hemochromatosis: Leads to excessive iron absorption, resulting in cirrhosis, diabetes, and bronze skin pigmentation.
Hemoglobinopathies:
Thalassemia: Results in ineffective erythropoiesis, causing iron accumulation.
Sideroblastic anemia: Characterized by defective heme synthesis.
Bantu siderosis:
Triggered by consuming iron-rich homemade beer, typically fermented in iron pots.

44. Koilonychia
(Notable for spoon-shaped nails)

45. Zinc
1. Basics
An essential nutrient recognized for over a century
Sources: Liver, dairy products, eggs, whole grains, legumes, and leafy greens
Total body zinc: Ranges from 1.4 to 2.3 grams
Highest concentrations: Found in skin and prostate (70–80 mg/100 g), bones and
teeth (10–15 mg/100 g)
Enamel/dentin: Approximately 0.02% zinc content (higher than other hard
tissues)
2. Absorption & Excretion
Absorbed in the duodenum and ileum (with limited absorption)
Facilitated by: Pancreatic zinc-binding factor
Inhibited by: High levels of calcium and phosphates
Excretion: About 9 mg/day through feces and urine; only 0.5 mg is retained
Daily requirement: Between 15 and 20 mg (0.3 mg/kg of body weight)

46. Key Functions
Enzymatic Role:
Includes superoxide dismutase, carbonic anhydrase, and leucine aminopeptidase
Vitamin A Metabolism: Releases vitamin A from the liver
Insulin Function: Integral part of protamine/globin zinc insulin
Wound Healing: Accumulates in granulation tissue; deficiency can slow the healing process
Diabetes Connection: Low zinc levels noted in the pancreas
Deficiency Disorders
Growth & Sexual Development:
Conditions such as dwarfism and hypogonadism (based on Prasad’s studies in Iran and Egypt)
Symptoms may include delayed bone age, atrophic testes, and lack of body hair
Characterized by low plasma, red cell, and hair zinc levels; increased zinc retention
Acrodermatitis Enteropathica:
A genetic disorder leading to zinc malabsorption, resulting in diarrhea, skin lesions (vesicles, plaques), hair loss, and
inflammation of the mouth
Additional Effects:
Impaired sense of taste, various skin disorders, delayed wound healing, and reproductive complications
Low leukocyte zinc levels indicate immune dysfunction
Reduced zinc levels observed in conditions such as leukemia, liver cirrhosis, and hepatitis

47. Acrodermatitis Enteropathica

48. A vital trace element commonly found throughout the Earth's crust.
Total body content ranges from 10–18 mg, with the highest concentrations in the kidney and liver.
Dietary sources include cereals, vegetables, fruits, nuts, and tea.
Normal blood levels are between 4–20 µg/100 ml, primarily found in red blood cells bound to
porphyrins.
It is transported in plasma through transmanganin (β₁-globulin).
Functions as a cofactor/activator for various enzymes, including arginase, cholinesterase, and
decarboxylases.
Plays a crucial role in mitochondrial enzyme function, bone development, and reproductive
health.
Deficiency can lead to bone abnormalities, ataxia, and infertility.
Excess may result in neurological damage, exhibiting Parkinsonism-like symptoms, psychosis,
and depletion of dopamine and serotonin.
Absorption rates are higher in anemic adults and premature infants.
Manganese

49. Cobalt
A crucial component of vitamin B₁₂.
Dietary sources are primarily animal-based; average intake is 5–8 µg/day
(Recommended Dietary Allowance: 1–3 µg/day).
Vital for:
The formation of cobamide enzymes (adenosyl coenzyme).
Proper bone marrow function and maturation of red blood cells (RBCs).
Deficiency results in vitamin B₁₂ deficiency, leading to macrocytic anemia.
Excess can lead to polycythemia due to the inhibition of respiratory enzymes,
such as cytochrome oxidase.
There is negligible storage of cobalt in the body.
Vitamin B₁₂ consists of about 4.5% cobalt; only minimal amounts are required to
address deficiencies (e.g., pernicious anemia).

50. Chromium
An essential trace element for glucose metabolism (discovered in 1959).
Normal blood concentration: 6–20 µg/100 ml.
Sources include cooking with stainless steel utensils and various foods.
Functions:
Aids in insulin binding through a "chromium bridge" (creates a complex with insulin
receptors).
A crucial part of the Glucose Tolerance Factor (GTF), with organic Cr³⁺ being more
bioactive than its inorganic counterpart.
Influences carbohydrate and lipid metabolism, but is not a direct hypoglycemic agent.
Deficiency:
Associated with impaired glucose tolerance, malnutrition, and diabetes.
Commonly observed in cases of protein-calorie malnutrition, gestational diabetes,
and maturity-onset diabetes.

51. Selenium
General Overview
A vital trace element for all species, including humans.
Initially recognized for its role in preventing liver cell necrosis.
Found in biological forms as selenium-containing amino acids:
Selenomethionine, selenocysteine, selenocystine (concentration < 0.2 µg/g).
Highest concentrations are located in the liver, nails, and kidneys.
Primary dietary source: plant material.
Absorbed in the duodenum (mainly as a methionine analog).
Total body selenium content: 4–10 mg.
Blood selenium levels average around ~0.22 µg/ml (can decrease to 0.009 µg/ml in deficient areas, such as China).
Metabolic Role & Function
An essential component of glutathione peroxidase (a selenoenzyme).
Present in both cytoplasm and mitochondria.
Aids in reducing hydroperoxides, thereby protecting cells from oxidative damage.
Functions as a primary antioxidant:
Scavenges reactive oxygen species (ROS) and free radicals.
Operates synergistically with vitamin E (each nutrient supports the other's requirements).
Deficiency in humans (noted in cases of protein-energy malnutrition):
Results in liver necrosis, exudative diathesis, and pancreatic degeneration.
Can lead to muscular dystrophies and myopathies.

52. Symptoms of Toxicity and Excess
Chronic exposure may result in:
Garlicky breath (caused by the excretion of dimethyl
selenide).
Dermatitis, hair loss, and brittle nails.
This is often seen in occupational exposure within
industries such as electronics, glass, and paint.

53. Fluorine
General Overview
A vital trace element sourced from food and water.
Key dietary sources include: tea, salmon, sardines, mackerel, and fluoridated
water.
Recommended intake: approximately 1 ppm (part per million) in drinking
water (around 1–2 mg/day).
Toxic threshold: >3 mg/day (excess can result in fluorosis).
Higher concentrations of fluoride are typically found in Indian foods (like rice,
salt, and spices) compared to Western diets.
Absorption & Excretion
Absorbed in the intestine through diffusion.
Blood fluoride levels are approximately 20 µg, predominantly in ionized form.
Excreted mainly through urine.
A calcium-rich diet can decrease fluoride absorption.

54. Biological Role
Dental Health:
Strengthens tooth enamel, making it more resistant to acid erosion.
Converts calcium phosphate into apatite crystals, which help harden teeth and bones.
Aids in preventing dental caries (cavities).
Bone Health:
Trace amounts found in bones contribute to mineralization.
Supports bone density, but excessive amounts can lead to osteosclerosis.
Deficiency (Rare)
In rats, a deficiency leads to severe dental caries, resulting in an inability to eat and ultimately, starvation.
While evidence in humans is limited, it may negatively impact tooth and bone development.
Toxicity (Fluorosis)
Causes:
Chronic intake exceeding 3 mg/day (e.g., from high-fluoride water or industrial exposure).
Industrial workers (e.g., those in cryolite processing) may inhale 20–80 mg/day.
Symptoms:
Dental fluorosis, characterized by mottled teeth.
Skeletal fluorosis:
Leads to osteosclerosis (abnormal hardening of bones).
Can result in calcification of ligaments/tendons, arthritis, and spinal rigidity.
In advanced cases, may cause crippling deformities.
Collagen Disruption:
Reduced proline uptake leads to weakened collagen fibers and abnormal calcification.

55. FLUOROSIS

56. Disturbance in Protein Metabolism

57. Protein Fundamentals
Proteins are intricate organic molecules made up of nitrogen, hydrogen, oxygen, carbon, and sulfur.
They exhibit greater structural complexity and functional diversity compared to carbohydrates or lipids.
Plants create proteins from nutrients in the soil and air, while animals must derive proteins from their food.
The process of digestion involves breaking down proteins into smaller, absorbable components through hydrolysis.
In a typical adult, protein comprises about 12–18% of body mass.
Studies on nitrogen balance help establish the minimum protein intake necessary for maintaining homeostasis.
Protein Needs
The recommended intake is 1 gram of protein per kilogram of body weight (with adjustments based on individual
requirements).
Increased protein consumption is essential during:
The latter half of pregnancy
Lactation
Infancy, childhood, and adolescence
Proteins are crucial for:
Cellular structure
Hormones, enzymes, antibodies, and plasma proteins
Categories of proteins:
Complete proteins (from animal sources) contain all essential amino acids.
Incomplete proteins (for instance, corn lacks lysine, while legumes are low in methionine).
Complementary proteins (mixing incomplete proteins to satisfy amino acid requirements).

58. Protein Metabolism & Function
The synthesis of body proteins occurs actively during periods of growth, pregnancy, and lactation.
Proteins play vital roles in:
Development of teeth (matrix formation for hard tissues).
Neutralizing acids produced by oral bacteria.
Protein-Energy Malnutrition (PEM)
A range of diseases characterized by:
Kwashiorkor (protein deficiency, edema, hypoalbuminemia).
Marasmus (severe calorie deficiency, significant weight loss).
Marasmic kwashiorkor (features of both conditions).
Nutritional dwarfism (long-term adaptation to low protein and energy).
Predominantly found in developing countries (including India, Africa, Southeast Asia, and Latin America).
Marasmus
Contributing factors include:
Rapid pregnancies, early weaning, and insufficient infant feeding.
Symptoms may present as:
Significant weight loss, muscle wasting, and an "aged" appearance.
Often associated with:
Chronic illnesses, burns, hypermetabolic states, and malabsorption issues.

59. Kwashiorkor
Caused by:
A low-protein diet following weaning.
Symptoms:
Edema (which disguises weight loss), diarrhea, changes in skin and hair, and increased susceptibility to
infections.
Oral manifestations:
A red, depapillated tongue, angular cheilosis, dry mouth, and mucosa that is caries-free but prone to
trauma.
Effects on Oral Health (Animal Studies)
Protein deficiency results in:
Delayed tooth eruption, enamel defects, and a rise in caries.
Degeneration of periodontal tissues.
Decreased salivary gland function (lower saliva volume, along with reduced DNA, RNA, and protein
content).
Genetic & Metabolic Disorders
Phenylketonuria (PKU):
The inability to metabolize phenylalanine necessitates a protein-restricted diet.
Gout:
Elevated uric acid levels require protein restriction to limit purine intake.

60. Protein Energy malnutrition

61. Marasmus

62. Kwashiorkor

63. Marasumus Vs Kwashiorkor

65. Definition: Abnormal protein deposits accumulate between cells within tissues and organs.
Microscopy:
Under light microscopy, it manifests as pink translucent material.
Electron microscopy reveals nonbranching fibrils characterized by a distinct "E-pleated sheet" structure.
Types of Amyloid:
Type A (secondary): Associated with chronic inflammatory diseases such as rheumatoid arthritis and tuberculosis.
Type B (primary): Likely immune-related, often linked to multiple myeloma.
Type C: Encompasses amyloid related to aging and localized forms.
Common Diseases Associated with Amyloidosis:
Conditions like rheumatoid arthritis, chronic infections (e.g., tuberculosis, osteomyelitis), multiple myeloma, and Hodgkin’s
disease.
Organs Affected:
Primarily the kidneys, heart, gastrointestinal tract, liver, spleen, respiratory tract, skin, nerves, and occasionally bone.
Diagnosis:
Staining Techniques: Congo red (which shows green birefringence under polarized light), crystal violet, and thioflavin-T
fluorescence.
The potassium permanganate test differentiates AA amyloid (which loses Congo red affinity) from AL amyloid.
Gingival biopsy may be conducted, though results can vary.
Macroscopic Features:
Affected organs may appear enlarged, gray, and waxy.
Staining with iodine and sulfuric acid reveals mahogany-brown deposits.
Nature of the Disease:
This condition is irreversible and leads to progressive cell destruction.
Amyloidosis

68. Definition: A group of inherited disorders resulting from errors in porphyrin metabolism, causing an
overproduction of uroporphyrin.
Two Main Types:
a.Erythropoietic Porphyria:
Characterized by early photosensitivity, splenomegaly, and abnormal porphyrin levels in red blood cells.
Subtypes include:
Uroporphyria (Congenital Porphyria): Notable for red urine at birth, photosensitivity, and scarring skin
lesions.
Protoporphyria: Generally presents with milder symptoms.
b.Hepatic Porphyria:
Comprises four subtypes:
Acute intermittent porphyria
Porphyria variegata
Porphyria cutanea tarda
Hereditary coproporphyria
Oral Findings in Congenital Porphyria:
Teeth may exhibit red/brown discoloration and fluoresce red under UV light.
This is due to porphyrin binding to calcium phosphate in teeth and bones.
The presence of porphyrin in deciduous teeth indicates that the disorder could initiate during fetal
development.
Porphyria

71. Lysosomal Storage Disorder
Lysosomal storage diseases (LSDs) are inherited, heterogeneous disorders caused by the buildup of undigested macromolecules within lysosomes.
This accumulation leads to an increase in both the size and number of lysosomes, resulting in cellular dysfunction and various clinical abnormalities.
Classification
LSDs are classified based on the substrate that accumulates.
They include:
Sphingolipidoses
Glycoproteinoses
Mucolipidoses
Mucopolysaccharidoses (MPSs)
Other variants
Expanded Concept of LSDs
The definition now encompasses deficiencies in:
Lysosomal enzymes
Noncatalytic lysosomal proteins
Functional abnormalities within lysosomes
Pathological Manifestations
The clinical manifestations depend on:
The type and quantity of accumulated materials
The specific organs that are affected
Vulnerable Cells:
Neurons (due to their inability to divide and regenerate)
The mononuclear phagocyte system (which contains a high concentration of lysosomes)
Genetic Basis
Advances in molecular genetics have led to the identification of defective genes responsible for LSDs.
These genes have been isolated, characterized, and their mutations identified.
Genetic heterogeneity: Despite exhibiting similar phenotypes and biochemical characteristics, the gene-level complexity remains significant.
Prevalence
There are more than 40 recognized lysosomal storage diseases.

73. Disturance in Carbohydrate Metabolism
Mucopolysaccharidoses (MPS)

74. Occurs due to abnormal degradation of glycosaminoglycans (GAGs) such as dermatan sulfate, keratan sulfate, heparan sulfate, and chondroitin sulfate.
Results in organ accumulation and dysfunction.
GAGs are typically present in the cornea, cartilage, bone, connective tissue, and reticuloendothelial system—these areas become storage sites.
Enzyme Deficiencies & Genetics
Deficiencies in catabolic enzymes hinder GAG breakdown.
Ten enzyme deficiencies lead to six distinct types of MPS.
Degradation involves:
4 glycosidases
5 sulfatases
1 nonhydrolytic transferase
Autosomal recessive inheritance applies (with the exception of MPS II, which is X-linked).
Mutation analysis is useful for correlating genotype with disease severity.
Clinical Features
Progressive disorders impacting various organs:
Brain, liver, spleen, heart, and blood vessels.
Common symptoms include:
Coarse facial features
Corneal clouding
Cognitive impairment (in many cases)
Diagnosis
Urine analysis reveals elevated GAG fragments.
Enzyme assays (in fibroblasts, leukocytes, and serum) confirm the diagnosis.
Heterozygous carriers may be difficult to identify based solely on enzyme activity.
Prenatal diagnosis can be performed through amniocentesis or chorionic villus sampling.
MPS Type I Subtypes
1.MPS I H (Hurler syndrome) – The severe form.
2.MPS I H/S – An intermediate form between Hurler and Scheie.
3.MPS I S (Scheie syndrome) – Biochemically akin to Hurler but less severe.

75. Cause: A chromosomal abnormality located at 4p16.3 disrupts
mucopolysaccharide metabolism.
Inheritance: Autosomal recessive.
Clinical Features:
Symptoms typically emerge within the first two years of life and progress
towards an early death (usually before puberty).
Facial characteristics include a large head, prominent forehead, broad
saddle nose, hypertelorism, thick lips, a large tongue, an open mouth,
and nasal congestion.
Additional symptoms involve corneal clouding, hepatosplenomegaly
(swollen abdomen), short neck, spinal abnormalities, and "claw hand"
resulting from flexion contractures.
Dwarfism and intellectual disability are also common.
Hurler Syndrome (Mucopolysaccharidosis I, MPS IH, Gargoylism)

76. Oral Manifestations
A short, broad mandible with a wide intergonial distance.
Teeth may appear small, widely spaced, and misshapen, although some cases report normal
teeth with delayed eruption.
Presence of gingival hyperplasia that varies in severity and may sometimes resemble
fibromatosis gingivae.
An enlarged tongue.
Histologic Features
Excessive accumulation of intracellular mucopolysaccharides in various tissues, including the
liver, spleen, nervous system, and cartilage.
Identification of "Hurler cells" (gargoyle cells) in gingival tissues, characterized by large,
metachromatic-staining cytoplasm.
Lab Findings
Elevated levels of urinary mucopolysaccharides.
Detection of Reilly bodies (metachromatic granules) in lymphocytes.

78. Cause: A rare autosomal recessive disorder linked to 1q21 due to a mutation in the ECM1 gene.
First Described: This condition was first identified by Urbach and Wiethe in 1929.
Clinical Features:
Generalized thickening of skin, mucosa, and internal organs.
Hoarse voice from birth resulting from laryngeal infiltration.
Beaded eyelid papules, thickened vocal cords, and dyspnea (may necessitate surgical intervention).
Skin Changes: Includes warty papules, scarring, alopecia, and nail dystrophy.
Neurological Issues: May experience epilepsy and neuropsychiatric abnormalities, occasionally with temporal
lobe calcifications.
Oral Manifestations:
Yellowish-white papular plaques on the oral mucosa, worsening with age.
Thickened, nodular lips and a firm, enlarged tongue, which can sometimes be bound to the floor of the mouth.
Recurrent parotitis due to parotid duct stenosis.
Congenital absence of teeth and severe enamel hypoplasia.
Histologic Features:
PAS-positive deposits found in the basement membrane, dermis, and surrounding blood vessels.
Hyaline (glycoprotein) material accumulation.
A decrease in type I collagen and an increase in type IV collagen due to overproduction in the basement
membrane.
Treatment: There is no cure, and management focuses on symptomatic relief.
Lipoid Proteinosis (Hyalinosis Cutis et Mucosae, Urbach-Wiethe Disease)

79. Thickened skin , mucosa, tongue
in Lipoid Proteinosis

80. Cause: An autosomal recessive disorder resulting from a
deficiency in fructose 1-phosphate aldolase.
Clinical Features:
Hypoglycemia and vomiting following fructose
consumption.
Strong aversion to sweets and fruits.
Oral Manifestations:
Significantly reduced sucrose intake due to dietary
restrictions.
Lower incidence of caries when compared to controls.
Hereditary Fructose Intolerance

81. Disturbance in Lipid Metabolism

82. Disturbances in Lipid Metabolism
Overview of Lipid Metabolism:
Encompasses the assimilation, utilization, replacement, and synthesis of fatty acids.
Fatty acids exist in cells as esters (with glycerol, cholesterol, etc.) or are linked with phosphoric acids, nitrogenous bases, or
carbohydrates.
While disturbances are uncommon, they can be categorized as:
Lipoid storage diseases
Xanthomatoses
Lipid granulomas
Gaucher’s Disease
Cause: Results from a deficiency of glucocerebrosidase, leading to the accumulation of glucocerebroside in macrophages.
Types:
Type I (Chronic, non-neuronopathic):
The most prevalent form (99%), often seen in Ashkenazi Jews.
Symptoms include hepatosplenomegaly, pancytopenia, and skeletal deformities (e.g., Erlenmeyer flask femur).
Type II (Infantile, acute neuronopathic):
Characterized by rapid neurovisceral progression; often results in death during infancy.
Type III (Juvenile, Norrbottnian):
Involves systemic and progressive CNS symptoms manifesting in teens or twenties.
Diagnosis:
Presence of Gaucher’s cells (large, foamy cells with a "crumpled silk" appearance) in bone marrow, spleen, and liver.
Treatment:
Enzyme replacement therapy is available (effective but costly).
Prognosis is poor for Type II, while Type I may persist into adulthood.

84. HEPATOMEGALY SEEN IN
GAUCHER DISEASE

85. Niemann-Pick Disease
Cause: Accumulation of sphingomyelin due to a deficiency in sphingomyelinase.
Types:
Type A: A fatal infantile form characterized by neurological involvement, often resulting in
death by age three.
Type B: Non-neurological with organomegaly, allowing survival into adulthood.
Type C: Biochemically distinct due to a cholesterol esterification defect.
Diagnosis: Presence of foamy Niemann-Pick cells with fat-stained vacuoles.
Treatment:
Experimental enzyme therapy is available, but the overall prognosis remains poor.

88. Letterer-Siwe Disease
A rare and aggressive histiocytic disorder primarily affecting infants (under
three years).
Symptoms: Includes skin rash, fever, organomegaly, and bone destruction.
Oral Manifestations: Symptoms may involve ulcerations, gingival
hyperplasia, and tooth loss.
Histology: Characterized by histiocytic proliferation without foam cells.
Prognosis: Generally poor; however, some patients may respond positively to
chemotherapy.

90. Avitaminoses (Vitamin Deficiency Diseases)

91. Definition and Characteristics of Vitamins
Vitamins are organic compounds that the body cannot produce.
They are soluble in either fat or water and required in small quantities.
They function as cofactors in various metabolic processes.
The term "vitamin" signifies their essential role in life (reflecting a functional, rather than chemical,
description).
Common Features of Vitamins
Found in minimal amounts in comparison to other nutrients.
Many are deactivated by heat and oxidation.
Some occur as provitamins (inactive forms) in nature, which are activated later (for example,
carotene converts to vitamin A in the liver).
Certain vitamins, such as D and A, may have hormonal functions, yet they remain classified as
vitamins due to historical context.
Avitaminoses (Vitamin Deficiency Diseases)
Result from a deficiency of essential vitamins, rather than harmful agents (such as infections).
The deficiency itself constitutes the disease (a negative effect rather than a positive cause).
Can manifest in mild (subclinical) or severe forms.
Initial stages may present symptoms that are difficult to identify.
Rarely severe enough to be an immediate cause of death.

92. Classification of vitamins

93. Fat soluble :- Vitamin A

99. Vitamin D

106. Vitamin E

108. Vitamin K

111. GINGIVAL BLEEDING
(Due to Vit K deficiency)

112. (Due to Vit K deficiency)

113. Vitamin C

115. SCURVY cause due vit C deficiency

116. Vitamin B

117. Vitamin B1 (Thiamine)

119. Vitamin B2 (Riboflavin)

122. Vitamin B3 (Niacin)

124. B Vitamins: Pantothenic Acid, Pyridoxine .

125. B Vitamins: Choline, Biotin, Inositol .

126. B Vitamins: Folic Acid & Vitamin B12

127. Disturbance in Hormone Metabolism

129. Pituitary Gland

132. Pitutary Dwarfism

133. Hyperpituitarism (Pituitary overactivty)

137. Thyroid Gland

139. Cretinism
Myxedma

143. Parathyroid Gland

151. Adrenal gland

165. CONCLUSION
The Impact of Metabolic Diseases on Oral Health
Metabolic diseases frequently present early in the oral cavity, highlighting the vital role dentists play in early
diagnosis and intervention.
Mineral imbalances (such as Ca, P, Mg, and trace elements) affect tooth development, enamel formation,
and bone density, potentially leading to conditions like enamel hypoplasia, osteoporosis, and pathologic
calcifications.
Protein-energy malnutrition (PEM) (e.g., kwashiorkor, marasmus) contributes to gingival atrophy,
delayed tooth eruption, and changes in the mucosa.
Carbohydrate metabolism disorders (e.g., Hurler syndrome) can result in coarse facial features, gingival
hyperplasia, and irregular tooth spacing.
Lipid storage diseases (e.g., Gaucher’s, Niemann-Pick) cause foam cell accumulation, bone deformities,
and involvement of oral soft tissues.
Vitamin deficiencies (A, B-complex, C, D, E, K) manifest through specific oral symptoms:
Vitamin C: Bleeding gums (scurvy)
Riboflavin (B2): Angular cheilitis and a magenta tongue
Niacin (B3): Stomatitis associated with pellagra
Vitamin D: Enamel hypoplasia and rickets/osteomalacia

166. Impact of Hormonal Disturbances and Other Conditions on Oral Health
Hormonal disturbances (involving the pituitary, thyroid, parathyroid, adrenal, and
pancreatic glands) can influence:
Tooth eruption: Hypothyroidism delays tooth eruption, while hyperthyroidism
speeds it up.
Bone density: Hyperparathyroidism can lead to osteopenia.
Gingival health: Diabetes heightens the risk of periodontitis.
Lysosomal storage diseases (such as mucopolysaccharidoses) result in dental
anomalies, macroglossia, and skeletal deformities.
Early detection of oral signs can assist in the diagnosis of systemic diseases,
ultimately enhancing patient outcomes.
Multidisciplinary care involving dentists, endocrinologists, and nutritionists is
crucial for effectively managing metabolic disorders with oral manifestations.

167. REFERENCE
1.Rajan, K., & Sivapathasundharam, B. (2023). Shafer’s
Textbook of Oral Pathology (10th ed.). New Delhi: Elsevier.

168. Multiple Choice Questions

169. 1. Which of the following is a key oral manifestation of hypocalcemia?
A) Gingival hyperplasia
B) Enamel hypoplasia
C) Caries susceptibility
D) Halitosis

170. Answer: B) Enamel hypoplasia
Explanation: Hypocalcemia disrupts enamel formation during
tooth development, leading to enamel hypoplasia (Page 12, 21).

171. 2. In Hurler syndrome (MPS I), oral findings typically include:
A) Microdontia and delayed eruption
B) Gingival hyperplasia and enlarged tongue
C) Dental fluorosis and mottled enamel
D) Angular cheilitis and glossitis

172. B) Gingival hyperplasia and enlarged tongue
**Explanation:** Hurler syndrome causes gingival
hyperplasia, macroglossia, and widely spaced teeth
(Page 75-76).

173. 3. Which mineral is critical for insulin function and glucose
tolerance factor (GTF) formation?
A) Iron
B) Chromium
C) Zinc
D) Selenium

174. Answer: B) Chromium
**Explanation:** Chromium aids insulin binding via a
"chromium bridge" and is part of GTF (Page 50).

175. 4. Vitamin C deficiency (scurvy) primarily affects oral tissues
by:
A) Causing enamel hypoplasia
B) Inducing xerostomia
C) Disrupting collagen synthesis, leading to bleeding gums
D) Promoting dental fluorosis

176. Answer:** C) Disrupting collagen synthesis, leading to bleeding gums
**Explanation:** Scurvy impairs collagen formation, resulting in
swollen, bleeding gums and poor wound healing (Page 122-123).

177. 5. Dystrophic calcification is characterized by:
A) Calcium deposition in dead/damaged tissues with normal serum
calcium
B) Calcium deposition in normal tissues with elevated serum
calcium
C) Skin calcification due to connective tissue disease
D) Reversible calcification upon metabolic correction

178. Answer: A) Calcium deposition in dead/damaged tissues
with normal serum calcium
**Explanation:** Dystrophic calcification occurs in necrotic
tissues without hypercalcemia (Page 23-24).

179. 6. Which vitamin deficiency causes angular cheilitis and a
magenta-colored tongue?
A) Vitamin K
B) Thiamine (B1)
C) Riboflavine (B2)
D) Vitamin A

180. Answer: C) Riboflavin (B2)
**Explanation:** Riboflavin deficiency leads to angular
cheilitis and glossitis (Page 114-115).

181. 7. In primary hyperparathyroidism, radiographic jaw findings
include:
A) Ground-glass appearance and loss of lamina dura
B) Periapical radiopacities
C) Thickened cortical bone
D) Delayed tooth eruption

182. Answer: A) Ground-glass appearance and loss of
lamina dura
**Explanation:** Hyperparathyroidism causes
osteopenia and loss of lamina dura (Page 141-142).

183. 8. Acrodermatitis enteropathica is caused by a
deficiency of ?
A) Copper
B) Iodine
C) Zinc
D) Magnesium

184. Answer: C) Zinc
**Explanation:** This genetic disorder results from zinc
malabsorption, causing skin lesions and diarrhea (Page
46).

185. 9. Which hormonal disorder is associated with "acromegalic
facies" and hypercementosis?
A) Hypothyroidism
B) Hyperpituitarism (excess GH)
C) Addison’s disease
D) Diabetes mellitus

186. Answer: B) Hyperpituitarism (excess GH)
**Explanation:** Excess growth hormone in adults causes
acromegaly, including jaw enlargement and
hypercementosis (Page 131-132).

187. 10. Gaucher’s disease, a lipid metabolism disorder, is
diagnosed by the presence of ?
A) Foamy Niemann-Pick cells
B) Gaucher cells with "crumpled silk" cytoplasm
C) Hurler cells in gingival tissues
D) Amyloid deposits in bone marrow

188. Answer: B) Gaucher cells with "crumpled silk" cytoplasm
**Explanation:** Gaucher cells are pathognomonic,
accumulating glucocerebroside (Page 82-83).

189. Thank you for
your attention‌