Diabetes Mellitus and Endocrine Diseases

APSARI INDRIYANIFAKHRANA A. AYUB

INKA SARASWATIMAJDA INFIRAJ

Dept. Penyakit Mulut FKG UI 2011

Diabetes Mellitus (DM): WHAT IS IT?

Diabetes mellitus (DM) is a clinically and genetically heterogenous metabolic disease characterized by: 1. abnormally elevated blood glucose levels (hyperglycemia), and,2. dysregulation of carbohydrate, protein, and lipid metabolism

Primary feature: chronic hyperglycemia

Cell’s resistance to insulin

Defect in insulin secretion

Diabetes mellitus: Classification• Etiologic classification of diabetes mellitus

(American Diabetes Association, 1997):

Type 2 diabetes mellitus (formerly adult-onset diabetes, non-insulin-dependent diabetes, or type II)

may benefit from insulin therapy but are not dependent on it for survival

Type 1 diabetes mellitus (formerly juvenile diabetes, insulin-dependent diabetes, or type I)

Truly dependent on insulin therapy

Gestational diabetes mellitus occurs during pregnancy and usually resolves after delivery

Other specific types of diabetes mellitus certain genetic disorders, pancreatic diseases, infections, injuries to the pancreas,

and endocrine diseases. Drug therapy with certain agents may also induce a diabetic state.

Diabetes mellitus: PathophysiologyNormal

conditionINSULIN SECRETION

(FROM PANCREATIC BETA CELLS)

GLUCOSE ENTRY INTO CELLS

LOWERED BLOOD GLUCOSE LEVEL

Hyperglycemia

Altered by disease insulin production is decreased

large amounts of glucose remain in the bloodstream

Inhibit glucose entry

Diabetes mellitus: PathophysiologyNormal

conditionINSULIN SECRETION

(FROM PANCREATIC BETA CELLS)

GLUCOSE ENTRY INTO CELLS

LOWERED BLOOD GLUCOSE LEVEL

Hyperglycemia

large amounts of glucose remain in the bloodstream

Insulin is not used properly by target cells due to cell’s resistance

to insulin

Diabetes mellitus: Pathophysiology• Other processes that could contribute to the elevation of

blood glucose levels glucose production by the liver

Glycogenolysisglycogen stores in the liver are

converted into glucose

Gluconeogenesisthe liver also produces glucose

from fat (fatty acids) and protein (amino acids)

When energy is required by the cells...

Elevating blood glucose levelsMultiple

hormones, except insulin

Diabetes mellitus: Type 1 DMAspects Descriptions

Prevalence 5-10% of DM cases

Etiology idiopathic autoimmune destruction of pancreatic beta cells leads to absolute insulin deficiency.

Predilection • 95% of type 1 DM cases occur before the age of 25 years.• more prevalent in caucasians

Risk factors family history of type 1 DM, gluten enteropathy (celiac disease), or endocrine disease

Subclassifications 1. Immune-mediated form of type 1 DM cellular-mediated autoimmune destruction of the insulin-producing beta cells in the pancreatic islets. This may be triggered by environmental event, such as: viral infection. May be associated with autoimmune disorders, such as: Hashimoto’s thyroiditis, Addison’s disease, vitiligo, pernicious anemia.

2. Idiopathic form of type 1 DM the cause of beta cell destruction is not understood

Complications Diabetic ketoacidosis

Insulin dependency absolutely dependent on exogenously administered insulin for survival since the pancreas has no longer produce insulin

In a known diabetic patients, period of stress or infection may precipitate diabetic ketoacidosis.

But more often, diabetic ketoacidosis results from:

poor daily glycemic control (for several days or longer) due to

excessive glucose intake or inadequate insulin administration

Diabetes mellitus: type 2 DMAspects Descriptions

Prevalence 90-95% of DM cases

Etiology Multifactorial (genetic predilection , advancing age, obesity, lack of exercises)•Characterized by insulin resistance in peripheral tissues and defective insulin secretion by the pancreatic beta cells.

Predilection more prevalent in African-Americans, Native Americans, Hispanics, and Pacific Islanders.

Pathophysiology Does not involve autoimmune beta cells disorders. Characterized by 3 disorders:Peripheral tissue resistance to insulin (esp. muscle cells)Increased glucose production by the liverInsulin secretory defect of the beta cellsIncreased tissue resistance to insulin generally occurs first, followed by impaired insulin secretion.

Risk factors Obesity (particularly intra-abdominal fat), advancing age, high caloric intake,low birth weight, impaired glucose tolerance, impaired fasting glucose, gestationalDM

Complications Dehydration, hyperosmolar nonketotic acidosis, atherosclerosis, microangiopathy

Insulin dependency do not require exogenous insulin for survival (since they still produce insulin).

Diabetes mellitus: other specific types of DM

Aspects Description

Prevalence 1-2% of DM cases

Etiology various specific genetic defects of beta cell function and insulin action, diseases of the exocrine pancreas, endocrinopathies, pancreatic dysfunction induced by drugs, chemicals, or infections.

Other genetic syndromes associate with this type of DM

Turner’s syndrome Down syndrome Wolfram syndrome Klinefelter’s syndrome Friedreich’s ataxia Huntington’s chorea Laurence-Moon-Biedl syndrome Myotonic dystrophy Porphyria Prader-Willi syndrome

Diabetes mellitus: Gestational DM

Gestational DM includes:•Development of type 1 DM•Discovery of undiagnosed asymptomatic type 2 DM during pregnancy

High incidence found in:•Older women•Overweight women•Women of minority ethnic groups

Pathophysiology: associated with increased insulin resistance

•Most patient with Gestational DM return to a normoglycemic state after parturition.However 30-50% of women with a history of gestational DM will develop type 2 DM within 10 yrs.

Table 1. Clinical Features Type 1 DM Type 2 DM

Polydipsia (excessive thirst) ++ +

Polyuria (excessive urination) ++ +

Polyphagia (excessive hunger) ++ -

Unexplained weight loss ++ +

Weakness, malaise ++ +

Nocturnal enuresis ++ -

Irritability ++ +

Dry mouth ++ +

Chronic skin infections ++ +

Ketoacidosis ++ +

Periodontal diseases ++ +

Changes in vision (vision impairment) + ++

Vulvovaginitis or pruritus + ++

Paresthesia, loss of sensation (neurologic symptoms) + ++

Impotence (sexual dysfunction) + ++

Postural hypertension + ++

Initially asymptomatic - ++

Diabetes mellitus: Diagnosis HOW TO DIAGNOSE PATIENTS WITH DM?

Clinical signs

Specific laboratory findings

fasting glucose and casual (nonfasting) glucose level

• determination of glucose levels at a single moment in time (at the time the blood sample is collected). Diagnosis is not made until the patients has exceeded threshold glucose levels on two separate occasions.

glycosylated hemoglobin assay (glycohemoglobin test)

• determination of blood glucose status over 30-90 days prior to blood sample collection.

Two different glycohemoglobin test: HbA1 test normal value: <8%. HbA1c test normal value: <6.0-6.5%

fructosamine test • determination of blood glucose status over 2-4 weeks prior to blood sample collection.

Normal range: 2.0-2.8 mmol/L

Diabetes mellitus: Diagnosis• Diagnostic criteria for diabetes mellitus:Table 2. Normal Impaired fasting

glucoseDiabetes mellitus

Fasting glucose <110 mg/dL 110-126 mg/dL ≥126 mg/dL

2 h postprandial plasma glucose

<140 mg/dL 140-200 mg/dL ≥200 mg/dL

Diabetes mellitus: Monitoring

Self-blood glucose monitoring has revolutionized patient management of DM development of small handheld glucometers at-home testing

Glucometers use a small drop of capillary blood from a finger-stick sample to assess glucose levels

within seconds.

Diabetes mellitus: ComplicationsSite Presentation

Eyes Retinopathy, cataracts, blindness

Kidney Nephropathy, renal failure

Nervous system Sensory: peripheral neuropathy, cranial neuropathy affecting cranial n. III, IV, VI, VII

Autonomic: gastroparesis, changes in cardiac rate/rhythm, and dysfunction, postural hypotension, G.I. Neuropathy, impotence

Skin and oral mucosa

Unusual infections, delayed wound healing

Periodontium Gingivitis and periodontal diseases

Cardiovascular system

Macrovascular disease (accelerated athersclerosis), coronary artery disease, cerebrovascular disease

Diabetes mellitus: Management

PRIMARY TREATMENT

GOALS

achieving blood glucose levels that are as close to normal as possible and prevention of diabetic

complications

Diet, exercise, weight control, and medications are the

mainstays of diabetic care.

The primary medication used in type 1 DM is insulin; while type 2

DM individuals frequently take oral medications, although many also use insulin to improve glycemic

controls

The most common complication of insulin therapy is hypoglycemia, a potentially life-threatening emergency.

Signs and symptoms of hypoglycemia are most common when blood glucose levels fall to <60 mg/dL

Oral agents for management of diabetes mellitus

Class Agent Generic name

Oral agents Sulfonylurea/first generation Chlorpropamide

Tolazamide

Tolbutamide

Acetohexamide

Sulfonylurea/second generation Glyburide

Glipizide

Glimeperide

Meglitinides Repaglinide

Nateglinide

Biguanides Metformin

Thiazolidinediones Rosiglitazone

Pioglitazone

A-glucosidase inhibitors Acarbose

Miglitol

Injectable Amylin analogues Pramlintide

Glucagon-like peptide-1 analogues Exanatide

Diabetes mellitus: Oral Manifestations

Tissues Manifestations (oral manifestations of DM usually related to the degree of glycemic control)

Mucosa Oral dysesthesiaAltered wound healingXerostomia Candidal infectionsIncreased incidence of infectionBilateral generalized salivary gland enlargement or sialadenitis (esp. parotid glands) may occur

Dental Increased incidence and severity of dental caries

Perio-dontal

Increased gingival inflammation in response to bacterial plaque to a greater extent than seen in well-controlled DM or nondiabetic individualsIncreased glucose levels in GCF altering periodontal wound healing significantly by changing the interaction between cells and their extracellular matrix within the periodontiumProgressive destruction periodontitis exacerbated by poor OH and smoking habit

Diabetes mellitus: Dental Management

In general, adults with well-controlled DM have similar risks for oral disease progression and respond similarly to most dental procedures as

nondiabetic individuals.

A patient presenting with signs and symptoms of undiagnosed or poorly controlled DM should be referred to a physician for diagnosis and

treatment

Oral health practicioners should have in-office glucose monitoring devices or glucometers to readily obtain immediate information about glycemic status if

needed

Diabetes mellitus: Dental Management

FIRST STEP determining the type of DM, methods of treatment (diet, oral hypoglycemics, insulin, or a combination of these), level of control, and presence of DM

complications

DM-associated medical complications which could

impact the dental care provision:Renal insufficiency should avoid or revise the dosage of potentially nephrotoxic drugs (acetaminophen, acyclovir, aspirin, NSAIDs)

Patients on hemodialysis are immunocompromised and at risk of endarteritis and endocarditis

The best time for dental treatment is either before or after periods of peak insulin activity. This reduces the risk of perioperative hypoglycemic reactions, which occur most often during peak insulin activity.

The greatest risk would occur in a patient who has taken the usual amount of insulin or oral hypoglycemic agent but has reduced or eliminated a meal prior to dental treatment.

Pretreatment blood glucose level can be

measured with a glucometer, and there should be

a readily available source of carbohydrates

in the dental office.

Diabetes mellitus: Specific Management Guidelines

Oral fungal infections can manifest in the presence of salivary hypofunction. The topical antifungal medications should be sugar-free.

If the DM patient also has renal insufficiency (renal failure), nephrotoxic antiviral drugs will require dose modifications

antibiotics considered for orofacial infections & oral surgical procedures in poorly controlled DM patients. Primary treatment of periodontal disease in DM patients nonsurgical combined with antibiotics.

Corticosteroid therapy for oral vesicobullous conditions can increase glucose levels. Therefore, corticosteroids should be used with caution.

Diabetes mellitus: Specific Management Guidelines

The decision to administer antibiotics should be based on multiple factors,

including:

The current level and duration of glycemic controlExtent of surgical procedures plannedPresence of underlying infectionsConcurrent medical problemsAnticipated level of postoperative pain and stressEstimated healing period

The most common emergency related to DM is hypoglycemia, a potentially life-threatening situation that must be recognized and treated expeditiously.

Signs and symptoms of hypoglycemia:ConfusionSweatingTremorsAgitationAnxietyDizzinessTingling or numbnesstachycardia

OTHER HORMONES

Mechanisms of Endocrine Diseases

Can be caused by:1. Neoplastic growth of

endocrine cells (eg, overgrowth of cortisol-producing adrenal cells causing Cushing’s syndrome)

2. Autoimmune disorders in which activating antibodies mimic trophic hormones (eg, Graves’ disease of thyroid gland)

HORMONE EXCESS HORMONE DEFICIENCY

Can be caused by:1. Glandular destruction (due

to autoimmunity, surgery, infection, inflammation, infarction, hemorrhage, tumor) eg. Autoimmune damage to pancreatic islet cells (DM type 1)

2. Hormone resistance (endocrine gland is resistant to the action of hormone, due to molecular defects in hormone receptors or molecules in the signaling pathway) eg. Insulin resistance in DM type 2

Pituitary GlandPITUITARY GLAND (Location: Sella tursica)

Hormones Function

Division Anterior pituitary(adenohypophysis)

GH Growth and development

ACTH Intermediaries in endocrine axes each responds to a specific hypothalamic hormone, and, in turn, acts upon an end-organ gland to bring endocrine response

TSH

LH

FSHProlactin Initiation and maintenance of lactation

Posterior pituitary(neurohypophysis)

AVP/ADH Maintaining water balance

Oxytocin -Contraction of the myoepithelial cells of the alveoli of the mammary gland- contraction of the uterus during childbirth and postpartum

*GH=Growth Hormone; ACTH=Adrenocorticotropic Hormone; TSH=Thyroid-stimulating Hormone; LH=Luteinizing Hormone; FSH=Follicle-stimulating Hormone; AVP=Arginine Vasopressin; ADH=Antidiuretic Hormone

• Simplified diagram of GH/IGF-1 axis involving hypophysiotropic hormones controlling pituitary GH release, IGF-1 production in the liver and elsewhere, and tissue responsiveness to GH and IGF-1. GH increases fat mobilization, decreases body fat and decreases adipocyte size and lipid content. Arrows denote stimulation (+) or inhibition (−). SRIF, somatotropin release-inhibiting factor; GHRH, GH-releasing hormone.

Anterior Pituitary Hyperfunction (GH excess)

During skeletal growth -> GIGANTISM• Excessively tall• Absence of early secondary sexual characteristics• Thickening of soft tissue: supraorbital ridge, thick fingers• Deepening of voice

After skeletal growth (epiphyses fused) -> ACROMEGALY• Enlarged mandible: prognathy, malocclusion, diastemata, elongated ramus and

increased oblique• Thickening of soft tissue: large ears, thick lips, frontal bossing. macroglossia,

hypertrophy of the pharyngeal and laryngeal tissues • Deepening of voice• Increased sweating• Hypertrophic arthropathy (knees, ankles, hips, spine)• Pinched nerve• Hypertension, DM• Left ventricular hypertophy• Cardiomyopathy -> increased mortality

Anterior Pituitary Hyperfunction (GH excess)

Diagnosis:• IGH-1 serum concentration• GH serum concentration -> rises and falls

Medical therapy:• Surgical resection through transsphenoidal approach• Somastatin receptor analogues: octreotide, lantreotide• GH receptor antagonist: pegvisomant

Dental consideration:• Taurodontism, hypercementosis• Enlarged sella tursica in skull radiography• Conscious sedation may be given if airway is clear• GA may be hazardous <- kyphosis, narrowed glottic opening• Dental management may be complicated by: DM, hypertension, hypopituitarism,

cardiomyopathy dysrhythmia• Thromboembolic phenomena

Anterior Pituitary Hypofunction(GH deficiency)

Clinical features:• Small facial appearance: disproportioned delayed growth• Abnormal tooth, delayed eruption and shedding• Abnormal alveolar growth, crowding, malocclusion• Poor OH -> gingivitis, periodontitis

Dental consideration: • correction of malocclusion

Adrenal glandADRENAL GLAND

Hormones Function

Division Cortex Cortisol(a.k.a glucocorticoid)

Essential (esp. in state of stress), for the maintenance of blood pressure and gluconeogenesis

Aldosterone(a.k.a mineralocorticoid)

Maintenance of blood pressure by intravascular volume expansion via retention of the mineral sodium

Medulla Epinephrine Acts in response to, and in conjunction with the activation of the sympathetic nervous system

Norepinephrine

Adrenocortical Hyperfunction (Cushing’s disease)

Clinical features:• Truncal obesity• Moon face• Buffalo hump• Hypertension• Osteoporosis• Loss of skin integrity• Menstrual irregularity• Mood disturbance• Acne & excessive facial hair (hirsutism)

Dental considerations: Easy bruising and hematoma, impaired wound healing Osteoporosis, hypertension, DM, heart failure, assessment of stress Immunosupressed if in glucocorticosteroid therapy: candidiasis, HSV, HZV,

periodontal disease, impaired wound healing

Adrenal Insufficiency (Addison’s Disease)

Clinical features:• Weakness, fatigue, anorexia• Abnormal cutaneous (tan-like) and oral pigmentation: often an early sign. Patchily

distributed on gingivae, buccal mucosa, lips• Gastrointestinal disturbance• Loss of weight• Hypotension

Treatment: exogenous corticosteroid

Dental consideration: • Immunosuppresed because of treatment: candidiasis, HSV, HZV, periodontal

disease, impaired wound healing• Beware of acute adrenal crisis: collapse, bradycardia, hypotension, hypoglycaemia,

vomiting, dehydration. Give IV 200 mg hydrocortisone, glucose if hypoglicaemia, and fluid replacement

Endocrine glands: Thyroid glandHormones Function

Thyroid gland Thyroxine (T4) Primarily responsible for regulation of metabolism- Every tissue in the body has thyroid hormone receptors and responds to the action of thyroid hormone, primarily with increased oxygen consumption and heat productionTriiodothyronine (T3)

Endocrine diseases: Thyroid gland disorders

HYPERTHYROIDISM (Thyroid hormone excess) symptoms: the patient feels hot when others feel cool, hungry and eating all the time but losing weight, has thinning hair, anxious and jittery, has tremors, tachycardia most common cause: TSH-stimulating autoantibodies (Graves’ disease), thyroid hormone-secreting nodules (toxic nodules), tumor classic feature: a “stare” with proptosis caused by deposition of glycosaminoglycans in the orbital musculature

Endocrine diseases: Thyroid gland disorders

HYPOTHYROIDISM (Thyroid deficiency) symptoms: chronically fatigued, the patient feels cold when others feel comfortable, gaining weight without eating more, constipated, bradycardic, slowed reflexes. Patients may develop mental slowing, depression, and hypothermia most common cause: autoimmune destruction of the gland (Hashimoto’s thyroiditis), loss of TSH-producing cells of the pituitary gland, pituitary adenoma classic feature: a slowed relaxation phase on the Achilles tendon reflex

Oral manifestations of thyroid gland disorders

Overview: Examine the thyroid gland with the patient’s head extended to one side.Next, the patient is instructed to swallow while the examiner evaluates the anatomic extent of the lobules using the last three fingers of one handThe presence of an assymetric thyroid gland enlargement should be referred for follow-up by an internist or endocrinologist

HYPERTHYROIDISM exacerbate the patient’s response to dental pain and anxiety excess sweatingEnlargement of the thyroid or the tongueDifficulty in swallowing Increased susceptibility to dental caries and periodontal diseases

HYPOTHYROIDISM facial myxedemaEnlarged tongue (macroglossia)Compromised periodontal healthDelayed tooth eruptionDelayed wound healingA hoarse voiceSalivary gland enlargementChanges in tasteBurning mouth symptomsXerostomia, impaired salivary output

Dental Management of Thyroid Gland Disorders

Overview:•The first concern in treating patients with thyroid disease is the level of metabolic control and the

second concern is concomitant medications.• Well-controlled hyperthyroidism and hypothyroidism should not present major risks to the

patient undergoing dental care.

Hyperthyroidism the risk of thyrotoxicosis (“thyroid storm”), symptoms: extreme irritability & delirium; hypotension; vomit; diarrhea. It can be triggered by surgery, sepsis, and trauma Epinephrine is contraindicated in patients exhibiting signs of thyrotoxicosis Stress management & short appointmentSusceptible to cardiovascular disease atrial dysrhthymia, tachycardia, hypertension check patient’s current medication (anticoagulants)Check patient’s current medication if patients use propylthiouracil increased susceptibility to infection (because propylthiouracil can cause agranulocytosis or leukopenia) and also cause sialolith formation and interacts with warfarin (increase the anticoagulant effect of warfarin)Certain analgesics must be used with caution aspirin and NSAIDs may cause increased levels of circulating T4 leads to thyrotoxicosis

Dental Management of Thyroid Gland Disorders

Hypothyroidism Lethargy is a common finding indicates poorly-controlled conditionSusceptible to cardiovascular disease consultations with medical providers current medications anticoagulants consider coagulation tests (prothrombin time, partial thromboplastin time, etc.) before invasive proceduresLocal anesthetic with epinephrine should be used cautiouslyConsider to give antibiotic prophylaxis before invasive procedures sensitive to CNS depressants and barbituratesFor postoperative pain control, narcotic used should be limited because there is greater susceptibility Long-standing hypothyroidism may exhibit increased bleeding after trauma or surgery , due to the presence of excess subcutaneous mucoploysaccharides , which decrease the ability of small vessels to constrict when cut result in increased bleedingDelayed wound healing due to decreased metabolic activity in fibroblasts

Endocrine glands: Gonads

Hormones Function

Male TestosteroneSecondary sexually development

Sperm

Female Ovarian estradiol

Endocrine disorders: Gonad disorders

PRECOCIOUS PUBERTYEarly signs of secondary sexually differentiation Puberty is generally considered precocious in boys if it starts before age 10 years and in girls before age 8.5 years Most common cause: early onset of pituitary hormone production, ectopic (exogenous) source of hormone (eg, adrenal gland produces androgen that can lead to early puberty)

DELAYED PUBERTYLate signs of secondary sexually differentiation Puberty is generally considered delayed in boys if there are no signs of sexual development by the age of 13 years in girls and 14 years in boys

HYPOGONADISMManifestations: In females = premature ovarian failure (before the age of 40 years) onset of menopause In males = loss of libido , decreased growth rate of facial hair and can lead to osteoporosis and

fractures

Oral manifestations of Gonadal Disorders

Hypersecretion of female sex hormones:

(commonly occurs in pregnancy)Bilateral brown facial pigmentation (melasma)High levels of female sex hormones cause increased capillary permeability susceptible to: gingivitis (pregnancy gingivitis)Gingival hyperplasiaPyogenic granuloma (pregnancy tumor)Complicate preexisting periodontal disease

Decrease in gonadal hormones: (at menopause)

Decrease in salivary flowDecrease in salivary compositionPredispose to dental caries, glossodynia, dysgeusia, metallic taste, oral candidiasisAtrophy of gingival tissueHigher tendency for plaque accumulationIncreased risks of gingivitis and periodontitisAfter dental extractions edentulous ridges rapidly undergo resorptionSusceptible to osteoporosis dental radiographs may demonstrate hypocalcified bone

Dental Management

• The specific dental management concerns in patients with gonadal diorders are focused on the associated secondary disorders.

1. The pregnant patient is susceptible to gestational diabetes insulin action is antagonized by estrogen and progesterones

2. Elective and stressful dental procedures should be avoided during the first trimester and the last half of the third trimester

3. The second trimester is the safest period to provide dental care during pregnancy emphasis on prevention, maintenance of optimal oral health, treatment of dental concerns that may lead to complications

4. Injudicious drugs use should be avoided in pregnancy avoid drugs with possible teratogenic effects

5. Evaluate panoramic radiographs the presence of a carotid atheroma in postmenopausal women

Endocrine glands: Parathyroid gland

Hormone Function

Four parathyroid glands

PTH (Parathyroid Hormone)

Maintenance of ionized calcium serum level

Endocrine disease: Parathyroid gland disorders

Hyperparathyroidism Hypoparathyroidism & hypocalcemia

Chronic excessive secretion of the PTH Leads to hypercalcemia

Deficiency in production, secretion, action of PTH Leads to hypocalcemia

Types: Primary caused by solitary

adenoma, hyperplasia, and carcinoma of the parathyroid gland

Secondary due to compensatory gladular enlargement in response to unusual hypocalcemia induced by metabolic disorders (eg, renal failure, vit.D deficiency, rickets,osteomalacia)

Tertiary secretion of PTH from enlarged parathyroid glands without control or response to feedback inhibition

Etiology: Surgical removal of parathyroid glandsCell-mediated autoimmune glandular destruction Mutations of the calcium-sensing receptors (autosomal dominant hypocalcemia)Other unusual causes radiation to the neck, metastatic cancer, infection, magnesium deficiency, damage to the glands by heavy metals (eg, copper in Wilson’s disease), transfusion hemosiderosisAbsence or underdevelopment of parathyroid glands in developmental abnormality (eg, DiGeorge syndrome)Renal resistance to PTH pseudohypoparathyroidism

Other causes of hypocalcemia: vitamin D deficiency, hyperphosphatemia, malabsorption of calcium, chronic renal failure

Endocrine disease: Parathyroid gland disorders

Hyperparathyroidism Hypoparathyroidism & hypocalcemia• Clinical findings: Skeletal disorders chronic bone resorption (may develop pathologic fractures), reduction in bone mass, cystic bone lesions on radiograph (known as “brown tumor” of hyperparathyroidism), bone painRenal disorders polyuria, polydypsia, development of kidney stones, excessive renal secretion of calcium and phosphateHypercalcemia nonspecific presentations: “abdominal groans” of constipation, indigestion, weight loss, peptic ulcer, nausea; and “psychic moans” of lethargy, fatigue, depression, loss of memory, paranoia, change in personality, coma

•Clinical findings:Acute hypocalcemia neuromuscular irritability. This leads to muscular and mental manifestations, including: paresthesia of the hands, feet, circumoral muscles, anxiety, confusion, depressionPositive Chvostek’s sign

may develop tetany tonic-clonic seizures, severe laryngospasm

•Laboratory findings: high alkaline phosphatase level in patients with bone lesions, elevation of serum calcium (>10.5 mg/Dl), elevation of PTH level

Laboratory findings: low PTH, low serum calcium level, elevation of serum phosphatase level, normal alkaline phosphatase level

Oral manifestations of Parathyroid glands disorders

HYPERPARATHYROIDISM

•Primary signs reflections of the systemic effects of hypercalcemia generalized osteoporosis

•Generalized osteoporosis visible on dental radiographs as:Cortical resorption and rarefactionLoss of trabeculation (“ground-glass appearance)Loss of lamina duraMetastatic calcificationsThinning and loss of cortical bone esp. in lower border of the mandibleBrown tumors may produce gingival swellingTeeth more radipaque appearance

HYPOPARATHYROIDISM•Radiograph appearance:The maxilla and mandible are abnormally dense, with well-calcified trabeculaeWhen teeh are still developing abnormality in the appearance and eruption pattern. There may be: enamel hypoplasia, poorly mineralized dentin malformed teethAnodontia; impacted teethshort blunt root apiceselongated pulp chambersPulp stonesMandibular exostosesThere are no abnormalities in erupted teethPatients may develop oral mucocutaneous candidiasis

Dental management of patients with parathyroid gland disorders

HYPERPARATHYROIDISMClinicians must be careful to avoid iatrogenic jaw fractures during oral

surgical procedures

HYPOPARATHYROIDISMLow serum calcium levels may precipitate cardiac arrhythmias, convulsions, laryngospasm, or bronchospasm consult with the patient’s physician to ascertain level of metabolic control Patients with dental abnormalities increased risk of dental caries associated with hypoplastic teethPeriodic radiograph evaluation screen for dentigerous cysts may develop at sites of impacted teeth

Thank you

• Intan: kortikosteroid pada pasien DM, bagaimana hati-hatinya?• Rahmi: beda hiperfunction adrenocortico dengan kelebihan

kortikosteroid?• MF: Mengapa hamil bisa DM? Efeknya seberapa besar, komp renal

disease?• Zerika: mengapa moon face?• Ranny: sialadenitis, xerostomia apakah efek dr DM atau obat?• Bani: mekanisme poliuria dan polidipsia di DM?• Putu: apa DM gestasional ada tanda yang spesifik? Drg boleh apa klo

ada pasien Acromegaly atau peny hormon lain?• Ica: dental management DM? Klo terjadi hipoglikemi?• Kristi: yg tes serum GH naik-turun, kpn naik kpn turun?• Anin: microvessel injury di DM, bisa terjadi di pulpa nggak?• Annisha: pertimbangan antibiotik di DM?• Sanny: bikin pertanyaan!• Kivon: knp hipertiodism lebih sering kena dental caries krn peny dental?• Arrad: drmn pasien DM tipe 1 yang <20 th bisa dpt DM? Obesitas pada

DM?