Bone Pattern.

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Presentation transcript:

Bone Pattern

Outline Normal bone pattern Localized change in bone pattern Radiographic changes in diseases affecting bone Systemic Diseases affecting bone Hyperparathtroidism Rickets Osteomalacia Osteopetrosis Paget’s disease Sickle cell anemia and Thalasemia Conclusion

Normal Bone Pattern * Cortical plates Cancellous bone To understand what abnormal bone looks like we must fully understand what normal bone pattern looks like. Normal: cancellous bone which lies between well defined cortical plates (dense compact bone). Important cortical plates look for: Inferior boarder of the mandible which is made of robust cortical bone Cotex of the anterior and posterior boarders of the ramus of the mandible IAN cotex Cortical boundries of the maxillary sinus *

Normal Bone Pattern Cancellous Bone: Trabeculae------thin radiopaque plates and rods, surrounding many small radiolucent pockets of marrow. The radiographic pattern of the trabeculae show intrapatient and interpatient variability Or Trabecular bone

Normal Bone pattern Maxilla Mandible Anterior Posterior Trabeculae: Thin, numerous---Fine granular dense pattern, random orientation. Marrow spaces: small, numerous Trabeculae: Thick, coarse, horizontally orientation Marrow spaces: Larger Posterior Same as above Larger marrow spaces More horizontally oriented trabeculae Larger marrow spaces in the periradicular area

Normal Bone Pattern The distribustion and size of the trabeculae throughout both jaws show a relationship to the thickness (and strength) of the adjacent cortical plates. So where the cortical plates are thick (posterior mandible), internal bracing by the trabeculae is not needed…….so there are fewer trabeculae. By contrast in the maxilla and anterior mandible were the cortical plates are less rigid trabeculae are more numerous----more internal bracing

Localized Change in bone Pattern

Dense Bone Island Or enostosis, internal counterpart of exostoses Localized growth of compact bone in the cancellous bone. Well-defined but may blend with the surrounding bone. No trace of a radiolucent margin or capsule. RARELY may cause external root resorpsion Or enostosis, internal counterpart of exostoses Seen more in the mandible

Marrow space Or Focal Osteoporotic Bone marrow Normal area of hematopoietic or fatty marrow, etiology is unknown but has be postulated to be: Bone marrow hyperplasia Persistent embryonic marrow remnants Site of “ abnormal” healing following extraction, trauma, or local inflammation. Or Focal Osteoporotic Bone marrow

Generalized Change in Bone Pattern

General radiographic changes of diseases affecting bone: Change in size or shape of bone. Change in number /size/ orientation of trabeculae. Altered thickness and density of cortical structures. Increase or decrease in overall density of bone Systemic disorders affect the entire bode, so the radiographic changes in the jaws are generalized. In most cases it is not possible to to identify diseases based on radiographic characteristics.

Mature are immune to systemic demineralization. Some Systemic diseases that occur DURING tooth formation may result in dental alterations Accelerated or delayed eruption. Hypoplasia Hypocalcification Loss of lamina dura Mature are immune to systemic demineralization.

Diseases affecting Bone Diseases that cause DECREASE in bone density Diseases that cause INCREASE in bone density Teeth stand out Against a radiolucent jaw Loss contrast of Inferior cortex of madndible Cortical structures Thin, less defined IAN canal stands out

Systemic Diseases Manifested in the Jaws Endocrine Disorders Metabolic Bone Diseases Others Hyperparathyroidism Osteoporosis Scleroderma Hypoparathyroidism Rickets Sickel cell anemia Hyperpituitarism Hypophosphatasia Thalassemia Hypophosphatemia Hypopituitarism Osteopetrosis Hyperthyroidism Hypothyroidism Diabetes Cushing’s Syndrome

Hyperparathyroidism Excess of serum PTH: Increases bone remodeling (osteoclastic resorption) Increases renal reabsorption of calcium Increases renal production of active vitamin D. Could be primary due to an adenoma in one of the glands Or secondary as a result of a compensatory increase in PTH in response to hypocalcemia. Condition of older patients 30-60 Increase serum calcium

Hyperparathyroidism Radiographic Features: (1 in 5 have obvious radiographic changes) CHANGES IN THE JAWS: Loss and thinning of cortical boundaries Decrease in density of jaw * Trabeculae: small, numerous, randomly oriented, Ground glass appearance, * Teeth stand out in contrast to the radiolucent jaws. Ground glass

Hyperparathyroidism Brown Tumours: Brown tumours regress spontaneously when the condition is treated. Resemble central giant cell granuloma. Histologically its identical to a giant cell granuloma. If giant cell granuloma occurs later than the second decade, patient should be screened for hyperparathyroidism.

Hyperparathyroidism CHANGES IN THE TEETH: Loss of lamina dura loss of lamina dura may give the root a tapered appearance because of decreased image contrast.

Rickets (infants) and Osteomalacia (adults) Inadequate serum and extracellular levels of calcium and phosphate (minerals required for normal calcification of bone and teeth). They result from a defect in the normal activity of vitamin D metabolites which is required for normal reabsorption of calcium from the intestines.

Rickets may result in hypoplasia of the dental hard tissues. These changes may manifest as: Large pulp chambers and widened root canals. Thinning or loss of tooth follicle cortices and laminae durae.

Osteopetrosis Is a disorder that results from a defect in the differentiation and function of osteoclasts Abnormal formation and remodelling of primary skeleton and generalized increase in bone mass. Dense, fragile bones susceptable to fracture and infection Obliteration of marrow---compromises hematopoiesis and compresses cranial nerves

Bones show great increase in density, which is bilaterally symmetrical Osteopetrosis It is homogeneous and diffused. Loss of Contrast between the outer cortical boarder and the cancellous bone Entire bone may be mildly enlarged Bones show great increase in density, which is bilaterally symmetrical

Osteopetrosis Increased radiopacity of the jaws. The radiographic image may fail to reveal any internal structure. Roots may fail to appear. Delayed eruption of teeth Malformed teeth

Paget’s Disease A condition of abnormal resorption and apposition of osseous tissue in one or more bones. Affects late middle and old age. Males>Females (2:1) Frequent in Great Britain and Australia. Ds may involve many bones simultaneously, but it is not a generalized skeletal ds.

Paget’s Disease Clinical Features: Enlargement of the skull Jaws Enlargement of the Jaws: Separation and movement of teeth Tight or ill fitting dentures Curvature of the spine “buffalo hump” Bowing of the legs Neurologic Pain– due to bone impingement on foramina and nerve canals

Paget’s Disease Three radiographic phases: Early radiolucent resorptive stage: Decrease density of bone. Decrease number of trabeculae. Granular second stage: Short, random distribution of trabeculae. Granular pattern of bone Dense radiopaque appositional late stage: Cotton-wool appearance Basically an intense wave of osteoclastic activity. Which results in irregular shaped resorption cavities. Vigorous osteblastic phase trying to for woven bone

Increase in dimension between the internal and outer cortex of skull Hypercementosis Cotton-wool pattern

Paget’s Disease Complications: Extraction sites heal slowly. Higher incidence of osteomyelitis. Development of osteosarcoma (10%).

Sickle Cell Anemia Hemolytic blood disorder. Abnormal hemoglobin: Under low oxygen tension results in sickeling of the RBCs. These RBCs have a reduced ability to carry oxygen. Because of their abnormal membrane proteins, they adhere to vascular endothelium and obstruct capillaries. Abnormal RBCs are destroyed by the spleen. Hematopoietic system responds to the anemia by increasing the production of RBCs. Which requires hyperplasia of the bone marrow. Sickle cell crisis

Thalassemia Defect in hemoglobin synthesis. It involves either alpha of beta globulin genes Resultant RBCs have reduced hemoglobin content and have a shortened life span.

Radiographic Changes: The hyperplasia of the bone marrow at the expense of cancellous bone is the primary reason for the radiographic manifestations of sickle cell anemia and thalassemia.

Radiographic Changes: General osteoporosis.

Radiographic Changes: Widening of the diploic space. Outer table of skull will not be apparent and a hair-on-end appearance. Linear alteration of the trabeculae.

Drugs That Affect Bone Density Corticosteroids Heparin Antiepileptic drugs Cytotoxic drugs Ciclosporin (immunodepressant)

Radiograph at a later time What do you do if you suspect the presence of disease (apparent absence of trabeculae)? Examine previous radiographs Change No Change Most probably abnormal Repeat R with lower exposure Change No Change Presence of expected but sparse trabecular pattern that was over exposed----Normal Follow up with a Radiograph at a later time