Radiology of Systemic Disorders Affecting the Foot and Ankle (Christman) Circle: 1

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Goals and Objectives Radiology of After completing this CME, the reader should be able to: • Discuss and recognize the radiographic features of Systemic Disorders osteopenia. • Distinguish between the radiographic findings associated with chronic and regional Affecting the Foot osteoporosis. • Describe and identify the radiographic features of met- and Ankle abolic, endocrine, and nutritional disorders that affect the lower extremity. • Describe and recognize Here’s a review of the findings seen the characteristic radiographic appearance of skeletal on foot and ankle x-rays. dysplasias seen in the lower extremity. 129 • List disorders that are associated with metastatic By Robert A. Christman, DPM, EdM calcification, calcinosis, and dystrophic calcification.

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any systemic disor- teoporosis, include several endocrine orders are frequently encountered in ders demonstrate as- and nutritional disorders (hyperpara- the foot and leg. sociated radiographic thyroidism, acromegaly, scurvy, and Decreased bone density, or in- findings in the lower rickets, for example). Paget’s disease creased radiolucency of bone,1,2 is extremity. Although may be localized in the lower extrem- a prominent radiographic feature of Mthese conditions typically are not ity. Skeletal dysplasias present char- numerous metabolic disorders. Mis- clinically diagnosed by their foot or acteristic presentations that may be conceptions abound regarding the ankle manifestations, the practitioner recognized as incidental findings; ex- use of terms relating to this finding;3 should be familiar with these radio- amples include osteopetrosis, osteo- therefore, the following definitions logic presentations so they are not poikilosis, osteochondromatosis, and are strictly adhered to in this article. misdiagnosed as other conditions. The osteogenesis imperfecta. Finally, soft The term osteopenia is used to refer metabolic diseases, in particular os- tissue manifestations of systemic dis- Continued on page 130 www.podiatrym.com JANUARY 2018 | PODIATRY MANAGEMENT CME Continuing

Medical EducationRadiology (from page 129)

to the non-specific radiographic finding of decreased bone density. The terms decalcification, under-mineral- ization, and demineralization are not used, because they refer more specifically to the underlying physiology and pathology of bone.4 Moreover, the term osteoporosis is reserved for the clinical entity. Generalized, diffuse osteopenia is a highly subjec- tive radiographic finding; one must be careful with this “finding” because radiographic technique and/or pro- cessing can profoundly influence the visual appearance (that is, the darkness or lucency) of bones. For example, a dark film can result from high-kVp technique, high- mAs technique, increased time in developer, or raised developer temperature. Instead, observe specific, more objective features involving the cortices and/or cancellous bone of the second, third, and fourth metatarsals in the dorsoplantar (DP) foot view. Patterns associated with cortical bone thinning in generalized (chronic, long-standing) osteopenia include endosteal resorption, Figure 4: Regional osteoporosis. A, Periarticular, spotty (acute) osteopenia of cancellous bone at metatarsophalangeal joints. B, Metaphyseal ill-defined 130 transverse bands of decreased density, all metatarsals (acute osteopenia). C, Severe acute osteopenia, with spotty, permeative decreased density of cancellous and cortical bone, and subperiosteal resorption. D, Severe osteopenia secondary to polio. Findings parallel those seen in chronic osteopenia (generalized osteoporosis).

intracortical tunneling, and/or subperiosteal resorption1 (Figure 1). A cancellous bone pattern associated with generalized osteopenia is prominent primary trabeculations, which may stand out in relief because secondary trabeculae are resorbed and subsequent bone is laid down on the remain- Figure 1: Chronic osteopenia, cortical bone. A, Normally, the endosteal and subperiosteal surfaces of the cortex are well defined and contin- ing primary trabeculae (Figure 2). uous and the remainder of the cortex is radiopaque and homogeneous Cortical and cancellous bone re- in density. B, In chronic cortical osteopenia, the endosteal surfaces are sorption is best identified using the ill defined, and lucent striations (intracortical tunneling) may be seen DP foot view and concentrating on running through the cortex, parallel to the shaft. C, Endosteal resorp- the second, third, and fourth meta- tion, resulting in cortical thinning. tarsals. The medial oblique view should not be used; striations that mimic intracortical tunneling normally are seen at the diametaphy- seal region. Caution should be ex- ercised so that these findings are not used to diagnose osteoporosis or other metabolic disease. Chronic osteopenia is commonly associated with systemic disorders, which are primarily diagnosed by other, more characteristic, radiologic features. Figure 3: Generalized In contrast, the primary radio- Figure 2: Chronic osteopenia, cancellous bone. A, Cancellous bone osteoporosis. This elderly, graphic feature of acute osteopenia postmenopausal patient is made of primary and secondary trabeculae. The primary trabecu- is spotty (mottled, moth-eaten) loss lae—also known as stress trabeculae—are found along lines of stress. demonstrates the characteristic features of chronic of bone density, particularly in peri- Secondary trabeculae are found perpendicular or oblique to the pri- articular regions. Acute osteopenia mary or stress trabeculae. Secondary trabeculae give spongiosa a fine, osteopenia, including is associated with causes of regional homogeneous appearance. B, With chronic osteopenia, secondary endosteal resorption, trabeculae are resorbed, leaving the primary trabeculae to stand out in intracortical tunneling, osteoporosis (discussed next), such relief. As bone is laid down on the remaining primary trabeculae, they and prominent, coarsened as immobilization or disuse. become coarse in appearance. primary trabeculae. Continued on page 131

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Radiology (from page 130) appearance of calcaneal trabecular patterns provide an index for assessing osteoporosis;5 however, Osteoporosis controversy exists as to whether or not these trabecular Osteoporosis is a metabolic disease that accompanies patterns correlate with actual bone density.6 Osteoporosis many other disease processes, including most of the en- has been classified according to its etiology: generalized, docrine and nutritional disorders discussed later in this regional, and localized.1 article. It is characterized by progressive loss of bone mass Generalized osteoporosis affects the entire skele- and may result in pathologic fracture. Osteoporosis is not ton and is associated with aging (senile osteoporosis), easily diagnosed with plain films, because 30% to 50% post-menopause, medications (steroids), endocrine states of bone calcium must be lost before osteopenia is visually (hyperparathyroidism, diabetes mellitus), deficiency apparent. Quantitative methods are necessary to detect states (scurvy, malnutrition), anemia, and alcoholism, early osteoporosis; studies include single-energy x-ray ab- to name a few. The radiographic features are more com- sorptiometry (wrist and heel), radiographic absorptiometry monly visualized in the axial skeleton. Typical radio- (hand), single-photon absorptiometry (wrist), quantitative graphic findings in the lower extremity (Figure 3) include computed tomography (spine), and dual-photon absorpti- one or any combination of the following: ometry (spine, hip, body). It has been suggested that the Prominent primary trabeculations Thinning of the cortices Intracortical striations (tunneling) Normal radiographic anatomy Normal radiographic anatomy may be misinterpret- may be misinterpreted as osteopenia. ed as osteopenia. For example, the trabeculations in the first-metatarsal head and neck are normally prominent and appear coarsened. Regional osteoporosis affects one 131 extremity. It is associated with disuse (immobilization) and reflex sympathetic dystrophy syndrome (RSD). Typical radiographic findings (Figure 4) include one or any combination of the following: Spotty (moth-eaten, mottled, patchy) osteopenia in cancellous bone, especially periarticular regions Ill-defined transverse bands of decreased density at subchondral or metaphyseal locations Figure 5: Rickets. A, Knee, lateral view. Characteristic features include an ill-defined, lucent and frayed Subperiosteal bone resorption (in zone of provisional calcification, with widening of the physis. B, Knee, anteroposterior (AP) view. Follow- severe cases, especially RSD) ing treatment, the zone of provisional calcification has become more defined, although still irregular and ill-defined medially. Rickets. C, Ankle, lateral view. Same date as A; similar findings demonstrated, with Long-standing disuse (paraly- additional metaphyseal cupping. D, Ankle, lateral view. Metaphyseal cupping very prominent following sis is often associated with coarse, treatment; also note defect along surface of talar dome. prominent primary trabeculations and cortical thinning) Continued on page 132

Figure 8: Acromegaly. Char- acteristic features include en- Figure 6: Hyperparathy- Figure 7: Renal largement of bones (especially Figure 9: Scurvy. A, Ankle. Note the transverse line of in- roidism. Subperiosteal osteodystrophy. metatarsal heads and shafts and creased density along the metaphysis. B, Knee (different bone resorption along Soft tissue calcifi- phalangeal bases) and soft tissue patient). In addition to the sclerotic line across the metaphysis, the medial aspects of the cation throughout thickening (increased soft tissue beaks are visible at the metaphyseal margins, and Wimberg- metatarsal shafts. the leg. density and volume). er’s sign is evident. www.podiatrym.com JANUARY 2018 | PODIATRY MANAGEMENT CME Continuing

Medical EducationRadiology (from page 131) Transversely oriented, incomplete radiolucencies, known as pseudofractures or Looser’s zones, may be seen in tu- Localized osteoporosis affects one bone. Examples of bular bones.1 pathology demonstrating localized osteoporosis include The radiographic features of rickets consist of both osteomyelitis, arthritis, and neoplasm. The medial aspect non-specific and characteristic findings (Figure 5). of the fifth-metatarsal head is normally radiolucent and Non-specific findings include general retardation of body should not be mistaken as pathology. growth, osteopenia, and bowing deformity of long tu-

Osteomalacia and Rickets The characteristic feature of Osteomalacia and rickets are characterized hyperparathyroidism is subperiosteal histologically as disorders with excessive amounts of bone resorption. uncalcified osteoid.7 Eti- ologies include vitamin D deficiency and hypophos- bular bones. Characteristic changes occur at the growth phatemia. When present plate region of tubular bones and include widening of the in the adult skeleton, os- physis, decreased density at the zone of provisional cal- teomalacia is the name cification, irregularity of the physeal margin of the zone given to this condition; in of provisional calcification (which has been described as the growing skeleton of “fraying” and a “paint-brush appearance”), and widening infancy and childhood, it and cupping of the metaphysis.1 Figure 10: Paget’s disease. A, Mor- 132 is called rickets. tise view; B, lateral view. The bone The radiographic fea- is predominantly sclerotic in the Hyperparathyroidism tures of osteomalacia are diaphysis and metaphysis, with The general term hyperparathyroidism refers to in- non-specific, consisting mixed well-defined lucent areas creased levels of parathyroid hormone.1 The characteristic primarily of osteopenia. intermixed. Probably the third stage. feature of hyperparathyroidism is subperiosteal bone re- Bowing deformity of long (Accompanying text on following sorption (Figure 6). Other sites of bone resorption include tubular bones may occur. page.) periarticular, intracortical, endosteal, subchondral, and at entheses. Soft tissue calcification and geographic, lucent lesions known as Brown tumors may also be seen.

Renal Osteodystrophy Patients with chronic renal failure demonstrate bony abnormalities known as renal Figure 11: Hereditary multiple exostoses. A, DP view, left foot. Small exostoses are becoming visible along the medial and osteodystrophy.1 The lateral aspects of the first-metatarsal distal metadiaphysis and along the lateral aspects of the third- and fourth-toe prox- radiographic findings imal phalangeal bases. B, Same patient, DP view, right foot. Significant involvement of the second and third metatarsals, manifested may parallel with shortening of the second. Hereditary multiple exostoses. C, Same patient, AP view, ankle. Exostoses are seen along those of hyperparathy- the medial aspect of the distal fibular diaphysis and the medial and lateral aspects of the tibial diaphysis. D, Different pa- roidism, osteoporosis, tient, adult. Involvement of the second through fourth metatarsals and third-toe proximal phalanx. and osteomalacia (or rickets if in the child). Figure 12: Osteogenesis imperfecta. A, DP view, foot. Characteris- Calcification of soft tis- tic features include narrowed girth of tubular bones and cancellous sue and vessels is a fre- osteopenia. B-D, Different patient demonstrating severe osteopo- quent finding (Figure 7). rosis and severe deformity of the fibula. Osteogenesis imperfecta. A, DP view, foot. Characteristic features include narrowed girth Acromegaly of tubular bones and cancellous osteopenia. Excess pituitary so- B-D, Different patient matotrophic growth demonstrating severe hormone results in ab- osteoporosis and se- normal growth of bone, vere deformity of the cartilage, and fibrous tis- fibula. Continued on page 133

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Radiology (from page 132) Figure 13: Osteopetrosis. A, DP view, 7-year- ology is unknown, and old; B, Lateral view, same patient at 3 years of occurs more frequently sue.7 In the adult, this is known age. Classic bone-within-bone appearance. in people who are 40 years as acromegaly; gigantism results and older. Paget’s disease is in the child with open growth typically asymptomatic in the plates. Radiographically (Figure foot, which may explain the in- 8), the patient with acromegaly frequent reports at this location has an increase in skin volume; in the literature.9 Four radio- the heel pad thickness is greater graphic stages have been rec- than 25 mm in the male and 23 ognized. The first stage is de- mm in the female (when local scribed as osteolytic. It starts in causes are excluded). The joint the subchondral area, spreading spaces are widened by cartilage thick- Hypovitaminosis C (Scurvy) to the metaphysis and eventually the ening. Bones become prominent; the Scurvy is caused by insufficient diaphysis resulting in what has been metatarsal heads and distal phalanx un- dietary intake of vitamin C.8 The char- described as a “blade of grass” ap- gual tuberosities are enlarged, metatar- acteristic radiographic features (Figure pearance. The second stage demon- sal shafts are thickened, and spurs are 9) occur in the developing child. In strates both osteolysis and osteoscle- found at entheses. Interestingly, how- the metaphyseal region they include a rosis. The diaphysis appears lucent, ever, the proximal phalangeal shafts transverse line of increased density, a whereas the epiphyseal and metaph- appear narrow in girth. transverse line of decreased density ad- yseal regions are sclerotic. Bone in the third stage is predominantly scle- Figure 14: Me- rotic. Findings include cortical thick- lorheostosis. The ening, bone enlargement, and coars- wavy, thickened 133 endosteal cortical ened trabeculae. The fourth phase is surface simulates malignant degeneration, reported in wax flowing down 1% to 10% of patients.8 Other com- a candle. This plications associated with Paget’s dis- patient also has ease are fracture, osteomyelitis, and osteopoikilosis, joint disease.1 as demonstrated by the circular Hereditary Multiple Exostoses increased densities Figure 15: Osteopoikilosis. Multiple is- (Osteochondromatosis) in periarticular lands of cortical bone density are iden- regions. Hereditary multiple exostoses is tified in the lesser-metatarsal heads. a skeletal dysplasia resulting from a

Figure 16: Osteopathia striata. Lateral view, ankle. Mixed linear The radiographic finding described bands of increased and as a “blade of grass” appearance is associated decreased density run through the metadi- with Paget’s disease. aphyseal region of the distal tibia, parallel to the bone’s long axis. jacent to this line of increased density disturbance of chondroid production (the scurvy line), and a small, beaklike resulting in heterotopic proliferation outgrowth of bone along the margins of epiphyseal chondroblasts.10 The in- Figure 17: Figure 18: Meta- of the metaphysis. Extensive dividual lesions appear identical to the Fibrous dys- static calcification: periostitis may be seen along bone tumor osteochondroma, that is, plasia. The secondary hyper- the entire length of the bone. multiple cartilage-capped exostoses geographic parathyroidism. The epiphysis appears as an adjacent to the diaphyseal side of the lesion in the The spectrum of outer shell of increased den- physis (Figure 11). This condition is distal fibular radiographic ab- sity surrounding a central lu- autosomal dominant and appears in diaphysis normality may be cency (Wimberger’s sign).1 the first two decades of life as painless demonstrates seen in these pa- bumps near the ends of long bones. a hazy, ground tients. This exam- Paget’s Disease (Osteitis Its distribution is frequently symmet- glass appear- ple demonstrates Deformans) ric, and it can cause bone deformity ance centrally. significant soft and shortening. Approximately 5 per- Notice its tissue calcification Paget’s disease (Figure intramedullary in the distal leg. 10) is characterized by ex- cent of these lesions transform into 7 location. cessive and abnormal re- chondrosarcoma. modeling of bone.1 Its eti- Continued on page 134 www.podiatrym.com JANUARY 2018 | PODIATRY MANAGEMENT CME Continuing

Medical EducationRadiology (from page 133)

Osteogenesis Imperfecta An inherited skeletal dysplasia that is the result of abnormal metaphyseal and periosteal ossification caused by deficient osteoid production is osteogenesis imperfecta.10 Abnormal maturation of collagen occurs in both mineralized and non-mineralized tissues. Radiographic features include diffuse osteopenia (occasionally coarse trabeculae and a honeycomb appearance), diminished bone girth, and flared metaphyses (Figure 12). An obvious complication is fracture. Figure 20: Dystrophic calcification: The Sclerosing Dysplasias Figure 19: Generalized calcinosis: tumoral calcinosis. trauma. This patient related a recent Four skeletal dysplasias are the result of abnormal injury to the heel. Multiple areas of metaphyseal and periosteal ossification caused by either A large periarticular mass demonstrates calcification ill-defined soft tissue calcification are excessive osteoid production or deficient osteolysis. The adjacent to the proximal in- identified (arrows). primary radiographic feature is increased bone density. terphalangeal joint of a toe. They include osteopetrosis, melorheostosis, osteopoikilosis, and osteopathia striata. Osteopetrosis (Albers-Schönberg disease) is an inherited, autosomal dominant (delayed type) condition Osteopoikilosis is characterized presenting radiographically with diffuse bone sclerosis by numerous small, (Figure 13). Its characteristic feature has been described 134 as a “bone within a bone” appearance.11 These patients well-defined and homogeneous circular are relatively aymptomatic.1 Melorheostosis is a rare dysplasia that is not believed foci of increased density. to be hereditary.1 the patient may or may not have associated symptomatology.9 The radiographic presentation bones.1 They may also be found in tarsal bones. Figure 21: Vascular Figure 22: Vascular Osteopathia striata is most likely inherited and calcification: phleb- calcification: Mo- is typically asymptomatic.9 Radiographically, linear, oliths. A, Phleboliths enckeberg’s sclerosis. may be solitary or The classic presenta- regular bands of increased density extend from the multiple, as demon- tion is shown in this metaphysis to the diaphysis, running parallel to the strated in this ex- diabetic patient (DP shaft (Figure 16). ample of the distal view). Tubular, ser- leg. B, Numerous piginous calcifications Fibrous Dysplasia phleboliths are seen are easily identified Pathologically, normal bone undergoing phys- throughout the calf in the first intermeta- iologic resorption is replaced with fibrous tissue.12 in this patient with tarsal space following It may occur in one (monostotic) or many (poly- chronic venous in- the course of arterial ostotic) bones. In tubular bones its location is insufficiency. vessels. tramedullary and diaphyseal, with only occasional is typically limited to a epiphyseal involvement.1 Radiographically the lesion single limb and consists Figure 23: Vascu- is somewhat radiolucent with a hazy, ground glass of hyperostosis along the lar calcification: (homogeneous) quality, and may appear expansile bone’s periphery, extend- atherosclerosis. In with endosteal scalloping (Figure 17). ing along its entire length contrast to Mo- in many cases (Figure enckeberg’s sclero- Soft Tissue Manifestations of Systemic isorders 14). This picture simu- sis, the calcifications The primary radiographic soft tissue findings are lates wax flowing down that follow the calcification and ossification. Calcification appears the side of a candle and course of arterial as irregular punctate, circular, linear, or plaque- vessels are patchy has a wavy, sclerotic bony like radiodense areas with no cortical or trabecular and solid. contour usually along the structure.1 Ossification, in contrast, demonstrates a bone’s endosteal surface. trabecular pattern and a thin, cortex-like periphery. Osteopoikilosis is an However, if the lesion is small, the distinction may inherited skeletal dysplasia that is not associated with be impossible to determine visually. symptomatology. Numerous small, well-defined and homogeneous circular foci of increased density are Calcification seen radiographically, mimicking multiple bone is- Conditions that lead to soft tissue calcification have lands (Figure 15). The distribution of these lesions is been categorized as metastatic calcification, generalized periarticular and symmetric, found at the ends of long Continued on page 135

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Radiology (from page 134) Figure 25: Soft along the tunica intima layer of the tissue ossification: vessel. Progressive calcification at calcinosis, and dystrophic calcifica- Achilles tendon. any particular site can lead to ob- tion.1 Metastatic calcification (Figure A, Notice the struction of the vessel. Radiographi- 18) results from a disturbance in trabeculations in cally, one notes patchy calcifications calcium or phosphorus metabolism. the lesion, which in the soft tissues that follow the Examples include hyperparathyroid- distinguish it from path of vessels (Figure 23). ism, hypoparathyroidism, renal os- calcification. B, A The site of soft tissue calcification much larger ossifi- teodystrophy, hypervitaminosis D, may provide a clue to the underly- cation; this image 1 and sarcoidosis. Generalized calci- also demonstrates ing systemic disorder. Periarticular nosis (Figure 19) presents as calci- Moenckeberg’s calcification is associated with hyper- um deposition in the skin and sub- sclerosis. parathyroidism, hypervitaminosis D, cutaneous tissue in the presence of and collagen vascular disease. Calci- normal calcium metabolism. Exam- and atherosclerosis. Moenckeberg’s fications of tendons and bursae are ples include collagen vascular disor- sclerosis (Mönckeberg’s arterioscle- associated with calcium pyrophos- ders (scleroderma, dermatomyositis), rosis, medial calcific sclerosis) is cal- phate dihydrate (CPPD) and calci- idiopathic tumoral calcinosis, and id- cification of the vessel’s tunica media um hydroxyapatite crystal deposition iopathic calcinosis universalis. layer. These lesions generally do not disease. Arterial calcification is fre- Tumoral calcinosis is rare in the obstruct blood flow foot but has been reported adjacent through the vessel. Figure 26: Generalized periostitis: venous stasis. A, to a sesamoid13 and a first-metatar- They are commonly Irregular, wavy periostitis is sal-head medial eminence,14 at the tip seen in patients with identified along the lateral of digits,15 and posterior to the ankle diabetes. and medial margins of the 135 joint. With dystrophic calcification Radiographically, distal tibia and fibular diaphy- (Figure 20), cal- Moenckeberg’s sclerosis, respectively. B, This cium is deposited sis has a characteristic patient, with chronic venous in damaged or de- appearance consisting insufficiency (AP view), vitalized tissue in of dual, curvilinear demonstrates solid periostitis the absence of a tubular calcifications along the distal tibial diaph- running ysis with diffuse soft tissue parallel to calcification (phleboliths).

The site of soft tissue calcification may provide a clue to the Figure 24: Calcific tendonitis. A, Achilles tendon calcification near its enthesis. B, Calcification of extensor tendons along the dorsum underlying systemic disorder.1 of the midfoot. generalized metabolic derangement. one an- Examples include neoplasm, inflam- other (Figure 22). They may be ser- quently seen with diabetes mellitus, mation, and trauma. Soft tissue cal- piginous and follow the anatomic hypervitaminosis D, and renal osteo- cification has been associated with course of the vessel. Not uncom- dystrophy. Calcification of cartilage local corticosteroid injection of the monly the path of calcification is (chondrocalcinosis) suggests CPPD heel16 and intra-articular corticoste- discontinuous. The term athero- deposition and hemochromatosis. roid injection of the small joints of sclerosis refers to plaque formation Sheet-like collections in the lower leg the hand.17 Extensive involvement of are associated with the foot suggests sarcoma.18 tissue injury and com- Vascular calcifications are fre- partment syndrome. quently encountered in the foot and The term calcific leg. Phleboliths, found in veins, are tendinitis (Figure 24) circular or elliptical in shape (Fig- has been used to de- ure 21); they possess a thin calcific scribe tendon calcifi- outline with a relatively lucent cen- cation resulting from ter. Phleboliths may be a solitary the deposition of cal- finding or multiple. Phleboliths have cium hydroxyapatite 20 also been described associated with Figure 27: Heterotopic soft tissue ossification. A, Myositis ossificans crystals. Its etiology 19 hemangioma of the foot. Two types circumscripta. A lesion identified in the plantar fascia musculature. is closely associated of arterial calcification have been B, Myositis ossificans associated with neuropathic osteoarthropathy, with trauma, but inju- described: Moenckeberg’s sclerosis posterior ankle. Continued on page 136 www.podiatrym.com JANUARY 2018 | PODIATRY MANAGEMENT CME Continuing pedic diseases, ed 4, Philadelphia, 1975, Medical EducationRadiology (from page 135) is the most common form (Figure 27A). Several cases in the foot have Saunders. 11 ry is not prerequisite. Pain is the been described.29-32 Forrester DM, Kricun ME, Kerr R: Im- most common associated symptom. 3) Myositis ossificans associated aging of the foot and ankle, Rockville, Md, Holt and Keats illustrate examples in- with neurologic disease (Figure 27B) 1988, Aspen. 12 Yochum TR, Rowe LJ: Essentials of volving the Achilles, peroneus, and may be due to a variety of neurologic skeletal radiology, vol 2, ed 3, Baltimore, 20 7 forefoot flexor tendons. Similar re- causes. 2004, Williams & Wilkins. ports include examples involving the 4) Pseudomalignant myositis os- 13 Slomowitz M, Nixon B, Mott RC: Tu- peroneal tendon,21,22 although they are sificans is similar to the circumscrip- moral calcinosis of the foot: case report and literature review, JFS 29(3):278, 1990. 14 Caspi I, Friedman B, Horoszovski H: Tumoral calcinosis simulating osteomyelitis, The term myositis ossificans JFS 28(6):547, 1989. is used to describe non-neoplastic heterotopic 15 Black JR, Sladek GD: Tumoral calcinosis in the foot and hand, J Am Podiatr soft tissue calcification. Assoc 73(3):153, Mar 1983. 16 Conti RJ, Shinder M: Soft tissue calcifications induced by local corticosteroid injection, JFS 30(1):34, 1991. not identified specifically as calcific ta form but without a history of an- 17 Dalinka MK, Stewart V, Bomalaski tendinitis. Radiographic evidence of tecedent trauma.33 JS, et al: Periarticular calcifications in as- adjacent bone erosion, mimicking ma- Yochum and Rowe34 warn that sociation with intra-articular corticosteroid lignancy, has been reported.23 the early stages of myositis ossifi- injections, Radiology 153:615, 1984. cans circumscripta may mimic sar- 18 Wu KK: Tumoral calcinosis with ex- 136 Ossification coma. It initially presents as a soft tensive pedal involvement, JFS 29(4):388, Causes of soft tissue ossifica- tissue swelling that proceeds to an 1990. 19 Miller SJ, Patton GW, Xenos D, Wulf tion include neoplasm (sarcoma), ill-defined calcific density followed MR: Multiple capillary hemangiomas of the trauma (myositis ossificans, os- by ossification. A radiolucent zone foot with associated phleboliths, J Am Podi- sifying hematoma), and venous may be seen between the lesion and atr Assoc 70(7):364, 1980. insufficiency. adjacent bone, which helps to distin- 20 Holt PD, Keats TE: Calcific tendinitis: Achilles tendon ossification (Fig- guish it from sarcomatous soft tissue a review of the usual and unusual, Skeletal ure 25) is frequently associated with extension. PM Radiol 22:1, 1993. pain.24-26 Interestingly, MRI analysis 21 Wirtz PD, Long DH, Vito GR: Calcifi- of several cases failed to demonstrate References cation within the peroneus brevis tendon, J 1 inflammatory changes, even with Resnick D: Bone and joint imaging, ed Am Podiatr Med Assoc 77(6):292, 1987. 3, Philadelphia, 2004, Saunders. 22 Lepow GM, Korfin DH: Calcification of acute symptoms.27 Morris and associ- 2 Bullough PG, Vigoria VJ: Orthopaedic an accessory peroneal tendon in an athlete, J ates have presented a classification of pathology, ed 5, 2009, Mosby. Am Podiatr Med Assoc 75(6):323, 1985. Achilles tendon lesion based on ana- 3 Christman RA: Misconceptions regard- 23 Hayes CW, Rosenthal DI, Plata MJ, tomic location, including calcification ing use of the term “osteoporosis,” J Cur Hudson TM: Calcific tendinitis in unusual and ossification.28 Podiatr Med 35(10):11, 1986. sites associated with cortical bone erosion, Generalized periostitis is associat- 4 Genant HK, Vogler JB, Block JE: Ra- AJR 149:967, 1987. ed with venous stasis (Figure 26), hy- diology of osteoporosis. In Riggs BL, Melton 24 Lotke PA: Ossification of the Achilles pertrophic osteoarthropathy (primary LJ, editors: Osteoporosis: etiology, diagno- tendon, J Bone Joint Surg 52A(1):157, 1970. and secondary), thyroid acropachy, sis, and management, Philadelphia, 1995, 25 Raynor KJ, McDonald RJ, Edelman and hypervitaminosis A.1,11 Radio- Lippincott Williams & Wilkins. RD, Parkinson DE: Ossification of the 5 graphically, varying degrees of peri- Jhamaria NL, Lal KB, Udawat M et al: Achilles tendon, J Am Podiatr Med Assoc The trabecular pattern of the calcaneum as 76(12):688, 1986. osteal new bone formation is possi- an index of osteoporosis, J Bone Joint Surg 26 Hatori M, Kita A, Hashimoto Y et al: ble, but typically it is thick and undu- 65B(2):195, 1983. Ossification of the Achilles tendon: a case lating (irregular). 6 Cockshott WP, Occleshaw CJ, Web- report, Foot & Ankle 15(1):44, 1994. The term myositis ossificans is ber C et al: Can a calcaneal morphologic 27 Yu JS, Witte D, Resnick D, Pogue W: used to describe non-neoplastic het- index determine the degree of osteoporo- Ossification of the Achilles tendon: imaging erotopic soft tissue calcification. Four sis? Skeletal Radiol 12:119, 1984. abnormalities in 12 patients, Skeletal Radiol categories are described in the liter- 7 Greenfield GB: Radiology of bone 23:127, 1994. ature, relating to underlying etiology diseases, ed 4, Philadelphia, 1986, 28 Morris KL, Giacopelli JA, Granoff D: (or lack of): Lippincott. Classification of radiopaque lesions of the 8 1) Myositis ossificans progres- Jaffe HL: Metabolic, degenerative, and tendo Achillis, JFS 29(6):533, 1990. inflammatory diseases of bones and joints, 29 Kaminsky SL, Corcoran D, Chubb siva is a rare genetic dysplasia Philadelphia, 1972, Lea & Febiger. WF, Pulla RJ: Myositis ossificans: pedal with associated congenital osseous 9 Berquist TH: Imaging of the foot and manifestations, JFS 31(2):173, 1992. 7 abnormalities. ankle, ed 3, Philadelphia, 2010, Lippincott 30 Fuselier CO, Tlapek TA, Sowell RD: 2) Myositis ossificans circum- Williams & Wilkins. Heterotopic ossification (myositis ossifi- scripta, caused by localized trauma, 10 Aegerter E, Kirkpatrick JA: Ortho- Continued on page 137

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Radiographic (from page 136) Fotiadou A, Arvaniti M, Kiriakou V, et osteoporosis. Semin Musculoskelet al.: Type II autosomal dominant osteopetro- Radiol 6: 197, 2002. cans) in the foot, J Am Podiatr Med Assoc sis: radiological features in two families con- Whitehouse RW: Paget’s disease of 76(9):524, 1986. taining five members with asymptomatic bone. Semin Musculoskelet Radiol 6: 313, 31 Herring KM, Levine BD: Myositis os- and uncomplicated disease. Skeletal Radiol 2002. sificans of traumatic origin in the foot, JFS 38: 1015, 2009. Wilson LC and Hall CM: Albright’s he- 31(1):30, 1992. Stoker DJ: Osteopetrosis. Semin Muscu- reditary osteodystrophy and pseudohypo- 32 Mandracchia V, Mahan KT, Pruzan- loskelet Radiol 6: 299, 2002. parathyroidism. Semin Musculoskelet Radi- sky J, Uricchio JN: Myositis ossificans: a Williams HJ, Davies AM and Chapman ol 6: 273, 2002. report of a case in the foot, J Am Podiatr S: Bone within a bone. Clinical Radiology Assoc 73(1):31, 1983. 59: 132, 2004. Dr. Christman is 33 Ogilvie-Harris DJ, Hons CB, Fornasier Berry JL, Davies M and Mee AP: Vita- currently a tenured VL: Pseudomalignant myositis ossificans: min D metabolism, rickets, and osteoma- professor at Western heterotopic new-bone formation without lacia. Semin Musculoskelet Radiol 6: 173, University of Health a history of trauma, J Bone Joint Surg 2002. Sciences’ College of 62A(8):1274, 1980. Morselli LL, Manetti L, Cosci C, et al.: Podiatric Medicine in 34 Yochum TR, Rowe LJ: Essentials of Bone and joint alterations in acromegaly. Pomona, CA. He is skeletal radiology, vol 1, ed 3, Baltimore, Journal of Orthopaedics and Traumatology the editor and author 2004, Williams & Wilkins. 7: 169, 2006. of the textbook Foot Mughal Z: Rickets in childhood. Semin and Ankle Radiolo- Additional References Musculoskelet Radiol 6: 183, 2002. gy; its 2nd edition was published in 2015. Martinez S: Tumoral calcinosis: 12 Pitt MJ, Morgan SL, Lopez-Ben R, et His website, www.FootRad.com, is devot- years later. Semin Musculoskelet Radiol 6: al.: Association of the presence of bone bars ed to all things podiatric imaging; he shares 331, 2002. on radiographs and low bone mineral densi- his knowledge and expertise via innovative Bansal A: The dripping candle wax ty. Skeletal Radiol 40: 905, 2011. learning environments to all interested sign. Radiology 246: 638, 2008. Quek ST and Peh WC: Radiology of learners worldwide. 137

CME EXAMINATION

See answer sheet on pagE 139.

1) Osseous resorption in cortical bone may B) hyperparathyroidism. appear as: C) fluorosis. A) band-like/transverse radiolucent D) hypervitaminosis A. areas in the metaphysis. B) subchondral spotty radiolucent 4) Generalized soft tissue thickening, areas. increased girth of metatarsals, decreased C) intracortical tunneling. girth of proximal phalanges, and joint space D) diffuse, homogeneous “coarsening” of widening are best associated with: trabeculae. A) hyperparathyroidism. B) pseudohypoparathyroidism. 2) A major cause of diffuse osteopenia is: C) acromegaly. A) osteoporosis. D) hypothyroidism. B) osteoarthritis. C) osteosarcoma. 5) Short metatarsals or phalanges are best D) osteopoikilosis. associated with: A) hypothyroidism. 3) Generalized subperiosteal bone resorption B) pseudohypoparathyroidism. is characteristic of: C) hyperparathyroidism. A) pseudohypoparathyroidism. D) hypervitaminosis A. Continued on page 137 www.podiatrym.com JANUARY 2018 | PODIATRY MANAGEMENT $ CME EXAMINATION PM’s Continuing

Medical Education CME Program 6) The following is NOT one of the three Welcome to the innovative Continuing Education classes of osteoporosis: Program brought to you by Podiatry Management A) generalized. Magazine. Our journal has been approved as a B) regional. sponsor of Continuing Medical Education by the C) localized. Council on Podiatric Medical Education. D) field. Now it’s even easier and more convenient to 7) A radiographic finding seen with reflex enroll in PM’s CE program! sympathetic dystrophy is: You can now enroll at any time during the year A) spotty loss of bone density. and submit eligible exams at any time during your B) intracortical tunneling. enrollment period. C) coarse trabeculations. CME articles and examination questions D) cortical thinning. from past issues of Podiatry Management can be found on the Internet at http://www. 8) A major cause of regional osteoporosis podiatrym.com/cme. Each lesson is approved 138 in the lower extremity is: for 1.5 hours continuing education contact hours. A) swimming. Please read the testing, grading and payment B) running. instructions to decide which method of participa- C) walking. tion is best for you. D) immobilization. Please call (631) 563-1604 if you have any questions. A personal operator will be happy to 9) A radiographic feature of rickets is: assist you. A) straight, narrow tubular bone. Each of the 10 lessons will count as 1.5 credits; B) sclerotic epiphysis. thus a maximum of 15 CME credits may be earned C) narrowing of the metaphysis. during any 12-month period. You may select any 10 D) irregular outline or in a 24-month period. zone of provisional calcification. The Podiatry Management Magazine CME program is approved by the Council on Podi- 10) Hypovitaminosis C is also known as: atric Education in all states where credits in A) rickets. instructional media are accepted. This article is B) scurvy. approved for 1.5 Continuing Education Contact C) lead poisoning. Hours (or 0.15 CEU’s) for each examination D) hypervitaminosis D. successfully completed.

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Home Study CME credits now accepted in Pennsylvania

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Note: If you are mailing your answer sheet, you must complete all there is no charge for the mail-in service if you have al- info. on the front and back of this page and mail with your credit ready enrolled in the annual exam CME program, and we receive card information to: Program Management Services, P.O. Box this exam during your current enrollment period. If you are not en- 490, East Islip, NY 11730. rolled, please send $27.00 per exam, or $220 to cover all 10 exams (thus saving $50 over the cost of 10 individual exam fees). Testing, Grading and Payment Instructions (1) Each participant achieving a passing grade of 70% or higher Facsimile Grading on any examination will receive an official computer form stating to receive your CME certificate, complete all information and the number of CE credits earned. This form should be safeguarded fax 24 hours a day to 631-532-1964. Your CME certificate will be and may be used as documentation of credits earned. dated and mailed within 48 hours. This service is available for $2.50 (2) Participants receiving a failing grade on any exam will be per exam if you are currently enrolled in the annual 10-exam CME notified and permitted to take one re-examination at no extra cost. program (and this exam falls within your enrollment period), and (3) All answers should be recorded on the answer form below. can be charged to your Visa, MasterCard, or American Express. For each question, decide which choice is the best answer, and cir- if you are not enrolled in the annual 10-exam CME program, cle the letter representing your choice. the fee is $27 per exam. (4) Complete all other information on the front and back of Phone-In Grading this page. You may also complete your exam by using the toll-free service. (5) Choose one out of the 3 options for testgrading: mail-in, fax, Call 1-800-232-4422 from 10 a.m. to 5 p.m. EST, Monday through or phone. To select the type of service that best suits your needs, Friday. Your CME certificate will be dated the same day you call and please read the following section, “Test Grading Options”. mailed within 48 hours. There is a $2.50 charge for this service if you are 139 Test Grading Options currently enrolled in the annual 10-exam CME program (and this exam Mail-In Grading falls within your enrollment period), and this fee can be charged to your to receive your CME certificate, complete all information and Visa, Mastercard, American Express, or Discover. If you are not current- mail with your credit card information to: Program Management ly enrolled, the fee is $27 per exam. When you call, please have ready: Services, P.O. Box 490, East Islip, NY 11730. PLEASE DO 1. Program number (Month and Year) NOT SEND WITH SIGNATURE REQUIRED, AS THESE 2. The answers to the test WILL NOT BE ACCEPTED. 3. Credit card information In the event you require additional CME information, please contact PMS, Inc., at 1-631-563-1604. Enrollment Form & Answer Sheet Please print clearly...Certificate will be issued from information below.

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Enrollment Form & Answer Sheet (continued) Continuing

Medical Education

EXAM #1/18 Radiology of Systemic Disorders Affecting the Foot and Ankle (Christman) Circle: 1. A B C D 6. A B C D 2. A B C D 7. A B C D 3. A B C D 8. A B C D 4. A B C D 9. A B C D 5. A B C D 10. A B C D

Medical Education Lesson Evaluation

140 Strongly Strongly agree Agree neutral Disagree disagree [5] [4] [3] [2] [1]

1) This CME lesson was helpful to my practice ____

2) The educational objectives were accomplished ____

3) I will apply the knowledge I learned from this lesson ____

4) I will makes changes in my practice behavior based on this lesson ____

5) This lesson presented quality information with adequate current references ____ 6) What overall grade would you assign this lesson? ABCD How long did it take you to complete this lesson? ______hour ______minutes

What topics would you like to see in future CME lessons ? Please list : ______

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