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Biomedical subjects

S C Marks

Publications and source records attributed to S C Marks.

At least 217 records · Page 12Linked to original sources
PubMed1981

The hematogenous origin of osteoclasts: experimental evidence from osteopetrotic (microphthalmic) mice treated with spleen cells from beige mouse donors.

The excessive skeletal mass and reduced bone resorption characteristic of osteopetrosis in microphthalmic (mi) mice can be corrected by irradiation and transfer of spleen cells from a normal littermate. Osteoclasts in beige (bg) mice, a mutation without osteopetrosis, have giant lysosomal granules. These two facts were exploited to trace osteoclast lineage. Microphthalmic mice treated with whole-body irradiation and spleen cells from a beige donor resorbed the excessive skeletal mass and recovered from osteopetrosis. Furthermore, osteoclasts in treated mi mice had giant lysosomal granules and resembled those found in bg donors when examined by light and transmission electron microscopy. These data provide direct evidence for a hematogenous origin of osteoclasts in mammals.

Animals↗
PubMed1981

Tooth eruption depends on bone resorption: experimental evidence from osteopetrotic (ia) rats.

Resorption of alveolar bone around erupting teeth is known to be independent of tooth eruption. However, the failure of tooth eruption and reduction in bone resorption in the osteopetrotic rat mutation, incisors absent (ia), suggest that tooth eruption depends upon bone resorption. This hypothesis was tested by determining the effects of neonatal restoration of bone resorption in ia rats on eruption of first molars. Newborn ia rats were treated with irradiation and spleen cells and tooth eruption and bone resorption were examined 30 days later. In 24 treated ia rats at least two molars erupted in every rat and all four molars erupted in 14. In 24 untreated ia littermates, no molars erupted in 21, one molar erupted in two and two molars erupted in one rat. All molars erupted in 38 untreated normal littermates. Alveolar bone overlying unerupted first molars in untreated ia rats was not present in treated mutant littermates. Neonatally treated ia rats had osteoclasts with ruffled borders and no skeletal sclerosis by 30 days. Within 48 hours after treatment two types of osteoclasts could be found in treated rats. One type resembled those found in untreated ia littermates and the other those found in normal rats. These data suggest that failure of tooth eruption in ia rats is directly related to the reduction in bone resorption and that alveolar bone resorption is required for tooth eruption.

Animals↗
PubMed1980

Experiences with learning about death and dying in the undergraduate anatomy curriculum.

Discussions about death, dying, and dissection during the first-year curriculum were initiated at the University of Massachusetts Medical School to deal with personal questions and emotions evoked by cadaver dissection. This report describes the evoluation of these discussions, their timing with respect to dissection, the present content of these sessions, and the importance of follow-up. Student response has been positive.

Anatomy↗
PubMed1980

Tooth eruption: evidence for the central role of the dental follicle.

The roles of the gubernaculum dentis, root formation, tooth crown and dental follicle in prefunctional eruption of a mandibular premolar have been studied in nine beagle dogs by radiographic and histologic evaluations of the effects of surgical ablation or removal of these structures on tooth eruption. The dental follicle was the only one of these structures required for the coordinated enlargement of the eruption pathway and formation of bone in the base of the bony crypt, the radiographic and histologic hallmarks of tooth eruption. These data, together with the topographic relationships of the dental follicle to areas of localized bone resorption and formation, are interpreted to mean that the dental follicle may influence, if not coordinate, these processes in tooth eruption.

Alveolar Process↗
PubMed1980

The anatomical basis for femoral nerve palsy following iliacus hematoma.

With increased use of anticoagulant agents, femoral neuropathy subsequent to hemorrhage within the iliacus muscle has become a frequent clinical problem. The mechanism for this type of femoral nerve palsy was studied in dissections of the iliac region and by injections of latex into fascial planes in that area. In most dissections, up to four fascial layers, parallel to the iliacus sheath, could be identified. Variable states of fusion of these layers often produced up to three pouches, separated by loose connective tissue or fat. These fasciae (called "lamina peritonealis," "lamina transversalis," "lamina preiliaca," and "lamina iliaca") appear to be variable adult remnants of distinct fascial layers present in the posterior abdominal wall during embryological development, and serve to strengthen the intrinsic fascia of the iliacus muscle. Latex injected into the iliacus sheath spread from the midlumbar region to the femoral triangle, surrounding, compressing, and stretching the femoral nerve in different parts of its course. These observations suggest an anatomical basis for femoral nerve palsy during iliacus hematoma.

Abdominal Muscles↗
PubMed1979

The cellular basis for extremity bone loss in leprosy.

Osteoclasts and osteolytic osteocytes have been observed in the majority of 60 samples of bone taken from five patients with lepromatous or tuberculoid leprosy. These results are interpreted to mean that bone loss in patients with leprosy is an acceleration of a normal cellular process and not the result of avascular necrosis. The acceleration of bone resorption could be due to local release of products from M. leprae or host cells, a hypothesis testable by organ culture methods. The presence of lymphocytes and mononuclear cells in bone samples in this and previous studies is discussed with respect to recent evidence of a role for lymphoid cells in bone resorption.

Acid Phosphatase↗
PubMed1978

Studies of the mechanism of spleen cell cure for osteopetrosis in ia rats: appearance of osteoclasts with ruffled borders.

After ia (osteopetrotic) rats receive whole body radiation and an injection of spleen cells from a normal littermate, the dense, sclerotic skeleton characteristic of osteopetrosis is rapidly remodeled and becomes normal in appearance radiographically and histologically within three weeks. The mechanism of this skeletal transformation has been explored in cured ia rats by light and electron microscopic examination of osteoclasts. In ia rats less than 25 days of age, osteoclasts viewed by electron microscopy lack a ruffled border - the extensive elaboration of plasma membrane next to the bone surface. Cured ia rats have osteoclasts with ruffled borders indistinguishable from those of normal littermates. In ia rats that receive only 600 rads whole body radiation, osteoclasts are still present three weeks later, but appear abnormal by light microscopy, with dense nuclei and lacking cytoplasmic vacuoles next to the bone surface. Cured ia rats have two types of osteoclasts, one type indistinguishable from osteoclasts of normal littermates by light microscopy, the other resembling osteoclasts of ia rats that received radiation only. These data indicate that the mechanism of the spleen cell cure for osteopetrosis in ia rats is rapid remodeling of the skeleton produced by osteoclasts with ruffled borders. Whether normal spleen cells produce these osteoclasts directly by cell division or indirectly by elaboration of some unknown local factor required for formations of ruffled borders by ia osteoclasts is not known.

Animals↗
PubMed1978

Studies of the cellular cure for osteopetrosis by transplanted cells: specificity of the cell type in ia rats.

Spleen cells from normal rats are known to cure osteopetrosis in ia littermates within 3 weeks. In this study cell suspensions from liver, thymus, bone marrow, salivary gland, skeletal muscle and brain from normal rats were tested for their ability to cure osteopetrosis in ia littermates whose ability to reject these cells had been suppressed by whole-body irradiation. Cells from liver, thymus and bone marrow cured the disease as effectively as spleen cells from normal littermates. Mutants that received cells from salivary gland, muscle and brain remained osteopetrotic. These data suggest that some cell found in spleen, liver, thymus and bone marrow of 10-day-old normal rats, such as a lymphoid cell or stem cell, can restore hemopoiesis and bone resorption in osteopetrotic (ia) rats.

Animals↗
PubMed1978

Parathyroid hormone stimulation of adenylate cyclase activity and lactic acid accumulation in calvaria of osteopetrotic (ia) rats.

We have examined the effect of parathyroid hormone (PTH) on the adenylate cyclase activity of newborn osteopetrotic rat calvaria, to study a possible molecular basis for the reduced response of this mutant to PTH. Phenotypically normal littermates served as controls. We also measured the effect of PTH on kidney adenylate cyclase activity and on lactic acid accumulation in short term cultures of calvaria. PTH stimulated calvarial adenylate cyclase activity in a dose-dependent manner in both mutant rats and normal littermates. Lactic acid production was also enhanced by PTH, and no significant difference between mutants and normal littermates was observed. These findings indicate that the reduced response of the young osteopetrotic rats to PTH is not due to an absence of PTH receptors coupled to adenylate cyclase.

Adenylyl Cyclases↗
PubMed1977

Pathogenesis of osteopetrosis in the microphthalmic mouse: reduced bone resorption.

Bone resorption, stimulated by injection of parathyroid extract, was measured in vivo in microphthalmic mice as the rate of release of 3H from bone after incorporation of 3H-proline. Bone resorption in these mice, which inherit osteopetrosis, was less than 10% of the in normal litermates. Autoradiography confirmed the reduction in removal of radioactive bone matrix and in bone growth in microphthalmic mice. The ability of these mice to raise the serum calcium concentration in response to PTE was also reduced. These results, that bone resorption is reduced in microphthalmic mice, are discussed in relation to the pathogenesis and cure of the disease.

Animals↗
PubMed1977

Osteopetrosis in the toothless (t1) rat: presence of osteoclasts but failure to respond to parathyroid extract or to be cured by infusion of spleen or bone marrow cells from normal littermates.

Osteoclast have been observe for the first time in toothless (t1) rats, a mutation with inherits osteopetrosis as an autosomal recessive. The ability of t1 rats to raise the serum calcium concentration after injection of parathyroid extract was severely limited when compared with normal littermates. In addition, osteopetrosis in t1 rats is not cured by radiation and infusion of normal spleen or bone marrow cells from normal littermates, a method know to cure osteopetrosis in mutants of this and other species. This indirect evidence for a reduction in bone resorption as a cause of osteopetrosis in this mutation and the failure of transplanted cells to cure the disease are discussed in relation to the development and function of osteoclasts.

Animals↗
PubMed1977

A radiographic and histologic study of fracture healing in osteopetrotic rats.

Repair of tibial fractures in osteopetrotic rats was delayed in comparison to that of normal littermates, due to reduced remodeling. Reduced bone resorption, known to be the cause of the disease in this mutation, is expressed in both skeletal development and fracture repair. The possible implications for human juvenile osteopetrosis are discussed.

Animals↗
PubMed1976

Osteopetrosis in the IA rat cured by spleen cells from a normal littermate.

Osteopetrosis in ia rats has been cured by combining whole-body irradiation with infusion of spleen cells from a normal littermate. The cure, first seen radiographically and histologically as areas of resorption below the epiphyseal plates of long bones, progressed to produce marrow cavities of normal proportions. Treatment of ia rats with either radiation or normal spleen cells alone was not successful. Furthermore, osteopetrosis was induced in normal littermates when radiation was combined with infusion of mutant (ia) spleen cells. These results show that spleen cells contribute to the resorbing capacity of the skeleton and suggest that osteoclasts might have a hematogenous origin.

Animals↗
PubMed1976

Tooth eruption and bone resorption: experimental investigation of the ia (osteopetrotic) rat as a model for studying their relationships.

The osteopetrotic (ia) rat was examined as an experimental model for studying the dependence of tooth eruption on bone resorption. In ia rats eruption of incisors and first molars was rare and eruption of second and third molars was reduced and delayed. Autoradiographic studies of 3H-proline incorporation showed that delayed eruption was not due to reduced tooth formation. Microscopic study revealed distortion and failure of posterior growth of the apical ends of incisors, unresorbed bone blocking the eruption pathway for molars, and ankylosis of incisors and first molars to alveolar bone. A reduction in bone resorption, known to be the primary cause of the disease in ia rats, is presumed to be the cause of the delayed or unerupted dentition. The effectiveness of attempts to increase bone resorption in ia rats at an early age by injection of vitamin A and/or parathyroid extract or by parabiotic union with a normal littermate was determined by measuring their effect on the relative size of the tibial marrow cavity. Only parabiosis had a beneficial effect on bone resorption but surgical union could not be performed in animals young enough to affect eruption of incisors and first molars in ia parabionts. These results suggest that parabiotic union of neonatal rats should allow resorption to begin early enough to test the presumed dependence of tooth eruption on bone resorption.

Animals↗