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At least 793 records · Page 44Linked to original sources
PubMed1987

Prevention of heterotopic bone formation: clinical experience with diphosphonates.

Heterotopic bone formation after total hip arthroplasty is a common occurrence in patients with osteoarthritis, and severe amounts of ectopic bone may limit motion or cause pain. Diphosphonates have been suggested as a method of preventing ectopic bone formation, but no long-term clinical evaluation of their effectiveness has been published. Because patients with osteoarthritis appeared to respond well to diphosphonate therapy in an earlier study, we thought that they would be an appropriate group of patients to study. We evaluated the results of 177 patients with 200 total hip arthroplasties performed for primary osteoarthritis. Considerable postoperative heterotopic bone formation (classes III and IV according to the classification system of Brooker and associates) was found in 36 hips (18%). The incidence of heterotopic bone formation was found to be as high as in the patients who had received either a placebo or no drug therapy. The postoperative range of motion of the hips, as well as ratings for pain, walking, and function, did not differ significantly between the treated and untreated groups. Diphosphonates (EHDP) have been demonstrated to inhibit the growth of hydroxyapatite crystals in vitro by chemisorption onto the crystal surface and thus have been thought to have the potential of preventing pathological calcification in vivo. However, diphosphonates have no inhibitory effect on the formation of osteoid matrix, and the delay in mineralization of matrix is reversed when therapy is discontinued. Although this delay in mineralization was known at the onset of these clinical trials, we hoped that the ultimate amount of heterotopic bone would be less in the treated patients and that the range of motion would be improved as a result of delaying the process of mineralization. Unfortunately, the final range of motion in the diphosphonate-treated patients did not differ significantly from that in the untreated group, and the final amount of heterotopic ossification was not reduced. Therefore diphosphonate therapy must be considered ineffective.

Clinical Trials as Topic↗
PubMed1994

Reaction of the pterygomaxillary fissure and the condylar cartilage to intermaxillary Class III magnetic mechanics.

The skeletal reaction to Class III intermaxillary magnetic mechanics was previously found to affect two target areas, the pterygomaxillary fissure (PMF) and the condylar cartilage. The objectives of this study were to analyze, radiographically and histologically, the response of these tissues to Class III intermaxillary functional orthopedic magnetic appliance (FOMA III), and to postulate possible models of their dichotomous biomechanism. Nine Macaca fascicularis monkeys received periodic administration of vital bone procion dye and were treated for 4 months with FOMA III (6 subjects) and sham appliance (3 subjects). The PMF (the target area of the midfacial complex) demonstrated a decreased skeletal reaction in inferosuperior and lateromedial directions. Cephalometrically, the lowermost PMF point was displaced inferiorly 1.98 +/- 1.74 mm and 0.42 +/- 0.38 mm and anteriorly 1.42 +/- 0.96 mm and 0.58 +/- 0.38 mm in the treated and control groups, respectively. The displacement of the uppermost PMF point, compared with the lowermost point, was three to five times lower. Histologically, two modes of response were found; first, a sutural response (disarticulation and osteogenesis) of the palatomaxillary and pterygopalatine sutures, which was distinctive of the lateral PMF aspect, and second, a dentosutural response, which was characteristic of the medial PMF aspect (bony microfractures between the third molar germ and the maxillary tuberosity in conjunction with mild sutural response). In the mandible, a discrepancy was found between the histologic and the cephalometric findings. Radiographically, mandibular length was unaffected after 4 months of treatment, and the distance condylion-pogonion was equally increased in the treated (0.75 +/- 0.78 mm) and the control animals (0.77 +/- 0.32 mm). Histologically, however, the condylar cartilage demonstrated increased osteoclastic activity at the zone of endochondral ossification and a decreased apposition rate at the adjacent bony trabeculae. Conceivably, the two target areas (PMF sutures versus condylar cartilage) demonstrate two diverse time-related responses that are either unrelated or interrelated to each other. An unrelated tissue response suggests that tissue stimulation (sutural) is always superior to tissue suppression (condylar). Another possible unrelated tissue reaction implies diverse response velocity (high sutural, low condylar). An interrelated mechanism suggests that an applied force will dissipate initially at the less resistant target area (sutures), and will subsequently affect the more resistant target area (condyle) once the sutural resistance exceeds a certain threshold. The fact that no pathologic change was found in the condylar cartilage encourages a long-term use of the FOMA III appliance, initiating treatment at an early skeletal age.

Animals↗
PubMed1977

Calcifying and osteoblastic tumors of the paranasal sinuses.

Calcifying and osteoblastic tumors of the paranasal sinuses comprise a large group of diseases, each characterized, however, by their own distinct pathologic features and correlated radiologic findings. The basic radiologic signs of such lesions comprise calcification, bone formation, and reactive bony sclerosis. It is the purpose of this presentation to define the radiologic signs which allow for appropriate diagnosis. These disorders are divided into three groups: calcifying and osteoblastic lesions simulating tumors, benign calcifying and osteoblastic tumors, and malignant calcifying and osteoblastic tumors.

Calcinosis↗
PubMed2001

Mast cell involvement in fibrodysplasia ossificans progressiva.

Fibrodysplasia ossificans progressiva (FOP) is a catastrophic genetic disorder of progressive heterotopic ossification associated with dysregulated production of bone morphogenetic protein 4 (BMP4), a potent osteogenic morphogen. Postnatal heterotopic ossification in FOP is often heralded by hectic episodes of severe post-traumatic connective tissue swelling and intramuscular edema, followed by an intense and highly angiogenic fibroproliferative mass. The abrupt appearance, intense size, and rapid intrafascial spread of the edematous preosseous fibroproliferative lesions implicate a dysregulated wound response mechanism and suggest that cells and mediators involved in inflammation and tissue repair may be conscripted in the growth and progression of FOP lesions. The central and coordinate role of inflammatory mast cells and their mediators in tissue edema, wound repair, fibrogenesis, angiogenesis, and tumor invasion prompted us to investigate the potential involvement of mast cells in the pathology of FOP lesions. We show that inflammatory mast cells are present at every stage of the development of FOP lesions and are most pronounced at the highly vascular fibroproliferative stage. Mast cell density at the periphery of FOP lesional tissue is 40- to 150-fold greater than in normal control skeletal muscle or in uninvolved skeletal muscle from FOP patients and 10- to 40-fold greater than in any other inflammatory myopathy examined. These findings document mobilization and activation of inflammatory mast cells in the pathology of FOP lesions and provide a novel and previously unrecognized target for pharmacologic intervention in this extremely disabling disease.

Cell Count↗
PubMedDate not supplied

Grade I and II acromioclavicular dislocations: results of conservative treatment.

The purpose of this study was to assess the results of acute grade I and II acromioclavicular (AC) joint sprains treated by conservative measures. Between 1993 and 1997, 37 consecutive patients were treated conservatively for AC joint sprains, grade I and II in the Tossy classification. Of these patients, 4 were excluded (three lost to follow-up and one sustained a further AC injury), leaving a series of 33 patients. Among them, in 9 (27%), chronic AC joint pathology that required subsequent surgery developed at a mean of 26 months after injury. The remaining 24 were reviewed clinically and radiologically at a mean of 6.3 years (range, 4-8 years) after injury. At the latest follow-up, 17 of the 33 patients (52%) remained asymptomatic. Of the 24 patients reviewed, 7 complained of activity-related pain. Eight patients presented with residual anteroposterior instability. Tenderness at the AC joint as well as a positive cross-body test was observed in 12 patients. The mean Constant score at follow-up was 82 points. The x-ray films showed degenerative changes in 13 patients, ossification of the coracoclavicular ligaments in 2, an association of degenerative changes with ossification of the coracoclavicular ligaments in 3, and distal clavicular osteolysis in 3. Only 4 cases had no radiographic changes after this kind of AC injury. On the basis of these results, we conclude that the severity of the consequences after grade I and II AC sprains is underestimated.

Acromioclavicular Joint↗
PubMed2001

Spinal toxoplasmic arachnoiditis associated with osteoid formation: a rare presentation of toxoplasmosis.

STUDY DESIGN: An extremely rare presentation of an isolated spinal toxoplasmic arachnoiditis is described. OBJECTIVE: To draw attention to the fact that spinal arachnoid membranes may be a potential reservoir for Toxoplasma gondii. SUMMARY OF BACKGROUND DATA: Central nervous system toxoplasmosis is a common manifestation in patients who are immunodeficient. Reports on the spinal toxoplasmosis are rare and focused on spinal cord involvement. METHODS: An adult patient presented with symptoms of spastic paraparesis that had begun 13 years before admission. Thoracic spinal magnetic resonance imaging showed small lesions in posterior subarachnoid space at Th7-Th8. A Th7-Th8 laminectomy was performed. Intradural-extramedullary lesions were excised. RESULTS: Clinical, immunologic, and pathologic examinations showed adhesive spinal arachnoiditis associated with osteoid formation caused by past toxoplasmic infection. There was no impairment of the immunologic defense system. CONCLUSION: Where no causative factor is found in serious spinal adhesive arachnoiditis, the possibility of spinal toxoplasmosis should also be investigated.

Adult↗
PubMed1979

Hip joint instability after the neonatal period. I. Value of measuring the acetabular angle.

The acetabular angle was measured by two independent observers in a consecutive series of 29 infants with idiopathic instability of the hip. The diagnosis was made at the age of 1 1/2 to 21 months, and was confirmed by arthrography. The average difference in the measurement values between the two observers was less than 2 degrees. In infants with unilateral instability the acetabular angle was always greater on the unstable side. This difference decreased after treatment. Criteria for pathologic angles are discussed. Measurement of the acetabular angle is of greatest value for assessing the effect of treatment, but is of limited usefulness in diagnosing instability, especially during the first 6 months of life, as the cartilaginous component of the joint is not included in the measurement. Arthrography is recommended in cases difficult to evaluate.

Acetabulum↗
PubMed1992

[Experimental study of hyperostosis induced by hypervitaminosis A].

Radiological and histological studies were made on retinoid-induced hyperostosis in rats. Vitamin A (VA) was administered intraperitoneally in rats for 6 months. Hyperostosis was observed in 94 percent of rats administered VA and in 38 percent of the control. Chondrocytes and vascular proliferation were observed in the attachment of the tendons and in the anterior corner of the vertebral body after 3 months. Hyperostosis was observed as osteophytes in the attachment of ligaments or tendons and as heterotopic ossification in the tendons or the joint capsules of the whole body after 6 months. Immature cells were observed around the osteophytes. These areas were stained with pH 4.1 toluidine blue and disappeared following streptomyces hyaluronidase treatment. This would indicate that hyaluronic acid increased around these areas. These results appear to demonstrate that hypervitaminosis A is capable of producing hyperostosis.

Animals↗
PubMed1986

[Diseases of the Achilles tendon].

In this report diseases of the Achilles tendon are discussed. First an anatomical survey of this region is presented including anatomical variations together with the results of the author's own investigations on corpses. Certain positions and insertions of the plantaris tendon with respect to the Achilles tendon may have pathological influence. Pathological aspects are discussed after a review of the physiology of the Achilles tendon, including functional and tensile tests. The clinical picture changes according to the location of the pathological disorder--tendon, paratenon, insertion and bursae--and whether the disease is acute or chronic. There are various reasons for degenerative changes in the tendon, which can even lead to rupture. Surgical and non-surgical treatment and their indications are presented. In conclusion treatment methods and their results for 36 cases are given.

Achilles Tendon↗
PubMed1990

Pseudomalignant, nonneoplastic osseous soft-tissue tumors of the hand and foot.

Seventeen patients with nonneoplastic osseous tumors in the soft tissues of the hands and feet were retrospectively studied. Three of the patients had a reliable history of trauma. Ten patients showed periosteal reaction associated with gradual formation of an osseous soft-tissue tumor, sometimes with a peripheral zone of bone density. Histologically (also radiographically), the lesions may be mistaken for malignant neoplasms such as osteosarcoma or parosteal osteosarcoma, especially when the pathologist does not receive representative material. In this series, malignancy was suspected in eight patients. Radiologic and pathologic criteria that may be helpful in the differential diagnosis of this lesion are presented. It is important that this nonneoplastic, benign, and self-limiting process in the hands and feet be recognized and treated accordingly. Local excision is adequate therapy in most cases, with little risk of local recurrence.

Adolescent↗
PubMedDate not supplied

Pathophysiology of cervical myelopathy.

BACKGROUND CONTENT: Cervical myelopathy is a group of closely related disorders usually caused by spondylosis or by ossification of the posterior longitudinal ligament and is characterized by compression of the cervical spinal cord or nerve roots by varying degrees and number of levels. The decrease in diameter of the vertebral canal secondary to disc degeneration and osteophytic spurs compresses the spinal cord and nerve roots at one or several levels, producing direct damage and often secondary ischemic changes. PURPOSE: Clinicians who treat cervical myelopathy cord injuries should have a basic understanding of the pathophysiology and the processes that are initiated after the spinal cord has been injured. STUDY DESIGN/SETTING: Literature review. METHODS: Literature review of human cervical myelopathy and clinically relevant animal models to further our understanding of the pathological mechanisms involved. RESULTS: The pathophysiology of cervical myelopathy involves static factors, which result in acquired or developmental stenosis of the cervical canal and dynamic factors, which involve repetitive injury to the cervical cord. These mechanical factors in turn result in direct injury to neurons and glia as well as a secondary cascade of events including ischemia, excitotoxicity, and apoptosis; a pathobiology similar to that occurring in traumatic spinal cord injury. CONCLUSIONS: This review summarizes some of the significant pathophysiological processes involved in cervical myelopathy.

Apoptosis↗
PubMed1994

"Wavy ribs". A reversible pathologic finding in rat fetuses.

A literature of 74 scientific papers addressing the occurrence of "wavy ribs" in fetuses of small rodents has been collected with the support of a computer-assisted search on MEDLINE, TOXLINE, BIOSIS and EXCERPTA MEDICA systems (1982-1993) and has been critically examined. Numerous compounds of a large variation in chemical structure and biological activity, if given to pregnant rats during the later period of organogenesis, are known to cause "wavy ribs" in their fetuses, a reversible pathologic finding which is rarely observed in untreated controls. According to literature, causative factors, like delayed development of alkaline phosphatase, decreased fetal protein, dietary contents, maternal toxicity, renal loop diuretics, myometrial constriction, endocrine disturbances and beta-adrenoceptor stimulation or blocking have been observed and discussed, but, a general explanation for the lesions is still missing. Therefore, the following hypothesis may be added: the high doses used in reproductive toxicology may induce maternal and placental circulatory disturbances leading to reductions in fetal serum proteins, with delayed development of osteoblast progenitors and low fetal serum alkaline phosphatase in the day 17-20 fetus. Normalization of the neonate's homeostasis (serum protein) leads to enhanced ossification and concomitant bone repair until weaning.

Animals↗
PubMed2002

Tissue-nonspecific alkaline phosphatase and plasma cell membrane glycoprotein-1 are central antagonistic regulators of bone mineralization.

Osteoblasts mineralize bone matrix by promoting hydroxyapatite crystal formation and growth in the interior of membrane-limited matrix vesicles (MVs) and by propagating the crystals onto the collagenous extracellular matrix. Two osteoblast proteins, tissue-nonspecific alkaline phosphatase (TNAP) and plasma cell membrane glycoprotein-1 (PC-1) are involved in this process. Mutations in the TNAP gene result in the inborn error of metabolism known as hypophosphatasia, characterized by poorly mineralized bones, spontaneous fractures, and elevated extracellular concentrations of inorganic pyrophosphate (PP(i)). PP(i) suppresses the formation and growth of hydroxyapatite crystals. PP(i) is produced by the nucleoside triphosphate pyrophosphohydrolase activity of a family of isozymes, with PC-1 being the only member present in MVs. Mice with spontaneous mutations in the PC-1 gene have hypermineralization abnormalities that include osteoarthritis and ossification of the posterior longitudinal ligament of the spine. Here, we show the respective correction of bone mineralization abnormalities in knockout mice null for both the TNAP (Akp2) and PC-1 (Enpp1) genes. Each allele of Akp2 and Enpp1 has a measurable influence on mineralization status in vivo. Ex vivo experiments using cultured double-knockout osteoblasts and their MVs demonstrate normalization of PP(i) content and mineral deposition. Our data provide evidence that TNAP and PC-1 are key regulators of the extracellular PP(i) concentrations required for controlled bone mineralization. Our results suggest that inhibiting PC-1 function may be a viable therapeutic strategy for hypophosphatasia. Conversely, interfering with TNAP activity may correct pathological hyperossification because of PP(i) insufficiency.

Alkaline Phosphatase↗
PubMed2002

[Outcome after total hip arthroplasty performed for rapidly progressive hip destruction].

PURPOSE OF THE STUDY: Rapidly progressive destruction of the hip joint occurs in approximately 5 to 10% of patients with degenerative hip disease. The cause and natural history remain unclear, but total hip arthroplasty is almost always necessary. We performed a retrospective analysis to determine the particular clinical and radiological features of this condition and to assess long-term outcome after total hip arthroplasty. MATERIAL AND METHODS: One hundred total hip arthroplasties were performed between 1984 and 1988 in patients with rapidly progressive hip destruction (67 women and 11 men, mean age 71 years). The transtorchanteric approach was used in all cases to implant cemented Charnley-Kerboull prostheses. Mean follow-up was 7 years 10 months. RESULTS: There were seven complications: two nonunions of the trochanter, three extensive periprosthetic ossifications, one case of recurrent dislocation, and one late hematogenous infection. At last follow-up, the Merle d'Aubigné classification showed an excellent or very good functional result in 95 hips. Stable fixation was observed for 94 acetabular implants and 97 femoral implants. Six acetabular implants showed signs of loosening: certain=1, probable=4, potential=1. Three femoral implants showed signs of loosening: certain=1, potential=2. All the femoral loosenings were associated with acetabular loosening. Four hips required revision surgery: one for nonunion of the trochanter, one for septic loosening, two for aseptic loosening. DISCUSSION: This series confirmed the radiological and clinical definitions of rapidly progressive hip destruction and demonstrated the reliability of pathological examination of the femoral head and joint capsule. Among the different hypotheses put forward to explain this condition, neither overloading nor use of antiinflammatory drugs would appear to be operating in this series. We were unable to confirm or infirm the micro-crystalline or vascular origin of this condition. Nevertheless, the vascular phenomena observed in the femoral head could be compared with those observed in ischemic joint disease. Arthroplasty led to major blood loss (2706 ml, hematocrit 35). This appears to be higher than observed for arthroplasty performed with the same technique in patients with the usual form of degenerative hip disease. Excepting this fact, the complications observed and the clinical results as well as the longevity of these implants suggest that arthroplasties performed for rapidly degenerative hips are not substantially different from those performed for common degenerative hip disease.

Aged↗
PubMedDate not supplied

Experimental otitis media following middle ear inoculation of nonviable Streptococcus pneumoniae.

The pathogenesis of otitis media is poorly understood, and the events leading to bacterial invasion of the middle ear cleft and resulting inflammation are a matter of conjecture. While Streptococcus pneumoniae is the most frequent microbe cultured from acute, purulent middle ear effusions, it is infrequently cultured from nonsuppurative serous and mucoid effusion. To explore the possibility that nonviable pneumococci persisting in the middle ear cleft might produce mucosal inflammation, a solution of heat-killed pneumococci was placed in the middle ear cavity of experimental animals. Mucoperiosteal pathology which followed inoculation included an active, early subepithelial inflammatory response, metaplasia of the lining epithelium and later new bone formation. Thus, nonviable pneumococci are capable of producing middle ear inflammation, and it is possible that persistence of whole nonviable organisms or subcellular components in either middle ear effusion or mucoperiosteum may lead to continued middle ear inflammation or nonsuppurative otitis media.

Animals↗
PubMed1995

Long-term healing of bone using recombinant human bone morphogenetic protein 2.

A 2.5-cm-long middiaphyseal plate-stabilized segmental defect in the right femora of 5 adult sheep was implanted with 1.5 mg of recombinant human bone morphogenetic protein 2 mixed with inactivated demineralized ovine bone matrix. Bone healing was evaluated for 12 months using clinical, radiographic, gross pathologic, and histologic techniques. Bone formation within the defect was first visible radiographically between Weeks 2 and 4 after surgery; bone union was apparent between Weeks 12 and 16, at which time the plates were removed. Recanalization of the medullary cavity with neocortex formation was near completion at Week 52. Bone mineral content at the defect sites equaled that of the nonsurgically treated intact femora by Week 16. Perifemoral soft tissue mineralization did not occur, and callus size was not greater than that formed with autograft. By Week 52, the sheep were not lame, and at necropsy the surgically treated femora were rigidly healed. Woven and lamellar bone bridged the defect site. An apparently normal sequence of ossification, modeling, and remodeling events had occurred. Recombinant human bone morphogenetic protein 2 mixed with a suitable carrier could provide an alternative to autograft for use in a variety of orthopaedic procedures.

Absorptiometry, Photon↗
PubMed1992

Interactions between growth hormone and dexamethasone in skeletal growth and bone structure of the young mouse.

The present study investigated the interactions of growth hormone (GH) and glucocorticoid on skeletal growth and bone structure in young mice. The purpose of this study was to examine the possible prevention by GH of the damage inflicted by dexamethasone (Dex) at sites of skeletal growth and ossification. Dex (1 mg/kg) with or without rat GH (rGH) or bovine GH (bGH), 1 mg/kg, was given for 4 weeks, from age 3-7 weeks, to female ICR mice. Tibiae, humerus, and vertebrae were analyzed morphometrically and biochemically. Growth, as determined by the mouse weight, tibial length, and humerus protein content was found to be compromised by dexamethasone. This was prevented by rGH or bGH. The epiphyseal growth plate width, trabecular bone volume, cortical bone width, mineral bone content, and alkaline and acid phosphatase activity were decreased by dexamethasone. These were prevented by rGH or by bGH. The findings of the present study suggest that in the mouse, GH can decrease or even avoid some of the pathological features in growing bones inflicted by high-dose glucocorticoid treatment.

Analysis of Variance↗