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MY'STORY

The MOVE Fire

This is a personal recollection on the Move fire on May 13, 1985 Philadelphia police fired thousands of rounds at the MOVE house, city officials approved dropping an explosive device on the roof, the resulting fire was allowed to burn, 11 people—including five children—died, and 61 homes were destroyed. Philadelphia City Council later called it a “brutal attack carried out by the City of Philadelphia on its own citizens” and acknowledged that no individual faced criminal consequences for the bombing. One timeline correction worth preserving for the BHP record: the major previous MOVE-police confrontation was August 8, 1978, about seven years before the bombing, not a year or two earlier. Officer James Ramp was killed, other police and firefighters were wounded, nine MOVE members were later convicted, and television cameras recorded police beating Delbert Africa during his arrest. The 1985 MOVE Commission later specifically criticized city planners for failing to adequately use lessons from that 1978 confrontation. And that actually strengthens the point you’re making: 1985 did not happen without precedent or institutional memory. There had already been a deadly confrontation with MOVE, years of conflict, negotiations and police involvement before Osage Avenue.

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BLACK FACTS
The Truths They Never Taught You...

Shirley Chisholm — Unbought and Unbossed

In 1968 Shirley Chisholm became the first Black woman elected to the United States Congress. In 1972 she launched a campaign for the Democratic presidential nomination, breaking another political barrier.

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BHP gathered finds from its connected research sources. Showing the 4 strongest Black History matches.
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Wikipedia

Osteoid

Osteoid
Light micrograph of osteoid, containing two osteocytes, being synthesized by osteoblasts.
Identifiers
FMA66830
Anatomical terminology

In histology, osteoid is the unmineralized, organic portion of the bone matrix that forms prior to the maturation of bone tissue.[1] Osteoblasts begin the process of forming bone tissue by secreting the osteoid as several specific proteins. The osteoid and its adjacent bone cells have developed into new bone tissue when it becomes mineralized.[citation needed]

Osteoid makes up about fifty percent of bone volume and forty percent of bone weight. It is composed of fibers and ground substance. The predominant type of fiber is type I collagen and comprises ninety percent of the osteoid. The ground substance is mostly made up of chondroitin sulfate and osteocalcin.[citation needed] Osteoblasts synthesize and secrete osteoid as an unmineralized organic matrix, and when the osteoid becomes mineralized through deposition of calcium salts, it transforms into mature bone tissue.[2]

Composition

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Osteoid is primarily composed of Type I collagen and ground substance.

Collagen fibers

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Type I collagen comprises approximately 85-95% of the organic matrix,[3] providing the structural scaffold and tensile strength necessary for bone formation.[4] These collagen fibers form a dense, highly cross-linked network that serves as the foundation for subsequent mineralization.[5]

The collagen molecules are arranged in layers that alternate parallel and orthogonal to the axis of stress loading, creating a sophisticated composite structure.[5]

Ground substance

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The ground substance of osteoid comprises approximately 10% of the bone matrix[6] and includes non-collagenous proteins:

  • Proteoglycans - Including chondroitin sulfate and heparan sulfate, which bind to collagen and may regulate collagen fibril diameters and play a role in mineralization[3]
  • Osteocalcin - A bone-specific protein involved in binding calcium during the mineralization process[3]
  • Osteonectin - May serve a bridging function between collagen and the mineral component[3]
  • Bone sialoprotein - Proteins rich in sialic acid that participate in matrix organization[2]
  • Growth factors - Including transforming growth factors, fibroblast growth factors, and insulin-like growth factors[3]

Formation and secretion

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Osteoid is synthesized and secreted by osteoblasts, specialized bone-forming cells.[7] Osteoblasts are large cuboidal cells characterized by abundant rough endoplasmic reticulum, reflecting their high synthetic activity.[4]

At their apical surface, osteoblasts secrete large amounts of type I collagen and smaller amounts of matrix organizing proteins, including osteocalcin and osteopontin.[5] The newly secreted osteoid forms a hydrated protein matrix layer between the mineralization front and the osteoblast layer.[5][7]

The synthesis of bone matrix occurs in two main steps: deposition of organic matrix (osteoid) and its subsequent mineralization.[7] During active bone formation, osteoblasts continuously produce osteoid matrix until mineralization occurs.

Mineralization

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The transformation of osteoid into mineralized bone involves the deposition of hydroxyapatite crystals [Ca10(PO4)6OH2] within the organic matrix.[6]

Mechanism of mineralization

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Mineralization occurs in two phases: the vesicular phase and the fibrillar phase.[7]

Vesicular phase: Matrix vesicles, measuring 30-200 nm in diameter, are released from the apical membrane of osteoblasts into the newly formed bone matrix.[7][3] These vesicles contain alkaline phosphatase, adenosine triphosphatase (ATPase), and inorganic pyrophosphatase, and act as seeding sites for hydroxyapatite crystal formation through localized enzymatic accumulation of calcium and phosphate.[3]

Role of alkaline phosphatase: Osteoblasts secrete alkaline phosphatase, which participates in bone mineralization by hydrolyzing pyrophosphate, an inhibitor of mineralization, thereby increasing local inorganic phosphate availability for hydroxyapatite formation.[2][4]

Crystal propagation: Crystal growth proceeds from initial foci in matrix vesicles to form spheroids, which gradually coalesce to form a network of apatite crystals.[3] As the matrix matures, hydroxyapatite microcrystals are organized into a sophisticated composite within the collagen layer by nucleation in the protein lattice.[5]

Clinical significance

[edit]

Disorders of osteoid mineralization

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Defective mineralization of osteoid leads to several important clinical conditions characterized by accumulation of unmineralized matrix.

Rickets: Occurs in children when defective mineralization affects the growth plate and osteoid.[8] The condition results from calcium or phosphate deficiency, either isolated or secondary to vitamin D deficiency.[9] In rickets, the mineralization defect leads to accumulation of osteoid in bone tissue below the growth plate, resulting in weak bones and deformities.[9]

Osteomalacia: The adult equivalent of rickets, osteomalacia is characterized by softened bones due to impaired mineralization of osteoid.[10] Vitamin D deficiency is the most common cause, though calcium or phosphate deficiency can also result in osteomalacia.[10] The condition manifests as bone pain, muscle weakness, and increased fracture risk.

Histomorphometric characteristics of osteomalacia include:[11][9]

  • Prolonged mineralization lag time (greater than 100 days)
  • Widened osteoid seams (increased osteoid thickness)
  • Increased osteoid volume

Vitamin D metabolism disorders: Rickets and osteomalacia develop in various clinical situations and have in common an absence or delay in the mineralization of growth cartilage and newly formed bone collagen.[12] Deficiency of vitamin D, essential for absorption of dietary calcium, has been a major cause historically.[12]

Osteoid in bone tumors

[edit]

Osteosarcoma: The most common primary malignant bone tumor, osteosarcoma is characterized by malignant cells that produce osteoid.[13][14] Osteosarcoma is a primary malignant tumour of the skeleton characterized by the direct formation of immature bone or osteoid tissue by the tumour cells.[14]

The production of osteoid by tumor cells is the histological hallmark distinguishing osteosarcoma from other bone tumors.[15] The malignant osteoid produced appears as irregular, immature structures in close proximity to malignant cells with enlarged hyperchromatic nuclei and abnormal mitotic figures.[16]

Osteoid osteoma: A benign bone-forming tumor characterized by formation of osteoid tissue, typically causing localized bone pain that worsens at night.[17]

Role in bone remodeling

[edit]

Osteoid plays a central role in the continuous process of bone remodeling.[2] During the bone formation phase of remodeling, osteoblasts deposit new osteoid at sites previously resorbed by osteoclasts.[7]

The bone remodeling cycle involves distinct phases:[2]

  1. Activation: Recruitment of osteoclasts to specific bone sites
  2. Resorption: Osteoclastic removal of old bone
  3. Reversal: Transition from resorption to formation
  4. Formation: Osteoblastic deposition of new osteoid
  5. Mineralization: Transformation of osteoid into mineralized bone

Throughout this process, osteoblasts produce the unmineralized organic matrix that subsequently undergoes calcification to form new bone tissue.[4]

Biochemical markers

[edit]

Several biochemical markers are associated with osteoid metabolism and bone formation:

  • Alkaline phosphatase: Secreted by osteoblasts during active bone formation; elevated levels indicate increased osteoid production[2][9]
  • Osteocalcin: A bone-specific protein synthesized by osteoblasts and incorporated into osteoid; serves as a marker of bone formation[5]
  • Type I collagen peptides: Degradation products measured to assess bone turnover

Physiology

[edit]

To allow bone mineralization to take place, osteoblasts secrete tissue-nonspecific alkaline phosphatase into the osteoid to break down pyrophosphate, an extracellular inhibitor of hydroxyapatite precipitation which otherwise prevents precipitation of hydroxyapetite crystals from extracellular fluid which is supersaturated in Ca2+ and PO3−4 ions.[18]

Disorders

[edit]

When there are insufficient nutrient minerals or osteoblast dysfunction, the osteoid does not mineralize properly and accumulates. The resultant disorder is termed rickets in children and osteomalacia in adults. A deficiency of type I collagen, such as in osteogenesis imperfecta, also leads to defective osteoid and brittle, fracture-prone bones.

In some cases, secondary hyperparathyroidism can cause a disturbance in mineralisation of calcium and phosphate.

Another condition is a disturbance in primitive transformed cells of mesenchymal origin, which exhibit osteoblastic differentiation and produce malignant osteoid. This results in the formation of a malignant primary bone tumor known as osteosarcoma or osteogenic sarcoma. This malignancy most often develops in adolescence during periods of rapid osteoid formation (commonly referred to as growth spurts).[19]

See also

[edit]

References

[edit]
  1. ^ Trammell, Lindsay H.; Kroman, Anne M. (2013-01-01), "Chapter 13 - Bone and Dental Histology", in DiGangi, Elizabeth A.; Moore, Megan K. (eds.), Research Methods in Human Skeletal Biology, Academic Press, pp. 361–395, doi:10.1016/b978-0-12-385189-5.00013-3, ISBN 978-0-12-385189-5, retrieved 2020-11-18
  2. ^ a b c d e f White, H. J.; Helwany, M.; Biknevicius, A. R.; Peterson, D. C. (2024). "Physiology, Bone". StatPearls. StatPearls Publishing. PMID 30855919.
  3. ^ a b c d e f g h Othman, D. (2012). "An Overview of Bone Cells and their Regulating Factors of Differentiation". Plastic Surgery International. 2012. doi:10.1155/2012/374398. PMC 3341892. PMID 22701169.
  4. ^ a b c d Cite error: The named reference histology_osteoblasts was invoked but never defined (see the help page).
  5. ^ a b c d e f Blair, H. C.; Larrouture, Q. C.; Li, Y.; Lin, H.; Beer-Stoltz, D.; Liu, L.; Tuan, R. S.; Robinson, L. J.; Schlesinger, P. H.; Nelson, D. J. (2017). "Osteoblast Differentiation and Bone Matrix Formation In Vivo and In Vitro". Tissue Engineering Part B: Reviews. 23 (3): 268–280. doi:10.1089/ten.TEB.2016.0454. PMC 5467150. PMID 27846781.
  6. ^ a b Han, D.; Wang, T.; Wang, R.; Chen, J.; Tang, Y. (2023). "A Brief Review of Bone Cell Function and Importance". Diagnostics. 13 (22). doi:10.3390/diagnostics13223443. PMC 10648520. PMID 37998580.
  7. ^ a b c d e f Sun, S.; Huang, S. Q. (2015). "Biology of Bone Tissue: Structure, Function, and Factors That Influence Bone Cells". International Journal of Clinical and Experimental Medicine. 8 (5): 8254–8258. PMC 4515490. PMID 26221406.
  8. ^ Baron, S. L.; Mathai, J. K. (2024). "Rickets". StatPearls. StatPearls Publishing. PMID 32809510.
  9. ^ a b c d Ghorpade, D. S.; Leyland, R.; Kurowska-Stolarska, M.; Patil, S. A.; Balaji, K. N. (2012). "Rickets–vitamin D deficiency and dependency". Molecular and Cellular Biology. 32 (12): 2239–2253. doi:10.1128/MCB.06597-11. PMC 3313732. PMID 22473996.
  10. ^ a b Majmundar, V. D.; Syed, H. A.; Baxi, K. (2024). "Osteomalacia". StatPearls. StatPearls Publishing. PMID 32644463.
  11. ^ Uday, S.; Högler, W. (2021). "Nutritional rickets & osteomalacia: A practical approach to management". The Indian Journal of Medical Research. 152 (4): 356–367. doi:10.4103/ijmr.IJMR_1961_19. PMC 8061584. PMID 33380700.
  12. ^ a b Berry JL, Davies M, Mee AP (2002). "Vitamin D metabolism, rickets, and osteomalacia". Seminars in Musculoskeletal Radiology. 6 (3): 173–82. doi:10.1055/s-2002-36714. PMID 12541194.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  13. ^ Rishor-Olney, C. R.; Hinson, M. R. (2024). "Osteosarcoma (Osteogenic Sarcoma)". StatPearls. StatPearls Publishing. PMID 32644347.
  14. ^ a b Fink-Retter, A.; Gschwantler-Kaulich, D.; Hudelist, G.; Mueller, R.; Kubista, E.; Czerwenka, K.; Singer, C. F. (2006). "Osteosarcoma (Osteogenic sarcoma)". Oncology Reports. 18 (2): 299–304. PMC 1794406. PMID 17611648.
  15. ^ Dahlin DC, Coventry MB (1967). "Pathology of osteosarcoma". Clinical Orthopaedics and Related Research. 111 (111): 23–32. doi:10.1097/00003086-197509000-00004. PMID 168999.
  16. ^ "Osteosarcoma". Holland-Frei Cancer Medicine - NCBI Bookshelf. BC Decker. 2003.
  17. ^ Exo, J.; Smith, C.; Smith, R.; Bell, M. (2010). "Update on Bone Forming Tumors of the Head and Neck". Pediatric Health. 3 (6): 533–541. doi:10.2217/phe.09.54. PMC 2807498. PMID 20191093.
  18. ^ Hall, John E.; Hall, Michael E. (2021). "Chapter 55: Spinal Cord Motor Functions; the Cord Reflexes". Guyton and Hall Textbook of Medical Physiology (14th ed.). Philadelphia, PA: Elsevier. pp. 994–995. ISBN 978-0-323-59712-8.
  19. ^ Ottaviani Giulia; Jaffe Norman (2009). "The Epidemiology of Osteosarcoma". Pediatric and Adolescent Osteosarcoma. Cancer Treatment and Research. Vol. 152. New York: Springer. pp. 3–13. doi:10.1007/978-1-4419-0284-9_1. ISBN 978-1-4419-0283-2. PMID 20213383.
  • Netter, Frank H. (1987), Musculoskeletal system: anatomy, physiology, and metabolic disorders, Summit, New Jersey: Ciba-Geigy Corporation
  • Jaffe, N.; et al. (2009). Pediatric and Adolescent Osteosarcoma. New York: Springer. ISBN 978-1-4419-0283-2.
[edit]

Source: Wikipedia. Article content is retrieved live through the MediaWiki API.

Wikipedia

Osteoid

In histology, osteoid is the unmineralized, organic portion of the bone matrix that forms prior to the maturation of bone tissue. Osteoblasts begin the process of forming bone tissue by secreting the osteoid as several specific proteins. The osteoid and its adjacent bone cells have developed into new bone tissue when it becomes mineralized. Osteoid makes up about fifty percent of bone volume and forty percent of bone weight. It is composed of fibers and ground substance. The predominant type of fiber is type I collagen and comprises ninety percent of the osteoid. The ground substance is mostly made up of chondroitin sulfate and osteocalcin. Osteoblasts synthesize and secrete osteoid as an unmineralized organic matrix, and when the osteoid becomes mineralized through deposition of calcium salts, it transforms into mature bone tissue.

MORE →
Wikipedia

Osteoid osteoma

An osteoid osteoma is a benign (non-cancerous) bone tumor that arises from osteoblasts and some components of osteoclasts. It was originally thought to be a smaller version of an osteoblastoma. Osteoid osteomas tend to be less than 1.5 cm in size. The tumor can be in any bone in the body but are most common in long bones, such as the femur and tibia. They account for 10 to 12 percent of all benign bone tumors and 2 to 3 percent of all abnormal bone growths. Osteoid osteomas may occur at any age, and are most common in patients between the ages of 4 and 25 years old. Males are affected approximately three times more commonly than females. Osteoid osteomas are different than osteomas, which are rather found in older patients and localized in the skull.

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Wikipedia

Osteosarcoma

An osteosarcoma (OS) or osteogenic sarcoma (OGS) is a cancerous tumor in a bone. Specifically, it is an aggressive malignant neoplasm that arises from primitive transformed cells of mesenchymal origin (and thus a sarcoma) and that exhibits osteoblastic differentiation and produces malignant osteoid. Osteosarcoma is the most common histological form of primary bone sarcoma. It is most prevalent in teenagers and young adults.

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Wikipedia

Curettage

Curettage ( or ), in medical procedures, is the use of a curette (French, meaning "scoop") to remove tissue by scraping or scooping. Curettages are also a method of abortion. It has been replaced by vacuum aspiration over the last decade. Curettage has been used to treat teeth affected by periodontitis. Gingival curettage is a surgical procedure designed to remove the soft tissue lining of the periodontal pocket with a curet, leaving only a gingival connective tissue lining. ... Gingival curettage, as originally conceived, was designed to promote new connective tissue attachment to the tooth, by the removal of pocket lining and junctional epithelium. Since there is no evidence that gingival curettage has any therapeutic benefit in the treatment of chronic periodontitis, the American Dental Association has deleted that code from the fourth edition of Current Dental Terminology (CDT-4). In addition, the American Academy of Periodontology, in its Guidelines for Periodontal Therapy, did not include gingival curettage as a method of treatment. This indicates that the dental community as a whole regards gingival curettage as a procedure with no clinical value. Curettage is also a major method used for removing osteoid osteoma and osteoblastoma. Curettage with subsequent culture is more accurate than ulcer base swan culture or aspiration and culture for diabetic foot ulcers. Curettage is also used when excising a chalazion of the eyelid.

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TOPIC OF THE DAY

Greenwood / Black Wall Street

Before the 1921 destruction of Tulsa’s Greenwood District, Black residents had created a remarkable center of business and community life. The district included stores, professional offices, entertainment venues and homes owned by Black citizens. Understanding Greenwood means learning what was built—not only what was burned.

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TRIVIA QUESTION OF THE DAY

Which Supreme Court case ruled state-sponsored public-school segregation unconstitutional?

Brown v. Board of Education in 1954.