Full transcript
0:01Hello everyone, welcome back to our
0:03biology 2401 lecture series. I am Dr. E.
0:07Today we explore chapter 6, bones and
0:09skeletal system.
0:11Bones are not just rigid support rods.
0:14They're living dynamic tissues that
0:16grow, remodel, store minerals, and even
0:19produce blood.
0:21We will explore how the skeleton
0:23protects vital organs, enables movement,
0:26and maintains homeostasis.
0:29By the end of this chapter, you will
0:31understand why bones are far more
0:33powerful and active than they appear.
0:36So, let's get started.
0:40Why does this matter?
0:43Bones and cartilage form the internal
0:46support of the body.
0:48So, understanding bone anatomy and the
0:51process of bone remodeling allows you to
0:54work effectively with patients with bone
0:57disease such as osteoporosis.
1:02We start with a brief overview of
1:04cartilage.
1:06The human skeleton initially consists of
1:08just cartilage, which is replaced by
1:11bone except in areas requiring
1:13flexibility.
1:15Skeletal cartilage
1:19is made up of highly resilient molded
1:21cartilage tissue
1:23that consists primarily of water.
1:26Cartilage contains no blood vessels or
1:28nerves.
1:30Surrounding the cartilage is the
1:32perichondrium.
1:36The perichondrium is a layer of dense
1:39connective tissue
1:41that helps cartilage resist outward
1:43expansion.
1:44It also contains blood vessels for
1:46nutrient delivery to the cartilage.
1:50Within the cartilage are cells. An
1:52example of such cells is chondrocytes.
1:55Chondrocytes are mature cells that are
1:57encased in small cavities called
1:59lacunae.
2:04Another cell type is chondroblast.
2:06Chondroblasts are immature cartilage
2:09cells that secrete the cartilage matrix.
2:14There are three types of cartilage in
2:16the body.
2:18Hyaline cartilage,
2:21elastic cartilage,
2:23and fibrocartilage.
2:25Hyaline cartilage provides support,
2:28flexibility, and resilience. It is the
2:31most abundant type and contains collagen
2:34fibers only.
2:36Elastic cartilage is similar to hyaline
2:39cartilage, but contains both collagen
2:42and elastic fibers.
2:45Fibrocartilage contains thick collagen
2:47fibers, which provides great tensile
2:49strength.
2:52This figure highlights different
2:55locations for the three types of
2:56cartilage.
2:58Hyaline cartilage includes cartilage in
3:00the nose, articular cartilage of joints,
3:04costal cartilages of ribs, thyroid
3:07cartilage, and trachea.
3:09Elastic cartilage is found in the
3:11external ear and the epiglottis.
3:15Fibrocartilage is found in the
3:16intervertebral disc, the pubic
3:19symphysis, and the meniscus of the knee
3:21joint.
3:25We begin our review of bones with
3:28functions. There are seven important
3:30functions of bones. Number one is
3:33support for the body and soft organs.
3:36Bones also provide protection of the
3:39brain, spinal cord, and vital organs.
3:42Bones act as anchorage and provide the
3:46levers for muscle action.
3:48They are important organs for mineral
3:51storage, for for calcium and phosphorus.
3:58Bones are the sites for blood cell
4:01formation or hematopoiesis. So, all the
4:04three types of blood cells, red blood
4:06cells, white blood cells, and platelets
4:08are made in the red bone marrow.
4:11Bones also store triglycerides,
4:14an important energy source.
4:17And finally, bones produce hormones. An
4:19example of hormone produced by bone is
4:22osteocalcin, that helps to regulate
4:25insulin secretion.
4:30Classification of bones. There are 206
4:33named bones in the human skeleton.
4:36The bones are divided into two groups
4:38based on location.
4:40The groups are axial skeleton and
4:43appendicular skeleton.
4:45Axial skeleton makes up the longitudinal
4:48axis of the body
4:50and includes the skull, the vertebral
4:53column or the backbone, and the rib
4:55cage.
4:57The appendicular skeleton includes bones
5:00of the upper and lower limbs
5:02and the girdles attaching limbs to axial
5:05skeleton.
5:06Examples include the clavicle or collar
5:09collar bone, the scapula or the shoulder
5:12blade.
5:16Bones are classified according to one of
5:18four shapes as long, short,
5:22flat, or irregular bones.
5:26Long bones are longer than they are
5:28wide. Examples [snorts] include the
5:31femur and the humerus.
5:35Short bones are cube-shaped. Examples
5:38include bones of the ankle and the
5:41wrist.
5:43A special type of short bones are
5:45sesamoid bones, which form within
5:48tendons and vary in size and number.
5:51An example of a sesamoid bone is the
5:53patella
5:54or the kneecap.
5:57Flat bones are thin, flat, and slightly
6:00curved. Example of a flat bone is the
6:02sternum.
6:04Other examples of flat bones include the
6:06cranial bones and the ribs.
6:10Irregular bones have complicated shapes.
6:12Examples are bones of the vertebral
6:15column or the backbone, as well as hip
6:17bones.
6:22Now, we zoom in on the structure of
6:25bone.
6:26Bones are organs because they contain
6:28different types of tissues.
6:31Bone or osseous tissue dominates.
6:35Bones also contain nervous tissue,
6:38cartilage, dense connective tissue,
6:41muscle cells, and epithelial cells in
6:44its blood vessels.
6:46There are three levels of structure in
6:49bones.
6:51Gross,
6:53microscopic,
6:55and chemical levels. We will review
6:57each.
7:02Bone can exist in two textures.
7:06Compact bone
7:08and spongy bone.
7:10Compact bone is the dense outer
7:14layer on every bone that appears smooth
7:17and solid.
7:21Spongy bone is made up of honeycombs of
7:24small,
7:26needle-like or flat pieces of bone
7:28called trabeculae.
7:31Open spaces between trabeculae are
7:33filled with red or yellow bone marrow.
7:38This figure highlights the key features
7:41of a typical flatbone.
7:44A flatbone consists of plates of spongy
7:47bone or diploë
7:49covered by
7:52compact bone.
7:55The compact bone is sandwiched by
7:57connective tissue membranes. There are
8:00two connective tissue membranes, the
8:02periosteum and endosteum.
8:05The periosteum covers the outside of the
8:08compact bone.
8:10While the endosteum covers the inside of
8:12the compact bone.
8:15Bone marrow is scattered throughout
8:17spongy bone
8:19with no defined marrow cavity.
8:23Hyaline cartilage covers areas of bone
8:25that is part of a movable joint.
8:30Now, let's review the structure of a
8:32long bone.
8:34All long bones have a shaft
8:37also called a diaphysis
8:40bone ends called epiphysis and
8:43membranes.
8:45The diaphysis is a tubular shaft that
8:48forms the long axis of the bone.
8:52It consists of compact bone
8:55surrounding a central medullary cavity
8:58that is filled with yellow bone marrow
9:00in adults.
9:03The epiphysis
9:05are the ends
9:06of long bones
9:08that consist of compact bone
9:11externally
9:13and spongy bone internally.
9:16On the epiphyseal end of long bones is
9:19articular cartilage
9:22which covers articular or joint
9:24surfaces.
9:27Between the epiphysis and the diaphysis
9:30is the epiphyseal line.
9:35This is a remnant of the epiphyseal
9:37plate from childhood
9:39>> [snorts]
9:39>> where growth of long bones occurs.
9:43Long bones have two membranes.
9:46The periosteum
9:48and the endosteum.
9:51The periosteum is a white double-layered
9:55membrane that covers external surfaces
9:58except at joints.
10:00It has two layers.
10:03An outer fibrous layer
10:05and an inner osteogenic layer.
10:09The fibrous layer contains dense
10:11irregular connective tissue
10:14consisting [snorts] of Sharpey's or
10:16perforating fibers that connect the
10:19periosteum to bone.
10:21The osteogenic layer contains primitive
10:24osteogenic stem cells that gives rise to
10:27almost all bone cells.
10:32The endosteum is a delicate connective
10:34tissue membrane covering internal bone
10:38surfaces.
10:39It covers trabeculae of spongy bone and
10:42lines canals that pass through compact
10:45bone.
10:46Like the periosteum, it contains
10:49osteogenic cells that can differentiate
10:52into other bone cells.
10:56As already mentioned, the red bone
10:59marrow is a site of hematopoiesis or
11:02blood cell formation.
11:04Red bone marrow is found within
11:06trabecular cavities of spongy bone and
11:09deploy of flat bones such as the
11:12sternum.
11:14In newborns, medullary cavities and all
11:18spongy bones contains red bone marrow.
11:21In adults, red bone marrow is located in
11:25the heads of femur and humerus.
11:28But most active areas of hematopoiesis
11:31are the flat bone deploy and some
11:32irregular bones such as the hip bone.
11:37Yellow bone marrow can convert to red
11:38bone marrow if a person becomes anemic.
11:43Our next topic of discussion is bone
11:46markings.
11:48Bone markings are sites of muscle,
11:51ligament, and tendon attachments on
11:53external surfaces.
11:56These are areas involved in joint
11:58formation or conduits for blood vessels
12:02and nerves.
12:06There are three categories of bone
12:08markings.
12:09Number one is projections.
12:12Projections are sites of muscle and
12:14ligament attachment.
12:17The second is surfaces.
12:20These are points where joints form.
12:23And finally, depressions and openings
12:28for blood vessels and nerves.
12:33This table highlights the main
12:34projections in bones. I'll mention just
12:37a few.
12:38The first is tuberosity.
12:40Large rounded projection which may be
12:43roughened. An example is ischial
12:46tuberosity in the hip bone.
12:49The second is crest.
12:52Crest A crest is a narrow ridge of bone
12:55which is usually prominent. An example
12:58is a iliac crest of the hip bone.
13:01Um trochanter.
13:05Trochanter is very large, blunt,
13:07irregularly shaped process.
13:10The only example we would find uh in the
13:13femur.
13:16I will skip here to spine.
13:20Spine is a sharp, slender, often pointed
13:23process or projection.
13:26An example is a spinous process of the
13:28vertebrae.
13:30And also we have process.
13:33A process is any bony prominence. An
13:36example of a process is a spinous
13:38process in the vertebrae.
13:42The first table here contains the main
13:45surfaces involved in joint formation.
13:48The head is a bony expansion carried on
13:51a narrow neck.
13:54A facet is a smooth nearly flat
13:56articular surface.
13:59And a condyle is a rounded articular
14:02projection.
14:03And [snorts] it often articulates with a
14:05corresponding fossa.
14:10The second table here highlights
14:12depressions and openings for passage of
14:15blood vessels and nerves.
14:18For example,
14:20a foramen is a round or oval opening
14:23through a bone.
14:26A notch is an indentation at the edge of
14:29a bone.
14:31A meatus is a canal-like passageway.
14:37A fossa
14:38is a shallow basin-like depression in a
14:41bone,
14:42often serving as an articular surface.
14:47Now, let's review the microscopic
14:50anatomy of bone.
14:52We start with cells in the bone.
14:54There are five major cell types in the
14:56bone,
14:57but we will review just four for this
15:00lecture.
15:01The first cell type is osteoprogenitor
15:04or osteogenic cell.
15:06The second is osteoblast, the third is
15:09osteocytes,
15:10and the [snorts] fourth is osteoclast.
15:15Osteoprogenitor cells are also called
15:18osteogenic cells.
15:20These are mitotically active stem
15:23in the periosteum and endosteum.
15:26When the cells are stimulated, they
15:28differentiate into osteoblast or bone
15:31lining cells.
15:33Some remain as osteogenic stem cells.
15:39Osteoblast are bone-forming cells that
15:42secrete unmineralized bone matrix called
15:45osteoid.
15:47Osteoid is made up of collagen and
15:49calcium-binding proteins.
15:52Collagen makes up 90% of bone protein.
15:56Osteoblasts are actively mitotic.
16:01Osteocytes are mature bone cells in
16:04lacunae that no longer divide.
16:07They maintain bone matrix and act as
16:10stress or strain sensors.
16:13They also respond to mechanical stimuli
16:16such as increased force on bone or
16:18weightlessness.
16:20Osteocytes communicate information to
16:23osteoblast and osteoclast so bone
16:26remodeling can occur.
16:30Osteoclast are derived from the same
16:33hematopoietic stem cells that become
16:36macrophages.
16:38They are giant multinucleated cells
16:40which function in bone resorption or
16:43breakdown of bone.
16:45When active, cells are located in
16:48depressions called resorption bays.
16:52The cells have ruffled borders that
16:54serve to increase surface area for
16:56enzyme degradation of bone.
16:58They also help seal off areas from
17:00surrounding matrix.
17:05Microscopic anatomy of compact bone.
17:09Compact bone is also called lamellar
17:11bone
17:12and consists of an osteon or Haversian
17:16system,
17:18Canals and canaliculi.
17:22Interstitial and circumferential
17:24lamellae.
17:28This cross-sectional view of the compact
17:30bone shows the basic structural unit.
17:34The osteon.
17:37In this electron micrograph of the
17:39osteon, you can clearly see the
17:41concentric lamellae and the central
17:43canal.
17:47An osteon is a structural unit of
17:50compact bone.
17:52It consists of an elongated cylinder
17:55that runs parallel to the long axis of
17:58bone.
18:00Osteons act as tiny weight-bearing
18:03pillars.
18:05An osteon cylinder consists of several
18:07rings of bone matrix called lamellae.
18:12Lamellae contain collagen
18:14that runs in different direction in
18:17adjacent rings.
18:19This helps to withstand stress and
18:21resist twisting.
18:23Bone salts are also found between
18:25collagen fibers.
18:30Each osteon has a central or Haversian
18:33canal
18:35which runs through the entire core of
18:37the osteon.
18:39Central canals contain blood vessels and
18:41nerve fibers.
18:43You will also find perforating or
18:45Volkmann's canals.
18:48These canals are lined with endosteum
18:50and occur at right angle to the central
18:52canal.
18:54Perforating canals connect blood vessels
18:56and nerves of periosteum, medullary
18:59cavity, and central canal.
19:02An osteon also has lacunae.
19:05Small cavities that contain osteocytes.
19:09Lacunae are connected to each other by
19:11hair-like canals called canaliculi.
19:15Canaliculi enable communication between
19:17all osteocytes of the osteon
19:20and permit nutrients and waste to be
19:22relayed from one cell to another.
19:26As already mentioned, osteons contain
19:28lamellae with collagen fibers.
19:32There are two main types of lamellae.
19:35Interstitial and circumferential
19:37lamellae.
19:39Interstitial lamellae are not part of
19:41the osteon.
19:43Some fill gaps between forming osteons.
19:47Others are remnants of osteons cut by
19:49bone remodeling.
19:52Circumferential lamellae are just deep
19:54to periosteum
19:56but superficial to endosteum.
19:59These layers of lamellae extend around
20:01entire surface of the diaphysis.
20:04They help long bones resist twisting.
20:10Microscopic anatomy of spongy bone.
20:13Spongy bone appears poorly organized
20:17but it is actually organized along lines
20:19of stress to help bone resist stress.
20:23Trabeculae, like cables on a suspension
20:26bridge confess strength to bone.
20:30There are no osteons present
20:32but trabeculae do contain irregularly
20:35arranged lamellae
20:37and osteocytes interconnected by
20:39canaliculi.
20:41Capillaries in endosteum supply
20:43nutrients.
20:47Our next topic is chemical composition
20:49of bones.
20:51Bone is made up of both organic and
20:54inorganic components.
20:57Organic components include osteogenic
21:00cells, osteoblasts, osteocytes
21:04bone lining cells
21:06osteoclast, and osteoid.
21:10Osteoid makes up about 1/3
21:13of organic bone matrix and is secreted
21:16by osteoblast.
21:19Osteoid consists of ground substance and
21:21collagen fibers, which contribute to
21:24high tensile strength and flexibility of
21:27bone.
21:29The inorganic components of bone include
21:34hydroxyapatite
21:36or mineral salts.
21:38Hydroxyapatite makes up approximately
21:4265% of bone by mass.
21:45It consists mainly of tiny calcium
21:47phosphate crystals
21:49in and around collagen fibers.
21:53Hydroxyapatite is responsible for the
21:56hardness and resistance of bone to
21:59compression.
22:03Next, we review bone development.
22:06Ossification or osteogenesis
22:09is the process of bone tissue formation.
22:13Formation of the skeleton
22:16begins around month two of embryonic
22:19development.
22:22After birth,
22:23bone growth occurs until early
22:25adulthood.
22:27And throughout uh growth and
22:29development,
22:30remodeling and repair take place, and
22:33these are typically lifelong processes.
22:38So, how does a bony skeleton form?
22:42Up to about 8 weeks of embryonic
22:44development, the skeleton consists only
22:47of fibrous membranes and hyaline
22:49cartilage.
22:50Bone tissue begins to develop at this
22:52time
22:53and eventually replaces most of the
22:55fibrous connective tissue and hyaline
22:57cartilage.
22:59Two mechanisms are involved. These are
23:02endochondral ossification
23:05and intramembranous ossification.
23:09In endochondral ossification,
23:12bone forms by replacing hyaline
23:14cartilage.
23:16The bones that are formed are called
23:18cartilage bones.
23:21And these bones form most of the
23:22skeleton.
23:24In intramembranous ossification,
23:27bones develop from fibrous membranes.
23:30Bones are called membrane bones.
23:36Endochondral ossification forms
23:38essentially all bones inferior to the
23:40skull except the clavicle.
23:44The process begins late in month two of
23:46development
23:48and uses previously formed hyaline
23:50cartilage models.
23:52Endochondral ossification requires
23:54breakdown of hyaline cartilage prior to
23:57ossification.
23:59It begins at a primary ossification
24:01center in the center of a shaft.
24:05Blood vessels infiltrate perichondrium
24:08and convert it to periosteum.
24:12Mesenchymal cells specialize into
24:14osteoblast.
24:18There are five main steps in the process
24:20of endochondral ossification.
24:22Around week nine, a bone collar
24:27forms around the diaphysis of the
24:30hyaline cartilage model.
24:33The model appears similar to the shape
24:35of a dumbbell.
24:37The primary ossification center
24:40is at the center of the model.
24:43The bone collar forms around the thinner
24:45middle portion.
24:49In stage two,
24:51cartilage calcifies in the center of the
24:54diaphysis and develops cavities.
24:58The area of deteriorating cartilage
25:00matrix grows along the length of the
25:03model.
25:07By month three, the periosteal bud
25:10invades the internal cavities and spongy
25:12bone forms.
25:14Spongy bone forms from the center
25:17along the length of the diaphysis.
25:20A blood vessel of the periosteal bud
25:23feeds the bud.
25:26Stage four occurs around birth.
25:30The diaphysis elongates and a medullary
25:33cavity forms.
25:35Secondary ossification centers appear in
25:38the epiphysis.
25:40The epiphysis have their own blood
25:42vessels called epiphyseal blood vessels.
25:46Stage five occurs from childhood to
25:49adolescence.
25:51The epiphysis ossifies.
25:54When ossification is complete, hyaline
25:57cartilage remains only in the epiphyseal
25:59plate
26:01and in articular cartilage.
26:07Intramembranous ossification begins
26:10within fibrous connective tissue
26:12membranes formed by mesenchymal stem
26:14cells.
26:16Intramembranous ossification forms
26:18frontal, parietal, occipital, temporal,
26:22and clavicular bones.
26:25Four major steps are involved in
26:26intramembranous ossification.
26:30In step one, ossification centers appear
26:33in the fibrous connective tissue
26:35membrane.
26:37Certain centrally located mesenchymal
26:39cells cluster and differentiate into
26:42osteoblasts
26:43forming an ossification center that
26:46produces the first trabeculae of spongy
26:48bone.
26:51In step two,
26:53osteoid is secreted within the fibrous
26:55membranes and calcifies.
26:59This process begins as osteoblasts start
27:02to secrete osteoid, which calcifies in a
27:04few days.
27:06Trapped osteoblasts become osteocytes.
27:11In step three, immature spongy bone and
27:14periosteum form.
27:16Accumulating osteoid is laid down
27:19between embryonic blood vessels in a
27:21manner that results in a network of
27:23trabeculae
27:24forming a honeycomb of immature spongy
27:26bone.
27:28Vascularized mesenchyme condenses on the
27:31external face of the bone and becomes
27:34the periosteum.
27:37In step four, compact bone replaces
27:40immature spongy bone
27:42just deep to the periosteum.
27:45Red marrow develops.
27:48Step four begins as trabeculae layers
27:50just deep to the periosteum thicken, are
27:52remodeled, and replaced with compact
27:54bone.
27:56Mature lamellar bone replaces them
27:58forming compact bone plates.
28:01The immature spongy bone in the center
28:03is remodeled into mature spongy bone
28:06that is eventually filled with red
28:08marrow.
28:10Spongy bone consisting of distinct
28:12trabeculae persists internally
28:15and its vascular tissue becomes red
28:18marrow.
28:20How do bones grow after birth?
28:25Long bones grow in length by
28:27interstitial
28:29or longitudinal growth of the epiphyseal
28:32plate.
28:36Bones grow in thickness
28:39by
28:41appositional growth.
28:45Bones stop growing during adolescence.
28:49However, there are some facial bones
28:52that continue to grow slowly throughout
28:55life.
28:58Growth of long bones occurs at the
29:01epiphyseal plate.
29:03Interstitial growth requires presence of
29:05epiphyseal cartilage in the epiphyseal
29:07plate.
29:09Epiphyseal plate maintains constant
29:11thickness. So, the rate of cartilage
29:13growth on one side is balanced by bone
29:16replacement on the other side.
29:19The epiphyseal plate consists of five
29:21zones.
29:22The resting zone,
29:24the proliferation or growth zone,
29:27the hypertrophic zone,
29:29calcification zone, and ossification
29:32zone.
29:36The resting zone is an area of cartilage
29:39on the epiphyseal side of the epiphyseal
29:42plate that is relatively inactive.
29:46The proliferation zone is an area of
29:49cartilage on the diaphysis side of the
29:51epiphyseal plate that is rapidly
29:53dividing.
29:55New cells formed move upwards, pushing
29:58epiphysis away from diaphysis, causing
30:01lengthening.
30:03The hypertrophic zone is an area with
30:07older chondrocytes closer to the
30:09diaphysis.
30:11Cartilage lacunae enlarge and erode,
30:14forming interconnecting spaces.
30:18The calcification zone is where
30:20surrounding cartilage matrix calcifies.
30:23Chondrocytes die and deteriorate.
30:29In the ossification zone, chondrocyte
30:32deterioration leaves long spicules of
30:34calcified cartilage at
30:36epiphysis-diaphysis junction.
30:39Spicules are then eroded by osteoclasts
30:43and are covered with new bone by
30:45osteoblasts.
30:47This zone is ultimately replaced by
30:49spongy bone.
30:51Medullary cavity enlarges as spicules
30:54are eroded.
30:57Towards the end of adolescence,
31:00chondrocytes divide less often.
31:04The epiphyseal plate thins, then is
31:06replaced by bone.
31:09Epiphyseal plate closure occurs when
31:12epiphysis and diaphysis fuse.
31:16At that point, bone lengthening ceases.
31:19In females, this occurs around the age
31:22of 18.
31:24In males, it occurs around the age of
31:2521.
31:30During growth, the epiphyseal plate
31:32maintains a constant thickness because
31:34the rate of cartilage growth on its
31:36epiphyseal facing side is balanced by
31:39its replacement with bony tissue on its
31:42diaphysis facing side.
31:44Longitudinal growth is accompanied by
31:46almost continuous remodeling of the
31:48epiphyseal end to maintain the
31:50proportions between the diaphysis and
31:53the epiphysis.
31:55Bone remodeling involves both new bone
31:58formation and bone resorption.
32:02Growth in width or thickness.
32:05Growth in thickness occurs through
32:08appositional growth.
32:12This can occur throughout life.
32:15Bones thicken in response to increased
32:18stress from
32:20muscle activity or added weight.
32:25Osteoblasts
32:26secrete the bone matrix
32:29while osteoclasts resorb or break down
32:33the bone.
32:35Usually, there is more bone build up by
32:38osteoblast than they are broken down by
32:40osteoclast,
32:42which leads to thicker, stronger bones
32:45that are not too heavy.
32:48Which hormones regulate bone growth?
32:52Number one is growth hormone.
32:57Growth hormone is the most important
33:00hormone in stimulating epiphyseal plate
33:02activity in infancy and childhood.
33:06Deficiency in growth hormone secretion
33:09in infancy causes dwarfism.
33:13The second is thyroid hormone.
33:17Thyroid hormone modulates activity of
33:20growth hormone
33:21ensuring proper proportions.
33:25Next is testosterone in males and
33:29estrogens in females at puberty.
33:33These hormones promote adolescent growth
33:36spurts.
33:37They also end growth by inducing
33:40epiphyseal plate closure.
33:43As you would imagine, excess or deficits
33:46of any of these hormones causes abnormal
33:49skeletal growth.
33:54Bone remodeling.
33:56Bone remodeling replaces approximately 5
34:00to 10% of bone every year.
34:03Spongy bone is replaced approximately
34:05every 3 to 4 years.
34:08While compact bone is replaced
34:10approximately every 10 years.
34:13Remodeling consists of both bone deposit
34:17and bone resorption.
34:22And occurs at surfaces of both the
34:24endosteum and the periosteum.
34:27Remodeling involves coordination between
34:30osteoblast, which make bone,
34:34and osteoclast, which break down bone.
34:40Bone resorption.
34:43Resorption is a function of osteoclast.
34:49Osteoclast dig depressions or grooves as
34:53they break down matrix.
34:56They also secrete lysosomal enzymes
35:00and protons or hydrogen ions
35:03that digest the matrix. Release of
35:05protons increases acidity.
35:08Acidity converts calcium salts to
35:11soluble forms.
35:14Osteoclast also phagocytize
35:17demineralized matrix and dead
35:20osteocytes.
35:23Digested products are transcytosed
35:26across the cell
35:28and released into the interstitial fluid
35:30and then into blood.
35:34Once resorption is complete, osteoclast
35:37undergo apoptosis.
35:41Osteoclast activation involves
35:43parathyroid hormone
35:45and immune T cell proteins.
35:51Bone deposition.
35:54New bone is deposited by osteoblast.
36:00Bone deposition begins as an osteoid
36:03seam,
36:05which is a band of unmineralized bone
36:07matrix that marks an area of new matrix.
36:13Between the osteoid seam and older
36:15mineralized bone is an abrupt transition
36:18zone called a calcification front.
36:25So, how does osteoid calcify?
36:28The triggers for deposit are not
36:30confirmed, but may include the
36:32following.
36:33One is mechanical signals.
36:37Number two, increased concentrations of
36:40calcium and phosphate ions
36:43for hydroxyapatite formation.
36:46Number three,
36:47matrix proteins that bind and
36:49concentrate calcium.
36:51And finally,
36:53appropriate amounts of the enzyme
36:55alkaline phosphatase for mineralization.
37:01How is bone remodeling regulated?
37:05Remodeling occurs continuously in the
37:07skeleton,
37:08but is regulated by two control loops
37:11that serve different purposes.
37:13The first is to maintain calcium
37:16homeostasis.
37:18This is achieved by hormonal regulation,
37:22principally parathyroid hormone.
37:28And the second reason is to keep the
37:30bone strong.
37:32So, mechanical and gravitational forces
37:35acting on bone drive remodeling to keep
37:38bone strong.
37:42Hormonal controls.
37:44Maintaining extracellular fluid calcium
37:46levels within homeostatic levels is
37:48critical for maintaining the resting
37:50membrane potential of cells.
37:53Calcium is required for nerves to fire
37:56and for muscles to contract.
37:58Approximately 99% of all the body's
38:01calcium is in the bones.
38:04Hormones maintain blood calcium within
38:07narrow limits.
38:09Two hormones are involved in calcium
38:11homeostasis.
38:13These include parathyroid hormone or PTH
38:17and calcitonin.
38:20Parathyroid hormone is produced by
38:22parathyroid gland in response to low
38:25calcium levels.
38:27It stimulates osteoclast to resorb bone.
38:31Calcium is released into blood, raising
38:33the levels of blood calcium.
38:37Calcitonin is produced by parafollicular
38:39cells of the thyroid gland
38:42in response to high levels of blood
38:43calcium.
38:47Parathyroid hormone or PTH is the most
38:50important hormone in controlling blood
38:52calcium levels.
38:54When blood calcium levels fall below
38:56normal,
38:57parathyroid gland is stimulated to
38:59release PTH, thereby raising the blood
39:01levels of PTH.
39:03PTH activates osteoclast to break down
39:06bone matrix
39:08and release calcium ions into blood
39:10until homeostasis is achieved.
39:14The second set of controls regulating
39:16bone remodeling is response to
39:18mechanical stress.
39:21Bones reflect stresses they encounter.
39:24Bones are stressed when weight bears on
39:27them or muscles pull on them.
39:31Wolff's law states that bones grow or
39:33remodel in response to demand placed on
39:35them.
39:37Stress is usually off-center, so bones
39:39tend to bend.
39:42Bending compresses one side and
39:44stretches the other side.
39:47Diaphysis is thickest where bending
39:50stresses are greatest.
39:52Bones can be hollowed because
39:54compression and tension cancel each
39:56other out in the center of the bone.
40:01This figure highlights the response of
40:03the femur to bending stress.
40:05A load on the head of the femur
40:07threatens to bend the bone along an arc
40:10that curves along the center of the head
40:12down through the diaphysis and back out
40:15under the head.
40:16Compression occurs below the head and
40:19tension occurs on the opposite side of
40:21the bone.
40:22The point of no stress is where the
40:24tension and compression on opposite
40:26sides cancel each other.
40:28In this case, at the distal point of the
40:30diaphysis.
40:32As a result, much less bone material is
40:36needed internally than superficially.
40:40Wolff's law also explains several other
40:43observations.
40:45For example, right or left-handedness
40:48results in thicker and stronger bones of
40:50the corresponding upper limbs.
40:54Curved bones are thickest where they are
40:57most likely to buckle.
41:01The trabeculae of spongy bone forms
41:04trusses or struts
41:06along lines of stress.
41:09Finally, large bony projections occur
41:12where heavy active muscles attach.
41:19Bone repair.
41:21Despite their remarkable strength, bones
41:24are susceptible
41:26to fractures or breaks.
41:30During youth, most fractures result from
41:32trauma
41:34that twist or smashes the bone.
41:37For example, sports injuries,
41:40automobile accidents, and falls.
41:44In old age, most fractures result from
41:47thinner and weaker bones.
41:53Fractures are the most common disorders
41:55of bone homeostasis.
41:58When we break bones, they undergo a
42:00remarkable process of self-repair.
42:05Three criteria can be used to classify
42:08fractures.
42:10The first is position of bone ends after
42:13fracture.
42:15In non-displaced
42:17fractures, bone ends retain normal
42:20position.
42:23In displaced fractures, the bone ends
42:26are out of normal alignment.
42:29The second criterion is completeness of
42:33break.
42:35If the bone is broken through, the
42:37fracture is a complete fracture.
42:41If not, it is described as an incomplete
42:45fracture.
42:49The third criterion is whether skin is
42:52penetrated or not.
42:55In open or compound fractures, the skin
43:00is penetrated.
43:03While in closed or simple fractures,
43:07the skin is not penetrated.
43:10In addition to these three
43:12classifications, all fractures can be
43:14described in terms of location of
43:17fracture, its external appearance, and
43:20or the nature of the break.
43:24This table summarizes the most common
43:26types of fractures.
43:28The first is comminuted.
43:31In this type of fracture,
43:33bones fragment into three or more
43:36pieces.
43:37It is particularly common in older
43:39adults, whose bones are more brittle.
43:44The second is compression.
43:47In compression, bones are crushed.
43:51This is common in porous bones, for
43:54example, in osteoporosis,
43:56where the bone is subject to extreme
43:58traumas, as in a fall.
44:02The next is spiral.
44:05In spiral fractures, a racked break
44:08occurs when excessive twisting forces
44:11are applied
44:12to a bone.
44:14This is very common in sports.
44:19The next is epiphyseal.
44:23In epiphyseal fractures, the epiphysis
44:26separates from the diaphysis along the
44:28epiphyseal plate.
44:31This type of fracture tends to occur
44:32where cartilage cells are dying and
44:35calcification of matrix is occurring.
44:41The next type of fracture is depressed.
44:45In depressed fractures, the broken bone
44:48portion is pressed inwards.
44:50This is very common in skull fractures.
44:54And finally, we have greenstick
44:56fractures.
44:58In greenstick fractures, the bone breaks
45:01incompletely.
45:02So, only one side of the shaft breaks
45:06while the other side bends.
45:09And this is common in children whose
45:11bones have relatively more organic
45:14matrix and are more flexible than those
45:16of adults.
45:19How are fractures treated?
45:22Treatment of fractures begins with
45:24reduction,
45:26the realignment of broken bone ends.
45:30In closed reduction,
45:33the physician manipulates the bone to
45:36the correct position.
45:38In open reduction,
45:41the bone ends are secured together
45:43surgically with screws and plates.
45:46After the broken bones are reduced,
45:49they are immobilized
45:54either by cast or traction to allow
45:57healing.
45:59The time needed for repair depends on
46:01the severity the break,
46:03the broken bone, and the age of the
46:05patient.
46:07For example,
46:08a simple fracture of a small or
46:10medium-sized bone in young adults heals
46:14in 6 to 8 weeks.
46:17Repair of a simple fracture involves
46:19four stages.
46:21The first step is hematoma forms,
46:24followed by formation of
46:24fibrocartilaginous
46:26callus,
46:28formation of bony callus, and bone
46:30remodeling.
46:33The first step is hematoma formation.
46:37When a bone breaks, blood vessels in the
46:39bone and periosteum are torn.
46:42The hemorrhage blood clots, forming a
46:45hematoma at the fracture site.
46:48Soon, blood cells deprived of nutrients
46:51die,
46:52and the tissue at the site becomes
46:54swollen, painful, and inflamed.
46:58The second step is fibrocartilaginous
47:01callus formation.
47:03Within a few days, capillaries begin to
47:05grow into the hematoma.
47:08Phagocytic cells clear debris, while
47:10fibroblasts secrete collagen fibers to
47:13span break and connect broken ends.
47:16Fibroblasts, cartilage, and osteogenic
47:19cells begin reconstruction of bone.
47:22They also create cartilage matrix of
47:24repair tissue.
47:27Osteoblasts form spongy bone within
47:29matrix.
47:31The mass of repair tissue is called
47:33fibrocartilaginous callus.
47:37Step three is bony callus formation.
47:42Within 1 week, new trabeculae appear in
47:45fibrocartilaginous callus.
47:47The callus is converted to bony or hard
47:50callus of spongy bone.
47:52Bony callus formation continues for
47:54about 2 months until firm union forms.
48:00In the final step, bone remodeling
48:03occurs and the fracture is healed.
48:07This begins during bony callus formation
48:09and continues for several months.
48:12The repaired area resembles the original
48:14unbroken bony region
48:16because it responds to the same set of
48:18mechanical stresses.
48:22Bone disorders.
48:25Imbalances between bone deposit and bone
48:29resorption
48:31underlie nearly every disease that
48:33affects the human skeleton.
48:36There are three major bone disorders we
48:38will discuss today.
48:41Osteomalacia
48:42and rickets,
48:44osteoporosis,
48:46and Paget's disease.
48:50In osteomalacia,
48:52bone is poorly mineralized.
48:55Osteoid is produced, but calcium salts
48:58are not adequately deposited,
49:00resulting in soft and weak bones.
49:03The main symptom in osteomalacia is pain
49:07when bones are bearing weight.
49:10Rickets is osteomalacia of children.
49:14Because young people are still growing,
49:17rickets is more severe than adult
49:20osteomalacia.
49:22Bowed legs and deformities of pelvis,
49:25skull, and rib cage are common.
49:28Osteomalacia and rickets are caused by
49:31insufficient calcium in the diet
49:33or by vitamin D deficiency.
49:37Increasing vitamin D intake and exposure
49:39to sunlight usually cures these
49:41disorders.
49:45The next disease is osteoporosis.
49:48Osteoporosis is a group of diseases in
49:51which bone resorption exceeds bone
49:53deposit.
49:55The matrix remains normal,
49:57but bone mass declines, and the bone
50:00becomes more porous and light.
50:03The bones become so fragile that they
50:05can break from something as simple as
50:07stepping off a curb.
50:11What are the risk factors for
50:13osteoporosis?
50:15Osteoporosis affects most often aged
50:18postmenopausal females.
50:21So, [snorts] it affects approximately
50:2230% of females aged 60 to 70 years old,
50:27and 70% by age of 80.
50:31Estrogen plays a role in bone density.
50:35So, when levels drop at menopause,
50:38females run higher risk of osteoporosis.
50:43Males are less prone due to protection
50:46by the effect of testosterone.
50:51Other risk factors for osteoporosis
50:53include
50:54insufficient exercise to stress bones,
50:58diet that's poor in calcium and
51:00proteins,
51:01smoking,
51:04genetics, osteoporosis runs in families.
51:07Also, there are hormone-related
51:09conditions. For example,
51:11hyperthyroidism
51:13and diabetes mellitus.
51:16And finally,
51:18consumption of alcohol or certain
51:21medications.
51:25How is osteoporosis treated?
51:28Osteoporosis can be prevented or at
51:31least delayed by minimizing the risk
51:33factors already discussed, especially
51:36the ones that can be controlled.
51:38Traditional treatments include
51:41ensuring adequate amounts of calcium
51:44and vitamin D in the diet.
51:48Osteoporosis is also treated with
51:50weight-bearing exercises.
51:54Other treatment
51:55focuses on hormone replacement therapy.
51:59This type of treatment slows down
52:02but does not reverse bone loss.
52:07Paget's disease In Paget's disease,
52:10there is excessive and haphazard bone
52:12deposit and resorption
52:15causing bone to grow fast and develop
52:17poorly.
52:19There is a high ratio of spongy to
52:21compact bone and reduced mineralization.
52:25It usually occurs in the spine, pelvis,
52:28femur, and skull
52:30and rarely occurs before age 40.
52:34It affects approximately 1% of the North
52:36American population aged 40 and above.
52:42The cause is unknown but possibly
52:44thought to be due to viral infection.
52:48Drug therapies against Paget's disease
52:50include bisphosphonates
52:53and high doses of calcitonin to prevent
52:56bone breakdown.
53:00Developmental aspects of bone
53:03Embryonic skeleton ossifies predictably.
53:07So, fetal age is easily determined from
53:09x-rays or sonograms.
53:11Most long bones begin ossifying by 8
53:14weeks
53:15with primary ossification centers
53:18developed by week 12.
53:22At birth, most long bones are fully
53:25ossified
53:26except at the epiphysis.
53:29The epiphyseal plate persists throughout
53:31childhood and adolescence.
53:33At approximately age 25 all bones are
53:37completely ossified and skeletal growth
53:40ceases.
53:43In children and adolescents,
53:46bone formation exceeds resorption.
53:50Males tend to have greater bone mass
53:53than females.
53:56In young adults, bone formation and
53:59resorption are balanced.
54:03In adults, bone resorption exceeds bone
54:06formation.
54:09Bone mass,
54:11mineralization,
54:13and healing ability decrease with age
54:16beginning in the fourth decade of life.
54:21That brings us to the end of chapter 6.
54:24Thanks for sticking around. Please stay
54:26tuned for chapter 7 coming out soon. Bye
54:29for now.