- Types of cementum
- Periodontal ligament
- Fiber groups
- Alveolar bone
- Clinical considerations
The includes cementum, , alveolar bone and gingival tissues. The gingiva contain a ← which develops from the of the ←. Underlying connective tissue layers develop from (as does most of the skull). The of these tissues contains ← and fibers. Cementum, PDL and alveolar bone develop from the of the . These three tissues share extracellular components, thanks to their shared , making for a strong connection between them. Like mesoderm-derived connective tissues, these tissues have a lot of collagen, but instead of elastic fibers, these tissues produce a special protein fiber type called fibers. Oxytalan fibers are found in a few other places in the human body, such as the aorta, whose lining is also derived from ←. ← plays an important role in the induction of these tissues, even if it is mostly fated to undergo ←.
Cementum forms a thin layer on the roots of teeth, attaching the teeth to the alveolar bone by way of the . The mineral content of cementum is lower than that of dentin, but not enough to make it appear different from dentin on a radiograph. The surface of cementum will feel grainier than enamel when probed with instruments.
After crown formation is nearly complete, ← grows apically, separating the from the . The of HERS the ← of , which begin ←. Without , the IEE cannot be induced to form . Instead, the IEE and secrete ← onto the surface of dentin, including members of the and families, but after that, these cells mostly undergo ←. Some of the epithelial cells of HERS may undergo an ← and differentiate into . With HERS out of the way, ← made by root odontoblasts contacts of the dental sac. Contact with pre-dentin and morphogens secreted from the dental papilla induces the neuro-mesenchymal stem cells of the dental sac to become cementoblasts. These cells, like odontoblasts, align next to one another, behaving more like a tissue derived from (an epithelium) than a connective tissue.
is the process of forming cementum. The word cementogenesis follows the pattern of and . Cementoblasts secrete the protein components of cementum. This immature matrix may be referred to as cementoid, which breaks from the pattern we used for and , or it may be referred to as . Layers of pre-cementum are laid down , and soon mineralize, at which time it is called cementum. Some cementoblasts become trapped in cementum, after which they are referred to as . Other cementoblasts remain near the surface of the cementum. These cells continue to lay down layers of pre-cementum throughout life, and can become more active during times of injury and repair to cementum. Because of the shared lineage between cementoblasts and , and the similarity of their , the is less distinct than the . In fact, the CDJ was once considered to be imaginary (
The major protein in cementum is ←. Collagen fibers extend out of cementum into of root dentin, and in the other direction become the collagen fibers of the . Collagen fibers of the PDL, in turn, become ← embedded in alveolar bone. Rather than thinking about alveolar bone, PDL, cementum and dentin as distinct tissues bonded to each other, think of their borders as a gradient, thanks to their shared . This makes for a stronger connection than could be produced by bonding 4 separate tissues, especially ones that are too thin for large ← and -like digitations. Other proteins secreted by cementoblasts include two (bone sialoprotein and osteopontin) which help collagen adhere to crystals. Cementoblasts also secrete enzymes that catalyze the formation of crystals, similar to those active in ←.
Types of cementum by area of the root
For most teeth, the apical one third of the root contains over . More cevical regions contain only acellular cementum. About 52% of the time, cementum completely covers root dentin, all the way up to the enamel. Roughly 33% of the time there is a gap between the cementum and enamel, with underlying dentin exposed. The rest of the time, roughly 15%, cementum extends over the enamel a short distance. These percentages are not for individual teeth, but for any area of the cervical region on a single tooth. Therefore, a single tooth may have all three patterns. The gap pattern is the most significant because of the increased risk of ←. Cementum found overlapping enamel contains no ← fibers, and does not connect to the .
The , like other ligaments, is a ←, composed primarily of ← fibers in the , plus the special fibers. These fibers are made by that differentiate from of the . In figure 11.6, fibroblast nuclei stain purple. From this image, you should be able to determine which side of the PDL is anchored to bone tissue versus anchored to cementum. Look at either border, are there cells within or not? The pink color is mostly collagen in all 3 of these tissues.
Like other ligaments, the contains and (mostly at the border with alveolar bone), but unlike other ligaments, the PDL also contains and a unique population of ←. The stem cells are different from , and may be referred to as Periodontal Ligament Stem Cells (PDLSCs). These stem cells can differentiate into , osteoblasts, , cementoblasts, or given the correct ←. This allows the PDL to play a role in the and repair of bone, cementum and dentin. Whether these stem cells are different from the found in the and is unclear. Their unique properties, however, make them useful:
stem cells from extracted teeth can be used to promote the healing of many other (non-tooth) tissues.
Unlike cementum and dentin, the is . The PDL is significantly more vascular than other ligaments, thanks to its . PDL secrete ← inlcuding
Vascular Endothelial growth Factor (VEGF) to promote . The of the VEGF is controlled by morphogens of the and families. BMPs the of and , while FGF induces fibroblast differentiation. Both morphogen signals are necessary to specify PDL fibroblast differentiation. What also makes PDL fibroblasts different from other fibroblasts is that they have a lineage. They have a higher capacity to undergo renewal (new ones forming from PDL ←) and trigger tissue repair than fibroblasts in other ligaments. In other ligaments, fibroblasts develop from , and are induced to differentiate from mesenchymal stem cells by FGF alone.
Oddly, the tissues that can best be repaired by cells from the PDL are bone and cementum, not the PDL itself. Keep this in mind as we discuss differentiation of the PDL. The first important concept is PDL fibroblasts are not like other fibroblasts. In addition to VEGF, PDL fibroblasts shared by other cells with a . For instance, PDL fibroblasts share features with , expressing RUNX2 and proteins. PDL fibroblasts also have similarities to neural tissue, expressing Neuronal (NCAMs)← and N-cadherin (a neuronal ← protein) (
scientific review article). These genetic details are less important to us, what is important is the PDL from neuro-mesenchyme.
One more unique feature of PDL fibroblasts is their ability to participate in an immune response. Unlike other ligaments, the PDL is often exposed to bacteria and bacterial toxins. In response to certain inflammatory signals, PDL fibroblasts down-regulate of involved in bone and behave more like white blood cells (
scientific article for further reading). This is not entirely unexpected given their . guide the of the thymus from the 3rd (The thymus is where
T cell lymphocytes develop).
of the begins during ←. PDL secrete ← fibers that become embedded in cementum and extend outwards (). This process begins at the and continues as the root grows. The other ends of collagen fibers are embedded within alveolar bone later, activated by tooth occlusion. By waiting to anchor one end of the fibers until tooth occlusion results in greater mobility of tooth roots during ←. PDL collagen fiber bundles run in different directions, which can be classified as alveolar crest, horizontal, oblique, (peri) apical, inter-radicular (on multirooted teeth) and trans-septal. are also collagen fiber bundles, but anchor cementum to the gingiva. These are also categorized based on their
location and fiber orientation. Depositing collagen in the correct orientation requires ← of the ← class. One example is a cell-surface membrane protein called
CD44 which binds to ←, collagen and ←. Similar morphogens are involved in the polarization of following their induction by the . Changes to polarity morphogens are likely necessary for re-orientation of fibroblasts during tooth occlusion and the production of collagen bundles in different directions.
Remnants of ← may linger after root formation is finished. These cells, the , may be involved in repair of cementum and the (the evidence is not definitive at this time). While these cells are epithelial, derived from , they may undergo an ← and then ← into or , if they receive the correct ←. Evidence for this comes primarily from studying transgenic mice, which must be intentionally injured and sacrificed (killed) before repair to tooth tissues can be measured. Obviously, this cannot be repeated in humans to determine whether we share this .
The vault of the skull by (including the maxilla). Thus, skull sutures contain dense connective tissue (unless they fully ossify). The base of the skull, on the other hand, develops by ←. The development of the mandible is even more complicated. First, forms two bands of cartilage (). The posterior portion is fated to become the ramus of the mandible (plus the malleus and incus bones), while the anterior portion disappears. Before the anterior portion disappears, the body of the mandible forms around it by intra-membranous ossification. Later, the condylar process, coronoid process and mandibular symphysis develop by . That is how the skull forms. What is forms from does not match as nicely. Most bones develop from , including the entire appendicular skeleton, plus most of the axial skeleton. The exceptions are the facial bones (including the hyoid) and inferior parts of the cranium, which develop from neuro-mesenchyme (the “new head”). In developmental biology classes, this is not a minor issue: ancient fish (either long extinct, or modern-day lampreys) have no lower jaw, they have seven branchial arches (←). Jawed vertebrates (gnathostomes), including you and bony fish, some arches into other structures, including a powerful mandible and ear parts. If you are curious, the lower jaw of a shark (and even the sturgeon) is not a mandible, it is Meckel’s cartilage (so sharks are a closer family member of yours than a lamprey, but more distant relative than a goldfish).
This brings us to alveolar bone (finally!). The alveolar ridge of both the mandible and maxilla from of the . in this area are to into by ← (including members of the family). This in turn activates such as members of the RUNX family and MSX ← family. These transcirption factors up-regulate of bone-specific proteins. From a development standpoint, it is important to understand that the basal bone of the mandible and maxilla are induced by signals from Meckel’s cartilage, while alveolar bone develops from the .
Alveolar bone contains numerous small , through which fiber bundles insert into bone tissue. This is the same name used for the perforating canals that run perpendicular to Haversian canals in compact bone, only those Volkman’s canals contain blood vessels. Like all bones, the outer portion of alveolar bone is compact bone and below that is spongy bone. The compact bone portion is referred to as the on a radiograph, as it shows up more radiopaque than the spongy bone deep to it (or the superficial to it). The is a triangular-shaped area between two teeth, which should be of uniform height between all teeth. The is the bone tissue between roots
The , including most of the gingiva, develop from and during embryonic development. Ectoderm forms the , while mesoderm forms the and . The exception is ←, which develops from a group of cells more specialized than ectoderm. During , ectodermal cells of the separate from oral ectoderm. During ←, it is the that develops into junctional epithelium.
Because are located at the surface of adult cementum (within the ), cementum has the ability to undergo and repair. This makes cementum similar to dentin but different from enamel. Excessive cementoblast function can result in . This occurs more frequently at the root apex due to excessive occlusal forces on a tooth. It may also be caused by ← disturbances, such as gigantism/acromegaly or
Enough can adhere two teeth together by the roots, which is called . This should illustrate one reason why a radiograph is necessary prior to tooth extraction. This most commonly occurs between the second and third upper molar.
is worrisome in part because it exposes the roots of teeth to the environment that only enamel is exposed to under healthy conditions. Because of its lower mineral content, spread quickly. can be passed quickly to dentin, and if untreated, pulp. Dental pain may not arise until infection of the pulp sets in. If that happens, treatment is generally limited to tooth extraction, rather than prevention and maintenance. Cemental caries can be detected early with radiographs or use of a dental mirror and explorer.
Both dentin and cementum have the capability to be repaired in response to mild or moderate trauma. This is because living are located in the outer layer of the pulp, and in the . If necessary, in the pulp or PDL may be induced to ← and lay down more . However, reparative cementum does not contain and does not contribute to tooth attachment to bone tissue.
Severe trauma, on the other hand, can induce the ← of into or , leading to the loss of cementum and dentin. It is possible that the precursor to cementoclasts and/or odontocalst may not be your average mesenchymal stem cell, but a related ← with a different . Possible candidates include and stem cells.
Loss of dentin and cementum from the roots of teeth is root resorption. Loss of dentin from deep layers is . As dentin is lost, the space is filled in by vascular pulp tissue, possibly causing the tooth to have a more pinkish coloration. This tooth may be referred to as a pink tooth of Mummery (named for the anatomist who first described the condition, it has nothing to do with a pantomime). If internal root resorption is caused by chronic inflammation, removal of inflamed pulp by ← may halt the condition.
is the loss of cementum and dentin from the superficial side of the root. External root resorption may be transient and resolve on its own, owing to the regenerative capability of cementum thanks to the in the . Chronic inflammation or tooth may trigger more severe resorption, and replace lost tooth tissues with bone tissue.
For those into crime shows, corpses that have suffered a traumatic death (e.g. asphyxiation) or have spent time in a humid environment before being discovered may have pink teeth. This is due to ruptured pulp blood vessels causing bleeding into dentinal tubules (
pdf download— warning: contains photos of a dead body).
Masses of may develop in abnormal locations, especially later in life. These are referred to as . Cementicles may be free (within the but unattached to the tooth), attached (on the surface of the layer of cementum) or embedded (once attached, but now surrounded by the cemental layer of the root). It is thought cementicles develop when encounter debris such as a blood clot (thrombus) lodged in a nearby capillary. This disrupts of cementum and instead creates a nucleus around which a cementicle forms.
Tooth discomfort following endodontic therapy
After ←, the pulp—including nerve endings– is replaced with a non-living polymer. Nevertheless, tooth discomfort may occur. This is because the is present and living. Besides functioning to attach the tooth roots to bone and gingival tissue, the PDL is involved in proprioception (kinesthesia), or the sensation of where the body is located. Nerve endings in the PDL relay information to the
somatosensory cortex about where the teeth are located and when they experience occlusal forces. This is very important in reducing or avoiding occlusal forces during mastication and speech. The jaws exert the greatest amount of force the human body can generate, but also exhibit great control. It is routine for people to bite down through substances of varying density and thickness without teeth hitting one another thanks to a large region of somatosensory cortex interpreting information from the teeth.
(or physiological drift) is the tendency of teeth mesial to the first molar to migrate in a mesial direction with age. The molars, on the other hand, tend to drift distally. It is a natural phenomenon caused by the assymetrical of alveolar bone tissue. There are two major concepts you should understand relevant to mesial drift. One, alveolar bone undergoes more bone remodeling than any other bone tissue. Two, this remodeling responds to occlusal forces: removing force causes bone loss to accelerate, adding force causes bone deposition to accelerate. When occlusal forces are assymetrical on a tooth, it leads to one side of the alveolar socket undergoing bone depostion and the other side bone resorption. Assymetrical remodeling, in turn, causes tooth movement (see Fig. 11.29 for a similar phenomenon). With age, teeth tend to wear down at their contact points, which leads to gaps between teeth, and a reduction in force on the gap side. Mesial drift causes teeth to move closer together, closing gaps as they form from wear. Too much movement can lead to crowding. Missing teeth can accelerate drift, causing neighboring teeth to bend inwards, changing the bite plane. This, in turn, can lead to abnormal forces on the temporo-mandibular joint, causing pain, discomfort and reduced range of motion.
Loss of alveolar bone
The loss of alveolar bone leads to an uneven level of the or . The consequence of this is reduced connection between tooth and bone, which can lead to tooth mobility and loss. This is often first observed in reduced opacity of the alveolar crest region(s) on a radiograph (Fig. 11.21). Under healthy conditions, alveolar bone—especially spongy bone—undergoes contant replacement by the ←. Chronic inflammation, such as result of , inhibits the rate of function without reducing the rate of function. This is likely due to the fact osteoclasts are related to white blood cells, their is from the bone marrow. White blood cells are more active during inflammation, unlike most other cells in the body.
Fenestration and dehiscence
With significant alveolar bone loss, portions of tooth roots may become exposed. A small window of root may become exposed, known as a (the Latin word for window). If the exposed root area connects all the way to the , the region is known as a (a general term for a wound that cannot close). This is distinct from or ←, where ← migrates to a region more apical on the root of the tooth, exposing cementum. A fenestration or dehiscence may still be covered by , but a lack of means oral bacteria may come into contact with cementum and bone tissue, neither of which is designed to resist infection the way partially epithelia are. This occurs much more frequently on the facial side than the lingual side.
There are many techniques that aim to stimulate the body to repair bone loss, including alveolar bone, by filling in the damaged area with a ←. The proper scaffolding material allows to migrate through the damaged area and into . Surgeries involving this method are referred to as Guided Bone Regeneration or (GTR). The major difference between these procedures and a ← is the use of a membrane to prevent neighboring tissue from growing into the damaged area.
First, a membrane must be placed over the injured area. Old-fashioned membranes, such as cotton gauze bandages, form a barrier between pathogens and exposed tissue. Membranes can also keep other tissues, such as epithelia or , from filling up the lost region with the wrong type of tissue. Cotton, however, does not contain molecules that bind to human or , and therefore does not act as a scaffold. Without a scaffold, healing of the injury occurs from the edges of the wound. Newer materials can be made of molecules that are recognized and used as a scaffold over which cells migrate. These membranes allow for healing to occur across the entire injured area, rather than just the edges. These membranes may be organic (Carbon-containing molecules similar to ←) or inexpensive inorganic polymers. Furthermore, these membranes may be gelatinous and molded into the injured area, or more like plastic and 3-D printed to fit the injured area. membranes add ← that promote the ← of mesenchymal stem cells into osteoblasts, rather than (which produce scar tissue). Similarly, morphogens (such as
VEGF) may be included to promote , speeding up the healing process. Antimicrobial agents may also be embedded within the polymer.
One consideration when choosing a membrane is whether it is resorbable, or whether it will need to be removed (requiring another surgery). Both organic and synthetic polymers may be capable of being resorbed, or not. For instance, cotton is organic, but is not resorbed readily by the human body. Poly-lactic acid (PLA) membranes (which are also organic, but synthesized in a laboratory) are readily absorbed during the healing process and get replaced by human tissues. Resorption of large molecules may occur without the activity of human cells. For example, PLA slowly degrades when exposed to heat and UV light. Other polymers might be removed by human enzymes, such as . Guided tissue regeneration is conceptually very different from replacing damaged tissues with a but inert material, such as latex in ←, or a filling made of metal, porcelain or plastic. The goal is not to fill in a gap, but to promote the healing of a gap.
Resorption of the alveolar ridge
Following tooth extraction or loss, regions of the alveolar ridge no longer anchored to and tooth roots undergo resorption (basal bone is unaffected). This occurs because all bone tissue undergoes ←, and a lack of tension slows down the activity of osteoblasts, but not . The opposite is why exercise maintains healthy bones. Chewing exercises the alveolar ridge.
Loss of alveolar bone reduces the vertical dimension of the mandible and maxilla. Without teeth to occlude, the mandible and maxilla can move closer together. This causes the mandible to protrudes forward, leading to a “popeye chin”.
can prevent loss of alveolar ridge by transmitting force onto bone tissue during mastication. respond to force by increasing the deposition of calcium and phosphate, increasing bone density and maintaining bone health. If bone loss has already occurred, a ← or procedure may need to be done allow for regeneration of lost bone tissue before the implants are installed. Afterwards, (including ←) may be involved if gingival tissue has receded significantly.
Dental Implant technology
Each dental implant consists of a core, abutment and crown. The core is made of titanium and is implanted into bone tissue. To get the shape and size of the core to fit properly within the alveolar ridge involves
computed tomography (CT scans) to image bone tissue and
computer-aided design (CAD) to specify the core’s dimensions. The abutment connects the core to the crown by a screw or dental cement. The crown is usually made of ceramic. Titanium is strong, durable and . It is more or less invisible to the cell surface that white blood cells use to detect
antigens. Unfortunately, this also makes titanium invisible to other cells in the body, including . As a result, titanium does not adhere well to the connective tissue it is embedded in. Knowledge of histology helps: coating the core with improves the connection between the core and the patient’s connective tissue.
Because dental implants fuse to bone tissue, they do not participate in proprioception. There is interest in creating coatings for the titanium core that might allow attachment to an implant. For instance, layering a core with with and PDL ←
promotes the connection of a dental implant to PDL in mice.
Another important connection that is lost with tooth extraction is ←. Because the junctional epithelium of each tooth is derived from the during ←, new junctional epithelium does not form on an implant. At best, may adhere to titanium via ←, creating peri-implant mucosa. Coating a ring of the core with ← (such as ) mimics the of junctional epithlium from REE, improving the connection between oral mucosa and the implant. Coating the titanium core with , on the other hand, promotes integration with bone tissue.
Failure to create a complete junction between the and the implant exposes underlying connective tissue to the oral microbiome, frequently leading to . Because the oral microbiome does not go away, chronic inflammation occurs, leading to loss of tissue around the affected implant, including gingival and bone tissue.
The ← is involved in both maintaining bone health and loss of bone tissue. Its activity is taken advantage of with . Pressure applied to a tooth causes the on one side to slacken, and on the other side to tense up. The side with lower amount of tension will undergo bone resorption, as are inhibited but maintain their speed of bone resportion. Higher tension triggers bone deposition on the opposite side. As a result, the location of the alveolar socket shifts in the jawline, without altering the overall dimensions of the socket itself. It is import that the correct amount of force be applied—to much stress can lead to bone resorption all around, increasing the size of the alveolar socket and increasing tooth mobility.
Common treatments for osteoporosis include drugs than inhibit the activity of , such as
bisphosphonates. Because the entire remodeling unit is required for orthodontia, patients using these medications cannot undergo orthodontic therapy. Another factor to consider with orthodontia is the activity of and . The ← that induce odontoclast ← and activity (RANKL) during orthodontic movement inhibit the activity of cementoclasts and odontoclasts. For this reason, there is significantly less resorption of cementum and dentin than there is bone tissue during orthodontic movements, even though force across the PDL is the same on bone and tooth root tissues. It is possible to experience root resorption with orthodontic treatment, especially as the orthodontic force increases, although the causes of root resorption are complex and multi-factorial.
Widening of the PDL space
With occlusal trauma, within the responds with increased activity, leading to a widening of the PDL. For example, in , a wider PDL space is temporarily generated on the side opposite of the direction of force, but this triggers bone deposition and returns the PDL space to its original width. A wider PDL space can be visualized on a radiograph, and may be accompanied by a thickening of the , bone loss, and/or . Other conditions besides occlusal trauma may lead to a widening of the PDL space, such as the use of certain medications. The term wider PDL space means that neighboring tissue is lost. It does not necessarily indicate PDL fibroblasts have made more ← fibers, only that a larger radiolucent gap exists between the root and the lamina dura. This space may contain more ← or pus, for instance, and not ←. This brings us to another example, which may seem contradictory to the first: reduced force can also lead to widening of the PDL space. For example, conditions that negatively affect bone health lead to changes in chewing behavior which in turn reduces occlusal forces. Reduced force is followed by bone loss and a widening of the PDL space. Similarly, chronic inflammation of nearby tissues, such as , can trigger widening of the PDL space. Whether these conditions stimulate production of ← by fibroblasts is unlikely because and osteoporosis are associated with increased tooth mobility. Common treatments usually aim to reduce the insult, such as using a nightguard if bruxism is suspected. help distribute the forces applied to remaining teeth in a partially mouth, reducing changes to the PDL space and maintaining tooth attachment.
Loss of the PDL apparatus
Loss of attachment between cementum and alveolar bone, known as , promotes tooth loss. Two common causes are smoking and bacterial biofilms located within periodontal pockets. With smoking, nicotine plays a role as a toxin. Nicotine activates
nicotinic acetylcholine receptors whose activity modulates blood flow, ←, chemotaxis and cell attachment to . These are all necessary for a to repair or regenerate the of ←. Bacterial biofilms contain toxins which can cause similar changes in fibroblast activity—but these toxins generally only diffuse 1 to 2 mm through ECM, which means biofilms located more than 2 mm away from the are too far away to harm fibroblasts of the PDL (Fig. 11.31).
Regeneration of the PDL following periodontitis
We have discussed of bone tissue using ← (), as well as promotion of to using protein coatings. The use of similar bioactive membranes to promote regeneration of the has only been
studied in animals at this time, not humans. PDL regeneration is conceptually more complicated—which is perhaps the reason why PDL regenerates poorly, and why we have made less progress on PDL regeneration than bone or . The PDL is good at tissure repair because it contains ← and ample vascularity. These two factors that make other connective tissues regenerate well, such as pulp, bone and the sub-mucosa of the oral cavity.
So why is the good at repairing bone and cementum, but not itself? First, the PDL is polarized. It is not enough to stimulate , the cells must be oriented correctly to create the proper attachments (similarly, a good coach won’t tell soccer players to kick the ball into a goal, or even the goal at the north end of the stadium, the target changes at halftime so polarity and time matter). Unfortunately, the ← signals involved in this process are poorly understood. Secondly, the two connections of the PDL form at different times: ← fibers are created within during root formation←, but fiber connections to alveolar bone are not made until ←. Again, the signals involved are poorly understood, it remains possible that the signals guiding these two connections could be mutually exclusive. We’ve covered examples where the same ← does different things at different times throughout this book. For example, -2 the of , , and . It may not be possible to get the PDL anchored to cementum and alveolar bone at the same time.
Without knowing more specifics, let us offer a metaphor: the two connections of the could be like car traffic at an intersection. For every green light you travel through, cross-traffic has a red light. With proper timing, you might be able to hit green lights all the way down the street, but the traffic light you drove through a minute ago is probably turning red now. It may not be possible to simultaneously get a green light occurring both at the light you are at and the light you were at 5 blocks ago. Urban planners realize that would be a horribly inefficient system. The two ends of the PDL might be controlled like traffic lights, a go signal at one end may be the stop signal at the other end.
Our final thought
Don’t worry about the red light 5 blocks behind you. You have the green light to go apply knowledge of histology and embryology to your clinical coursework. If the light turns yellow,
yellow means go faster.
Chapter review questions
Specialized tissues that surround and support the teeth, including gingival tissue, PDL, cementum and alveolar bone.
Periodontal Ligament, a group of specialized connective tissue fibers that attach a tooth to alveolar bone.
Epithelia that have more than one layer of cells, with the cells at the apical surface having a flat shape.
he most exterior of the three primary germ layers formed in the gastrula, it gives rise to the epithelial tissue covering the body and the CNS.
A series of externally visible anterior tissue bands lying under the early brain that give rise to the structures of the head and neck.
The middle of the three embryonic layers that develop during gastrulaton, mesoderm becomes most of the body's muscle and connective tissues.
Extra-Cellular Matrix: Materials in the body, but outside of cells. A network of macromolecules, such as fibers, enzymes, and glycoproteins, that provide structural and biochemical support to surrounding cells.
The main structural protein in the ECM of connective tissues
Thin protein fibers in the ECM, capable of stretching and returning to their original length, made of the protein elastin.
A subset of mesenchymal stem cells derived from neural crest cells rather than mesoderm, or mesoderm-derived mesenchymal stem cells induced by neural crest morphogens to adopt a more neural fate.
Neuro-mesenchymal cells and fibres surrounding the enamel organ and dental papilla of a developing tooth.
The developmental history of a differentiated cell traced back to the embryonic cell from which it arises.
Elastic-like fibers made of the protein Fibrillin that run parallel to the tooth surface and bend to attach to cementum.
A temporary group of cells that arise from the embryonic ectoderm, and in turn give rise to a diverse cell lineage—including melanocytes, cranio-facial cartilage and bone, teeth and periodontal tissue, smooth muscle, peripheral and enteric neurons and glia.
Hertwig's Epithelial Root Sheath: A proliferation of epithelial cells located at the cervical loop of the enamel organ in a developing tooth which initiates the formation of root dentin.
Programmed cell death
A condensation of ecto-mesenchymal cells seen in histologic sections of a developing tooth.
Inner Enamel Epithelium: a layer of columnar cells located next to the dental papilla, these pre-ameloblast cells will differentiate into Ameloblasts which are responsible for secretion of enamel during tooth development.
The embryonic process in which one group of cells directs the development of another group of cells.
When one cell begins to look different from another. This process involves limiting cell fate by altering gene transcription to become more specialized.
A cell of neural crest origin that is part of the outer surface of the dental pulp, and whose biological function is the formation of dentin.
The formation of dentin.
A group of star-shaped cells located in the center of the enamel organ of a developing tooth, they synthesize glycosaminoglycans.
Shared equally by two parties.
Cells present only during the embryonic period that deposit tooth enamel.
Outer Enamel Epithelium: a layer of cuboidal cells located on the periphery of the enamel organ in a developing tooth.
A substance whose non-uniform distribution governs the pattern of tissue development and pattern formation.
Fibroblast Growth Factors are a family of morphogens involved in a wide variety of processes, including important roles in development and tissue regeneration, especially connective tissues.
Signaling molecules first identified for their role in carcinogenesis, then for their function in embryonic development, including body axis patterning, cell fate specification, cell proliferation and cell migration.
A process by which epithelial cells lose polarity and cell-cell adhesion, and gain migratory and invasive properties to become mesenchymal stem cells, this normally occurs during embryonic development and wound healing.
Differentiated cell that deposits cementum matrix.
Newly formed dentin before calcification and maturation.
Bone Morphogenetic Proteins are a group of signaling molecules, initially discovered for their ability to induce bone formation, now known to play crucial roles in all organ systems.
The process of cementum formation which covers the tooth root by cementoblasts of mesenchymal origin.
The formation of enamel.
The initial un-mineralized form of enamel secreted by ameloblasts.
The thin unmineralized layer present on the surface of developing cementum.
The increase in diameter by the addition of tissue at the surface,
Terminally differentiated cell found within mature cementum lacunae.
A layer of dark granules that lie parallel to the outer surface of root dentin.
Bundles of strong type I collagen that anchor the periosteum to bones by penetrating the outer layers of compact bone tissue
Fingerlike projections of the epidermis, the downward-pointing counterparts to the dermal papillae.
Fingerlike projections of the apical side of the dermis, increasing the surface area between the epidermis and dermis, strengthening their connection and increasing exchange of oxygen, nutrients, and waste.
A protein that has had sugar residues attached to it in the Golgi apparatus and is often secreted.
Ca5(PO4)3(OH), the inorganic ECM material composed of calcium, phosphate and hydroxide ions that makes up the bulk of bone tissue.
Cementum containing cells and collagen fibers anchoring the tooth to alveolar bone.
Cementum covering the cervical portion of the tooth root, important for attachment of the periodontal ligament (PDL) to the root surface.
Pain derived from exposed dentin in response to chemical, thermal tactile or osmotic stimuli which cannot be explained as arising from any other dental defect or disease.
A type of connective tissue found in tendons and ligaments that is composed primarily of parallel collagen fibers, secreted by fibroblasts, with very little ground substance.
The basic connective tissue cell type capable of secreting ECM components, including fibers and ground substance proteins.
Lakes, or spaces within cartilage of bone connective tissue where cells reside.
A differentiated connective tissue cell that secretes bone ECM, including collagen, calcium and phosphate.
A cell derived from bone marrow stem cells capable of demineralizing bone tissue by the secretion of acids and enzymes, releasing calcium into the blood.
Undifferentiated or partially differentiated cells that can differentiate into various cell types, and proliferate to produce more of the same stem cell.
Multipotent cells of a connective tissue that can differentiate into a variety of cell types, including osteoblasts, fibroblasts, chondrocytes, myoblasts, blood cells and adipocytes.
Resorptive cell capable of demineralizing cementum by the secretion of acids and enzymes.
Resorptive cell capable of demineralizing dentin by the secretion of acids and enzymes.
Reorganization or renovation of existing tissues, either physiological or pathological. The process can either change the characteristics of a tissue such as in blood vessel remodeling, or result in the dynamic equilibrium of a tissue such as in bone remodeling.
Containing blood vessels
Growth of endothelial cells, creating new blood vessels within a tissue.
Copying DNA into a functional product, such as a RNA and/or protein. Controlled by the activity of transcription factors binding to gene promoter regions to recruit RNA polymerase.
A sequence of nucleotides in DNA that encodes the synthesis of a gene product, either RNA or protein.
Mesenchyme tissue that contains neural crest cell derivatives.
Cell Adhesion Molecules: proteins located on the cell surface involved in binding with other cells or with the extracellular matrix.
Trans-membrane structure specialized for cell-to-cell adhesion.
The process by which animals and plants grow and change.
An endodermal pouch between two pharyngeal arches on the internal surface of the embryo.
A process in tooth development in which the teeth enter the mouth and become visible.
The main principal fiber group is the alveolodental ligament, which consists of five fiber subgroups: alveolar crest, horizontal, oblique, apical, and interradicular on multirooted teeth. Principal fibers other than the alveolodental ligament are the transseptal fibers.
Cemento-Enamel Junction, found in the cervical region of the tooth.
The top (or apex) side of a cell or tissue, usually facing the lumen.
Collagen fibers in the gingiva that, in general, attach the tooth to the gingival tissue (rather than the tooth to the alveolar bone like the PDL fibers).
A polarity axis that organizes cells in the plane (side-to-side) of the tissue.
A very large glycosaminoglycan distributed widely throughout connective tissue ECM, epithelial, and neural tissues.
A large glycoprotein found in the ECM which binds to integrin proteins on the cell surface, involved in cell adhesion, growth, migration, and differentiation.
Clusters of epithelial cells found within the PDL, remnants of Hertwig's Epithelial Root Sheath (HERS).
The shape (or form) of.
Formation of bone tissue from a dense connective tissue model
The formation of bone tissue from a cartilage model
Apiece of cartilage from which the mandibles (lower jaws) of vertebrates evolved, originally the lower of two cartilages which supported the first branchial arch in early fish.
A protein that controls the rate of transcription of DNA to mRNA, by binding to a specific DNA sequence.
A group of 235-300 related genes that code for a transcription factors, which control the activity of other genes involved in development, including directing the formation of limbs and organs along the anterior-posterior axis.
An aggregation of cells that eventually forms a tooth, composed of the enamel organ, dental papilla and dental sac.
Small channels in the bone that transmit blood vessels from the periosteum into the bone and that communicate with the haversian canals, or small holes in alveolar bone through which PDL fiber bundles are embedded.
Compact bone that lies adjacent to the periodontal ligament, in the tooth socket.
The bony partition across the alveolar process between adjacent teeth that forms part of the tooth sockets.
The bony septum lying between tooth roots.
The mucous membrane lining the inside of the mouth. It is a stratified squamous epithelium, named the oral epithelium, and an underlying areolar connective tissue named the lamina propria.
The stratified squamous epithelium of the oral mucosa.
The areolar connective tissue layer of the oral mucosa (or hollow organ), homolgous to the papillary layer of the dermis.
The dense irregular connective tissue layer found below the oral mucosa (or mucosa of a hollow organ), homologous to the reticular layer of the dermis.
Epithelium on the inner wall of the gingiva that attaches to connective tissue of the lamina propria on the basolateral side and to the surface of the tooth on the apical side.
Formation and eruption of the teeth.
Reduced Enamel Epithelium: the OEE and ameloblasts found on the surface of the crown prior to tooth eruption.
Idiopathic, non-neoplastic condition characterized by the excessive buildup of normal cementum on the roots of one or more teeth.
A signaling molecule capable of stimulating cell proliferation, wound healing, and cellular differentiation.
A condition of teeth where the cementum overlying the roots of at least two teeth join together.
The exposure in the roots of the teeth caused by a loss of gum tissue and/or retraction of the gingival margin from the crown of the teeth.
Decay of cementum.
The wearing away of tooth enamel by excess acids.
The type or types of cell(s) a stem cell can possibly differentiate into in the future, determined by which genes are methylated and stored around histones, or free to be transcribed.
A pulp disease characterized by the loss of dentin as a result of the action of osteoclastic cells stimulated by pulpal inflammation.
Also known as a root canal, is a treatment for infected pulp of a tooth, result in the removal and replacement of pulp and the protection of the decontaminated tooth from future microbial invasion.
When the body's own immune system dissolves the tooth root structure. It can occur following tooth infection, orthodontic treatments or in the presence of unerupted teeth in the jaw.
Abnormal stiffening and immobility of a joint (including tooth-to-alveolar bone)
Spherical calcified bodies lying free in the periodontal membrane.
Materials used in surgical implants, not harmful to living tissue and unlikely to be rejected by the host immune system.
The tendency of teeth to move in a mesial direction within the arch, maintaining interproximal contact between teeth.
Osteoblasts and osteoclasts working together to remove old bone tissue and replace it with new bone tissue, necessary for the maintenance of healthy bones.
Inflammation that damages soft tissue and bone that anchors the teeh, including the gingiva plus PDL, cementum or alveolar bone tissue.
A roughly circular defect of the cortical plate which exposes the underlying root surface, but does not involve the alveolar margin of the bone.
A lack of the facial or lingual alveolar cortical plate resulting in a denuded root surface
A pathologically deepened gingival sulcus around a tooth at the gingival margin.
located at the bottom of the sulcus, consisting of approximately 1 mm of junctional epithelium and 1 mm of gingival fiber attachment.
Having the protein keratin, which lends resistance to abrasion and water loss.
Without blood vessels
Extracellular matrix material involved in the repair of injured and missing tissues, allows stem cells to migrate into the injured area. It is usually replaced during regeneration.
Procedures attempting to regenerate (as opposed to replace) lost periodontal structures.
A medical procedure in which ground up bone tissue or synthetic bone tissue is placed in an injured site to act as a scaffold, promoting the formation of new bone tissue by the patient's own cells.
A strong but immovable connective tissue quickly made by fibroblasts, consisting primarily of highly cross-linked collagen fibers.
A trans-membrane protein which allows cells to bind to the ECM protein fibronectin, it is involved in cell adhesion, growth, migration, and differentiation.
A compound that has an effect on a living organism, tissue or cell, such as by mimicking a morphogen or growth factor.
Enzymes that degrade all kinds of extracellular matrix proteins, or process a number of bioactive molecules. They play a major role in cell proliferation, migration, differentiation, angiogenesis, and apoptosis.
An artificial tooth root that is surgically placed into bone tissue.
The use of connective and epithelial tissue from the roof of the mouth or neighboring gingiva, attached to the gum area being treated.
The most common method used to treat root exposure, involving the transplantation of healthy connective tissue from a donor site to the damaged area, which acts a scaffold aiding in tissue regeneration.
A cell-surface, trans-membrane or cytoplasmic protein that binds to (receives) a signaling molecule and transmit the signal further.
Half of a desmosome, specialized for cell-to-ECM adhesion.
A destructive inflammatory process affecting the soft and hard tissues surrounding dental implants.
The treatment of irregularities in the teeth (especially of alignment and occlusion) and jaws, including the use of braces.
Gel-like substances in the ECM, composed of water held in place by large molecules (proteins, glycoproteins and glycosaminoglycans).
Inflammation of the pulp.
Damage to the structures that support the tooth; results from periodontitis and is characterized by relocation of the junctional epithelium to the tooth root, destruction of the fibers of the gingiva, destruction of the periodontal ligament fibers, and loss of alveolar bone support from around the tooth.
The process of cell division, where one cell divides into two identical clones (daughter cells).
After partial loss of as tissue, based on the remaining part, the tissue grows the same structure and function as the lost part.