11 Periodontium development

Figure 11.1: H&E stain of the periodontium. Figure legend: 1) gingival sulcus, 2) gingival crest, 3) lamina propria, 4) PDL. Image credit: "Histological section of an incisor tooth of a Rhesus monkey displaying the elements of the periodontal apparatus" by András Mihály1 and Eszter Mihály is licensed under CC BY 4.0


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 .

photo of a tooth cross section
Figure 11.2: Cross section of a tooth to show hard tissues, including cementum. Image credit: "What is inside a human tooth" by Mohamed A.M. Ahmed is licensed under CC BY-SA 4.0 / cropped


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 explored with instruments.

animtion of HERS
Figure 11.3: Disintegration of HERS and the formation of cementum.

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 . A few of the epithelial cells of HERS may undergo an and differentiate into . However, most cementoblasts arise differently. 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. Cementoblasts secrete the protein components of cementum. This immature matrix is commonly 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 (reviewed here).

illustration of the periodontium
Figure 11.:4 Illustration of the periodontium, highlighting bundles of collagen fibers (dark pink) that extend from Tomes’ granular layer through to alveolar bone.

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 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 .

Figure 11.5: Patterns of cementum at the CEJ

Types of cementum by area of the root

For most teeth, the apical one third of the root contains over . More cervical regions contain only acellular cementum. Most of the time, roughly 60%, cementum extends over the enamel a short distance. About 30% of the time, cementum completely covers root dentin, all the way up to the enamel. Roughly 10% of the time there is a gap between the cementum and enamel, with underlying dentin exposed.  Rarely, about 1% of the time, enamel may overlap cementum (rare because begins much earlier than ). 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 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 .

Histology of periodontal tissues.
Figure 11.6: Histology of the PDL. Image credit "Immunohistochemistry of CXCL12 in PDL of rat molars” by Yashiro Y et al is licensed under CC BY-SA 4.0 / cropped

Periodontal ligament development

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.

photo of stem cell media
Figure 11.7: Collection of stem cells from an extracted tooth (the fluorescent green color lets you know this is science!). Image credit: “Sample embedded in tooth preservation cocktail and nourishment media” by PM Sunil et al is licensed under CC BY-NC-SA 4.0

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.

Confocal image of HERS
Figure 11.8: Confocal image of developing mouse tooth. Legend: BV = blood vessel, Od = odontoblasts, Dp = dental pulp, PDL = periodontal ligament. Colors: purple = DNA (nuclei), red and green = experimental trans-genes. Image credit: “Lineage studies by mapping Cre activity in the root region of a second molar in a 2-week-old mouse by confocal microscopy using the Olympus FV 1000.” by Rakian A, et al is licensed under CC BY-NC-ND 4.0

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 , whgingival ile 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).

illustration of the periodontium
Figure 11.9: The periodontium. Legend: A. Enamel, B. Dentin, C. Alveolar bone, D. Gingiva, E. Oral epithelium, F. Free gingival margin, G. Gingival sulcus, H. Principal gingival fibers, I. Alveolar crest fibers of periodontal ligament, J. Horizontal fibers of periodontal ligament, K. Oblique fibers of periodontal ligament. Image credit: "the periodontium” by Goran tek-en is licensed under CC BY-SA 4.0

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 multi-rooted 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.

histology of the PDL
Figure 11.10: Histology of the epithelial Rests of Mallasez (ERM). T = tooth, B = alveolar bone. Image credit “Photomicrograph of the periodontal ligament showing clusters of epithelial cell rests” by HD Miniggio and EJ Raubenheimer is licensed under CC BY-NC 4.0

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 from studying transgenic mice.

photo of a model skull
Figure 11.11: Alveolar bone (roughly above dotted red line)

Alveolar bone

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 humans 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. 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 .

bite wing radiograph
Figure 11.12: Bitewing noting PDL and lamina dura.

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 the height of the alveolar crest. The is the portion of alveolar bone between roots

Gingival development

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.

Clinical applications

radiograph of hypercemtosis
Figure 11.13: Hyper-cementosis. Image credit: “Periapical radiograph showing radiopaque halo around the root of tooth #36” (international numbering system) by Antonione Santos Bezerra Pinto is licensed under CC BY-NC-SA 4.0


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 Paget’s disease.

Concrescence: can the teeth involved be moved or separated?
Figure 11.14: Concrescence examples. Image credit : “Second and third molars joined by cement, in teeth with and without hypercementosis” by Consolaro A et al is licensed under CC BY 4.0


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.

photo of cemental caries
Figure 11.15: Cemental caries. Image credit: “Photograph showing root caries in 33 & 34” (international numbering system) by B Gupta is licensed under CC BY-SA 4.0

Root caries

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. Caries pass 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. Root caries can be detected early with radiographs or use of a dental mirror and explorer.

radiograph of root resorption
Figure 11.16: Root resorption. Image credit: “Own work” By Bin im Garten is in the Public Domain CC0

Root resorption

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 odontoclasts may not be your average mesenchymal stem cell, but a related with a different . Possible candidates include and stem cells.

photo of a pink tooth
Figure 11.17: Lateral maxillary incisor has undergone root resorption, evident by its pinkish appearance. Image credit: “Mummery” by DRosenbachis licensed under CC BY 3.0

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). 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. This occurs because cementum has a high regenerative capacity because of 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).

histology of a cementicle
Figure 11.18: Cementicle. Labels: PDL = periodontal ligament, CEM = cementicle, BV = blood vessel, CC = cellular cementum. Image credit: “Cementicles” by Mandana Donoghue is licensed under CC BY-NC-ND 4.0


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.

photo of a cat and kitten
Figure 11.19: Example of the importance of tooth proprioception. Image credit: “Tortoiseshell cat carrying her kitten up a flight of stairs. She grips the kitten's scruff in her teeth” by Margo Akermark is licensed under CC BY 2.0

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.

photo of mesial drift
Figure 11.20: Mesial drift. Image credit: “Class II human Molar relationship” by Dr. Vipin C. P. is in the Public Domain, CC0

Mesial drift

(or physiological drift) is the tendency of teeth to migrate in a mesial direction with age. It is a natural phenomenon caused by the assymetrical of alveolar bone tissue. There are two major concepts  relevant to mesial drift. One, alveolar bone undergoes more bone remodeling than 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 lean lingually, changing the occlusal plane. This, in turn, can lead to abnormal forces on the temporo-mandibular joint, causing pain, discomfort and reduced range of motion.

Image result for periodontitis xray
Figure 11.21: Loss of alveolar bone. Image credit: “Own work” by By Bin im Garten is licensed under CC BY-SA 3.0

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 from , 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.

animated illustration of fenestration
Figure 11.22: Illustration of fenestration and dehiscence of alveolar bone tissue, exposing underlying tooth roots.

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.

medical photos of guided tissue regeneration
Figure 11.23: Guided tissue regeneration. Legend: A) bony defect after root planing and debridement. B) Bone graft C) Collagen-membrane D) Gingival flap surtured over graft materials. Image credit: “Chronic periodontitis, Collagen, Guided tissue regeneration” by Young Mi Chung is licensed under CC BY-NC-SA 4.0

Guided Tissue Regeneration

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 may incorporate molecules covered in this book, and be recognized as a scaffold over which stem cells migrate. These molecules may include components of ECM, or . Some morphogens promote the of mesenchymal stem cells into osteoblasts, rather than (which produce scar tissue), others can be used to promote , speeding up the healing process.

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.

photo of an edentulous mouth
Figure 11.24: Changes to an edentulous alveolar ridge. Image credit: “Own work” by JASFUS assumed in the Public Domain CC0

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.

animated illustration of changes to alveolar ridge
Figure 11.25: Changes to the vertical dimension of the maxilla and mandible in an edentulous mouth.

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 protrude forward, leading to a “popeye chin”.

radiograph ofnttl implants
Figure 11.26: Dental implants. Image credit: “Own work” By Danjhon  is licensed under CC BY-SA 4.0

Dental implants

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.

photo of a dental implant
Figure 11.27: Ceramic root analog implant (RAI) compared to a traditional titanium screw-type implant. Image credit: “Own work” by Logicwhatelse is licensed under CC BY-SA 4.0

Dental Implant technology

Each dental implant consists of a core, abutment and crown. The core is traditionally made of titanium and is implanted into bone tissue, although other technologies exist (Fig. 11.27). 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.

animated radiograph of peri-implantitis
Figure 11.28: Peri-implantitis leading to bone loss. Image credit: “Bone loss following peri-implantitis in a smoker” by Coronation Dental Specialty Group is licensed under CC BY-SA 3.0


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.

animation of orthodontia
Figure 11.29: Changes inthe  force applied to bone tissue from the PDL during orthodontic movement leads to changes in the activity of the bone remodeling unit on both sides of the alveolar socket.


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 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.

radiograph of wide PDL
Figure 11.30: Widening of the PDL space. Image credit: “Widening of periodontal ligament space in tooth 36” by CH Chuh is licensed under CC BY-NC-SA 4.0

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 unknown 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.


illustration of a tooth
Figure 11.31: Illustration of a healthy pocket versus severse periodontitis, including fibers of the PDL. Image credit: “Line diagram of a tooth showing the gingiva, bone, periodontal ligament with a scale showing the pocket depth of severe periodontitis” by Ian Furst is licensed under CC BY-SA 4.0

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).

scientific diagram of PDL regeneration
Figure 11.32: PDL regeneration schematic. Figure Legend: a) loss of bone and soft tissue during periodontitis. b and f) Long Junctional Epithelium (LJE) repair. c and g) ideal repair. e) Guided Tissue Regeneration schematic. C = cementum, NC = new cementum, D = dentin, NB = new bone, NPLF = new PDL fibers. Arrowhead = apical end of JE. Image credit: “Periodontal regeneration” by Jin Liu, et al is licensed under CC BY 4.0

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.

illustration of a traffic light
Figure 11.33: Like the programming of traffic lights, development involves timers (such as cyclins) and signal buttons (morphogens), internal electric changes (gene transcription changes) that lead to externally visible changes (morphogenesis). Like a well-planned city traffic light system, there is significant cross-talk between developing structures in a human embryo not illustrated here. Image credit: “FSA of a traffic light system” by Pluke is in the Public Domain, CC0 / colors added

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.

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