Basic Civil Engineering first year Notes- Chapter 4 Building.pptx
The periodontal ligament
1. GOVT.DENTAL COLLEGE & HOSPITAL
DEPT. OF PERIODONTICS
THE PERIODONTAL LIGAMENT
(22/06/19)
GUIDED BY PRESENTED BY
DR. P. SURESH CH. SUMA PRIYANKA
PROF & HOD PG STUDENT
GDC, KADAPA GDC, KADAPA
2. CONTENTS:
INTRODUCTION
DEFINITIONS
DEVELOPMENT OF PDL & PRINCIPAL FIBERS
STRUCTURE OF PDL
FUNCTIONS OD PDL
PDL HOMEOSTASIS
BLOOD & NERVE SUPPLY TO PDL
AGE CHANGES IN PDL
CLINICAL CONSIDERATIONS
IMPLANTS & PDL
PDL – TISSUE ENGINEERING
PDL – STEM CELLS
CONCLUSION
BIBLIOGRAPHY
3. INTRODUCTION:
The periodontium is a connective tissue organ covered by the epithelium that attaches the teeth
to the bones of the jaws and provides a continually adapting apparatus for support of the teeth
during function.
Normal periodontium is a unique and complex dynamic structure, each of its components
having distinct functions that are capable of adaptation during the life of the structure.
DEFINITIONS:
“The periodontal ligament is composed of a complex vascular and highly cellular connective
tissue that surrounds the tooth root and connects it to the inner wall of the alveolar bone”.
(Carranza 11th ed)
“It is a narrow and highly cellular connective tissue that forms the interface between alveolar
bone and cementum”.
(Perio 2000)
“Soft, richly vascular and cellular connective tissue which surrounds the roots of the teeth and
joins the root cementum with the socket wall”.
(Jan Lindhe 5th ed)
“The periodontal ligament occupies the periodontal space , which is located between the
cementum and the periodontal surface of alveolar bone and extends coronally to the most apical
part of the lamina propria of the gingiva”.
(Orban’s Oral histology 13th ed)
At the apical foramen, it is continuous with the dental pulp.
Collagen fibers of the PDL are embedded in cementum and alveolar bone so that the ligament
provides soft tissue continuity between the mineralized connective tissues of the periodontium.
PDL ranges in width from 0.15-0.38mm. It is thinnest around the middle third of the root, with
an “hourglass” appearance.
It shows a progressive decrease in thickness with age.
4. Acc. to age…
* 0.21mm – young adult
* 0.18mm – mature adult
* 0.15mm – older adult
Acc. to functional state of the tissues-
* Time of eruption – 0.1-0.5mm
* At function – 0.2-0.35mm
* Hypo function – 0.1-0.15mm
In radiographs, the ligament appears as the periodontal space of 0.4-1.5mm, a radiolucent area
between the radio-opaque lamina dura of the alveolar bone proper and the radio-opaque
cementum.
The periodontal space of permanent teeth are narrower than those of deciduous teeth.
DEVELOPMENT OF PDL:
The development of PDL begins with the root formation, prior to the tooth eruption.
The continuous proliferation of the internal and external enamel epithelium forms the cervical
loop pf the tooth bud.
This sheath of epithelial cells, grow apically, in the form of “Hertwig’s epithelial root sheath”,
between the dental papilla and dental follicle.
At this stage, the sheath forms a circumferential structure encompassing dental papilla
separating it externally from dental follicle cells.
5. Dental follicle cells located between the alveolar bone and epithelial root sheath are composed
of 2 sub-populations-
i) Mesenchymal cells of the dental follicle proper
ii) Peri-follicular mesenchyme
Peri-follicular mesenchymal cells are more widely separated than cells of dental follicle proper
and contains an euchromatic nucleus, a very little cytoplasm, RER, mitochondria, free
ribosomes and an inactive golgi.
As the root formation continues, cells in the peri-follicular area, gain their polarity, and the
cellular volume and the synthetic activity increases.
These cells become elongated and contain an increases RER, mitochondria and an active golgi
complex.
As a result, they actively synthesize and deposit collagen fibrils ad glycoproteins in the
developing PDL.
The developing PDL and mature PDL contains undifferentiated stem cells that retain the
potential to differentiate into osteoblasts, cementoblasts, and fibroblasts.
Studies suggest that these stem cells occupy the perivascular sites in the PDL and in adjacent
periosteal spaces.
6. As the root formation continues, cells in the peri-follicular mesenchyme gain their polarity,
cellular volume and become widely separated
Actively synthesized & deposit collagen fibrils in developing PDL
Type I collagen is secreted
Assembles as collagen bundles on bone & cementum surfaces
Establish continuity across the ligament space
DEVELOPMENT OF PRINCIPAL FIBERS:
Immediately before tooth eruption, active fibroblasts adjacent to the cementum of the coronal
third of root, appear to become aligned in an oblique direction to the long axis of the tooth.
Soon thereafter, the first collagen fiber bundles of the ligament become discernible.
These are the precursors of the “alveolar crest fiber bundle group”.
By the time of 1st
occlusal contact of the tooth with its antagonist, the principal fibers around
the coronal third of the root, the “Horizontal group” are almost developed.
The “Oblique fibers” in the middle third of the root are still being formed and there is a
progressive apical maturation of oblique fibers upon eruption.
With the formation of apicacl fiber group, the definitve PDL is established.
7. Originate at the surface of newly formed root dentin in relation to highly
polarized fibroblasts
Nascent fiber bundles are tightly packed by the action of cementoblasts during initial
development of AEC
As PDL matures, fringe fibers merge across the width of the ligament to form
principal fiber bundles.
8. STRUCTURE OF PDL:
Cellular elements
Periodontal fibers
Ground substance
SYNTHETIC CELLS:
OSTEOBLASTS:
The osteoblasts covering the periodontal surface of the alveolar bone constitute a modified
endosteum.
Surface of the bone is covered largely by osteoblasts in various stages of differentiation as well
as by osteoclasts.
These are the bone forming cells lining the tooth socket. These are cuboidal in shape, with a
prominent nucleus at the basal end of the cell.
RER, mitochondria, and vesicles are abundant in active cells.
The cells contact one another through desmosomes & tight junctions and also with the
underlying osteocytes through cytoplasmic processes.
9. FIBROBLASTS:
Predominant cells in PDL.
These cells originate in part from the ectomesencyme of investing layer of dental papilla and
from the dental follicle.
These cells are different from cells in other connective tissues in a number of respects.
Eg; Rapid degradation of collagen by fibroblast phagocytosis is the basis for very fast turnover
of collagen in PDL.
Also, fibroblasts on the bone side of the ligament show abundant alkaline phosphatase activity
than those on tooth side.
Fibroblasts near cementum are derived from ectomesenchymal cells of the investing layer of
dental papilla while fibroblasts near alveolar bone are derived from perivascular mesenchyme.
These are fusiform shaped cells arranged parallel to the tooth surface with extensive cytoplasm
and abundant organelles with protein synthesis and secretion.
During development and initial formation of PDL, fibroblasts appear very active with
extensive network of RER, well developed golgi apparatus and abundant secretory granules
containing type I collagen molecules.
Cell-cell & cell-matrix connections are through gap junctions & adherens.
These cells produce growth factors and cytokines such as IGF-1, BMP’s, PDGF & IL-1. TGF-
β stimulates the synthesis of collagen and inhibits the synthesis of collagenase.
The role of fibroblast is to produce the structural CT proteins, collagen and elastin, as well as
proteoglycans, glycoproteins and glycosaminoglycans that compromise the PDL ground
substance.
These cells also secrete an active collagenase and MMP’s.
These cells are characterized by rapid turnover of collagen.
These are also responsible for the formation and remodeling of PDL fibers, and a signaling
system to maintain the width of PDL and thickness.
10. CEMENTOBLASTS:
These are cuboidal cells that line the surface of cementum.
These cells have abundant mitochondria and less amounts of RER than periodontal ligament
fibroblasts.
These cells actively deposits cellular cementum.
RESORPTIVE CELLS:
OSTEOCLASTS:
Resorbs bone.
Large & multi-nucleated osteoclasts are formed by fusion of precursor cells similar to
circulating monocytes.
The part of the plasma membrane lying adjacent to bone that is being resorbed is raised in to
characteristic folds and is termed as “Ruffled / striated border”.
The bone related to the ruffled border undergoes resorption.
FIBROBLASTS:
It shows rapid degeneration of collagen by fibroblast phagocytosis and that is the basis for
rapid turnover of collagen.
Some studies suggested that collagen degradation is “Intracellular” in all healthy tissues
through intracellular collagen profiles and “Extracellular” in tissues where the changes are
pathological or where degradation is rapaid.
Hence, degradation of collagen may be intracellular & extracellular.
11. INTRA-CELLULAR DEGRADATION OF COLLAGEN:
Lysosomal cysteine proteases of lysosomal granules are capable of rapid degradation of
internal collagen fibrils.
EXTRA-CELLULAR DEGRADATION:
The altered integrity of ECM causes increased water to enter the collagen bundles causing
loosening of the bundles, thus allows the cells that secrete degrading MMP’s to enter the
bundles.
CEMENTOCLASTS:
Resembles osteoclasts and are occasionally found in normal functioning PDL.
Resorption of cementum can occur under certain circumstances, and in these instances
mononuclear cementoclasts or multi-nucleated giant cells, often located in Howship’s lacunae,
are found on the surface of cementum.
12. EPITHELIAL RESTS OF MALESSEZ:
These cells were 1st
described by “Malassez” in 1884 and are the remnants of the epithelium
of Hertwig’s epithelial root sheath.
These are most numerous in the apical area and cervical area.
These cells form a lattice work and appear as either isolated cluster of cells or interlacing
strands. They diminish in number with age and may undergo calcification to form
“Cementicles”.
These cells are attached to one another by desmosomes.
Contain leratinocyte growth factors.
These cells can proliferate and participate in the formation of peri-apical cysts and lateral root
cysts.
DEFENSE CELLS:
i) Mast cells
ii) Macrophages
iii) Eosinophils
MAST CELLS:
These are relatively round / oval cells having a diameter of about 12-15μm.
Mast cells releases histamine that plays a role in the inflammatory reaction, and these have
been shown to degranulate in response to antigen – antibody reactions on their surface.
Release of histamine into the extracellular environment causes proliferation of endothelial cells
and mesenchymal cells.
These cells also play a role in regulating endothelial and fibroblast cell populations.
MACROPHAGES:
These are derived from monocytes and phagocytize particulate matters and invading microbes.
In PDL, macrophages may play a dual role-
i) Phagocytizing dead cells
ii) Secreting growth factors that regulate the proliferation of adjacent
fibroblasts.
13. Macrophages also synthesize a range of molecules like interferons, prostaglandins, and factors
that enhance the growth of fibroblasts and endothelial cells.
EOSINOPHILS:
These are occasionally seen in PDL.
They possess granules that consists of one or more crystalloid structures that are capable of
phagocytosis.
EXTRACELLULAR SUBSTANCE:
It consists of fibers and ground substance.
Fibers Collagen
Elastic – Oxytalin
Reticular
Secondary
Indifferent fiber plexus
Ground substance Glycosaminoglycans
Proteoglycans
Glycoproteins
CT fibers are mainly collagenous, but there may be small amounts of oxytalin and reticulin
fibers.
COLLAGEN:
Collagen is a protein composed of different aminoacids; the most important being glycine,
proline, hydroxylysine and hydroxyproline.
Amount of collagen in a tissue can be determined using hydroxyproline content.
All collagens are composed of 3 polypeptide chains coiled around each other to form the
typical “Triple helical configuration”.
VARIATIONS ARE BROUGHT ABOUT BY:
i. Differences in assembly of the basic polypeptide chains.
14. ii. Different lengths of the helix.
iii. Various interruptions in helix
iv. Differences in the terminations of the helical matrices.
Collagen fibrils have transverse striations with a characteristic periodicity of 64nm. These
striations are caused by the overlapping arrangement of the tropocollagen molecules.
Collagen fibril diameter of PDL are small with a mean diameter of 45-55nm. This small
diameter of the fibrils could be due to high rate of collagen turnover or the absence of mature
collagen fibrils.
Main types of collagen in PDL are type I & type III.
Collagen inparts a unique combination of flexibility and strength to the tissues.
Principal fibers of PDL are arranged in 6 groups-
i. Transseptal
ii. Alveolar crest group
iii. Horizontal
iv. Oblique
v. Apical
vi. Inter-radicular
TRANS-SEPTAL FIBERS:
These fibers extend inter proximally over the alveolar bone crest and are embedded in the
cementum of the adjacent teeth.
These are reconstructed even after destruction.
These fiberes may be considered as belonging to the fobers of gingiva as they do not have any
osseous attachment.
ALVEOLAR CREST GROUP FIBERS:
These fibers extend obliquely from the cementum just beneath the JE to the alveolar crest.
Fibers also run from the cementum over the alveolar crest and to the fibrous layer of the
periosteum covering the alveolar bone.
These fibers prevent the extrusion of the tooth and resists lateral tooth movements.
The incision of these fibers duting periodontal surgery doesn’t increase tooth mobility.
15. HORIZONTAL FIBERS:
These fibers extend at right angles to the long axis of the tooth from the cementum to the
alveolar bone.
OBLIQUE FIBERS:
These are the largest group in the PDL, extend from the cementum in a coronal direction
obliquely to the bone.
They bear the brunt of the vertical masticatory stresses and transform them into tension on
alveolar bone.
APICAL FIBERS:
These fibers radiate in a irregular manner from the cementum to the bone at the apical region
of the socket.
These do not occur in incompletely formed roots.
INTER – RADICULAR FIBERS:
These fibers fan out from the cementum to the tooth, in the furcation areas of multi-rooted
teeth.
16. Though PDL doesn’t contain mature elastin, 2 immature forms are found-
* Oxytalin
* Elaunin.
Oxytalin fibers run parallel to the root surface in a vertical direction and bend to attach to the
cementum in the cervical third of the root. They are thought to regulate vascular flow.
In addition to these, small collagen fibers associated with larger principal fibers have been
describes called “Indifferent fiber plexus”.
GROUND SUBSTANCE:
It fills the space between fibers and cells.
It consists of a biochemically complex, highly hydrated, and semisolid gel.
Consists of - Water content – 70%
- Glycosaminoglycans – hyaluronic acid, proteoglycans
- Glycoproteins – fibronectin, laminin, vibronectin, tenascin.
PROTEOGLYCANS:
These are a large group of anionic macromolecules that consists of a protein core to which
hexose amine containing polysaccharides called “gag chains” are attached.
The 2 main tyoes of proteoglycans present in PDL include..Dermatin sulfate & Chondroitin
sulfate.
These helps in * Cell adhesion
* Cell-cell & cell-matrix interactions
* Cell repair
* Binding to various growth factors.
GLYCOPROTEINS:
The primary function of these molecules is to bind cells to the extracellular elements.
Most widely studied glycoprotein is “Fibronectin”.
It promotes the attachment of cells to the collagen fibrils. It may also be involved in cell
migration and orientation.
Other glycoproteins preset in PDL include- Tenascin & Vitronectin.
17. Tenascin ia a adhesive glycoprotein synthesized at specific times and location during
embryogenesis.
It may act to transfer the forces of mastication and stresses of tooth support to specific protein
structures.
It binds to fibronectin and to proteoglycans.
It blocks the binding capacity of syndecan and thereby enables the cell to move freely.
FUNCTIONS OF PDL:
Physical
Formative & remodeling
Nutritive
Sensory
Regulation of PDL width
PHYSICAL FUNCTIONS:
i. Provision of a soft tissue ‘casing’ to protect the vessels and nerves from injury by mechanical
forces.
ii. Transmission of occlusal forces to bone
iii. Attachment of teeth to bone.
iv. Maintenance of gingival tissues in their proper relationship to the teeth.
v. Resistance to the impact of occlusal forces (Shock absorption).
RESISTANCE TO THE IMPACT OF OCCLUSAL FORCES:
2 theories – i) Tensional theory
ii)Visco-elastic theory
18. TENSIONAL THEORY:
• States that principal fibers are major factor in supporting the tooth and transmitting forces to
the bone.
20. TRANSMISSION OF OCCLUSAL FORCES TO BONE:
• Arrangement of principal fibers is similar to suspension bridge or a hammock.
• When an axial force is applied –
When horizontal / tipping forces are applied - i) within the confines of PDL
ii) produces a displacement of the facial
& lingual bony plates.
In areas of tension, principal fibers are taut rather than wavy.
In areas of pressure, fibers are compressed, tooth is displaced, and a corresponding distortion
of bone exists in the direction of tooth movement.
21. In single rooted tooth, the axis of rotation lies in between the apical third & middle third of the
root.
In multi-rooted tooth, the axis of rotation lies in the bone between the roots.
FORMATIVE & REMODELLING FUNCTIONS:
Cells have the capacity to resorb and synthesize the extracellular substance of the connective
tissue ligament, bone & cementum.
Participate in physiologic tooth movements and in repair of injuries.
PDL is constantly undergoing remodeling, old cells and fibers are broken down and replaced
by new ones.
Radio autographic studies indicate a very high turnover rate of collagen in PDL. A rapid
turnover of sulfated GAG’s in the cells and amorphous ground substances also occurs.
Sodek (1977) has demonstrated that PDL incorporates proline atleast 5 times faster than
gingiva or bone and the biological half life of mature collagen was 20% & 17& less than found
in gingiva & bone respectively.
NUTRITIONAL FUNCTIONS:
Supplies nutrients to cementum, bone and gingiva by the way of blood vessels and also
provides lymphatic drainage.
Highly vascularized compared to other ligaments and tendons.
This may provide hydrodynamic damping to applied forces, as well as high perfusion rates to
PDL.
22. Rich vascular plexus are present at apex & cervical part.
SENSORY FUNCTIONS:
• Periodontal ligament provides the most efficient proprioceptive mechanism
• 4 types of neural terminations are seen
1. Free nerve endings -pain
2. Ruffini like mechanoreceptors (apical area)
3. Meissner’s corpuscles - mechanoreceptors (middle3rd)
4. Spindle like pressure and vibration endings (apex)
TOOTH SUPPORT MECHANISM:
• Primary role of the ligament is to act as a medium of force transfer during mastication.
• “Matsuo” et al. - blood vessels in the ligament -“Shock absorber” to cushion the alveolus from
occlusal load.
• The ligament exhibits visco-elastic behavior, where the fluid component of the tissue modifies
the action of the fibers in withstanding transmitted loads.
• Evidence suggests that ligament collagen crimps play a role in the preliminary stages of
masticatory loading, which permits some movement prior to the tissue experiencing tension.
23. • Recent biochemical analysis of the proteoglycans within the ligament shows that under
different loading regimens, the degree of aggregation / disaggregation of proteoglycans may
have role in the tooth support.
REGULATION OF PDL WIDTH:
• The ability of periodontal ligament cells to synthesize and secrete a wide range of regulatory
molecules is essential in accurately maintaining the width of the periodontal ligament (McCulloch,
1983)
• Transforming growth factor-β isoforms - can dose-dependently down- regulate osteoblastic
differentiation of periodontal ligament cells (Brady TA et al. 1998).
• Prostaglandins - can inhibit mineralized bone nodule formation and prevent mineralization by
periodontal ligament cells in vitro (Ogiso B, Hughes FJ, et al. 1991,1992).
• Paracrine factors - inhibit bone resorption (Ginger MS, et al 1991)
• Pro-inflammatory cytokine (IL-1) and one of the isoenzymes responsible for prostaglandin
synthesis are induced by applied mechanical force on periodontal ligament cells in vitro. (Shimizu
N et al 1995).
• As prostaglandins and interleukin-1 can strongly induce matrix degradation, there is evidently an
important relationship between mechanical forces, cytokine production and regulation of the
periodontal ligament space.
24. BLOOD SUPPLY:
• Inferior & superior alveolar arteries to the mandible & maxilla - reaches the PDL from 3 sources:
1. Apical vessels (Dental artery)
2. Transalveolar vessels (rami perforantes-penetrating vessels from bone)
3. Intraseptal vessels (anastomosing vessels from the gingiva)
• Branches of the intraseptal vessels – perforate the lamina dura & enter the ligament.
• After entering the PDL, perforating rami anastomose & form a polyhedral network which
surrounds the root like a stocking.
• More abundant in the maxilla than in the mandible, & more in the posterior than in the anterior
teeth.
• This dual supply allows the ligament to survive following removal of the root apex during
certain endodontic procedures.
• Arteriole in PDL – diameter – 15 to 50 µm.
NERVE SUPPLY:
• The nerve follow almost the same course as the blood vessels.
• Nerve bundle divide → myelinated fibers → lose their myelin sheath → end in one of the 4
types of neural termination
25. • The PDL has double innervation:
Axons arising from the mesencephalic nucleus - Unconscious reflex pathways &
proprioceptors – position control of the mandible.
Axons from the trigeminal ganglion - Conscious sensation of touch, pain & temperature.
The vast majority of the nerve endings are the unenscapsulated, Ruffini like mechanoreceptors
and free nerve endings.
In experimental animals, innervation from the trigeminal ganglion is very dense – tooth apex,
circular & interdental ligaments.
Innervation from mesencephalic nucleus – most dense – subapical region, especially for the
canines & incisors, with no innervation in the zone of the circular & interdental ligaments.
LYMPHATICS:
• Lymph vessels - originate as cul-de-sac in PDL.
• Course apically - pass through the fundus of the socket or they may pass through the cribriform
plate to empty into larger channels pursuing intraosseous paths.
26. AGE CHANGES IN PDL:
• Decreased number of fibroblasts.
• Decreased cell activity and therefore normal function of tissue is diminished.
• Scalloping is seen.
• Decreased organic matrix production and epithelial cell rests.
• Increased amounts of elastic fibers.
CLINICAL CONSIDERATIONS:
The primary role of periodontal socket is to support the tooth in the bony socket.
Its thickness varies in different individuals and in different teeth in the same person and in
different locations on the same tooth.
“ACUTE TRAUMA” to PDL, accidental blows or rapid mechanical destruction may produce
pathological changes such as fractures or resorption of the cementum, tear of fiber bundles,
hemorrhage and necrosis.
The adjacent alveolar bone is resorbed and the PDL is widened and tooth becomes loose. when
trauma is eliminated, repair usually takes place.
“ORTHODONTIC TOOTH MOVEMENT” depends on resorption and formation of bone and
PDL.
These activities can be stimulated by properly regulated pressure and tension.
If the movement of teeth is within the physiologic limits, the initial compression of PDL on
the pressure side is compensated for by bony resorption whereas on tension side, opposition is
seen.
Application of larger forces results in necrosis of PDL and alveolar bone on the pressure side
and movement of the tooth will occur after the necrotic bone has been removed completely by
osteoclasts.
“INFLAMMATORY DISEASES OF THE PULP” progress to the apical PDL and replace its
fiber bundles with granulation tissue.
This lesion is called “periapical granuloma”, may contain epithelial cells that undergo
proliferation and produce a cyst.
27. “CHRONIC INFLAMMATORY DISEASE” is the most common pathology related to PDL.
The toxins released from the dental plaque and metabolites of the host’s defense mechanism
destroy the PDL and the adjacent bone very frequently.
This leads to tooth mobility and further loss of tooth.
To repair the existing destruction of PDL, can be quite challenging. It involves limiting the
disease process and to regenerate the host tissues to their original form in such a way that
reattachment of PDL to bone becomes possible.
Various surgical techniques like GTR are being used for correction of periodontal destruction.
Fusion of alveolar bone and cementum with obliteration of periodontal ligament is termed as
“ANKYLSOIS”.
It occurs in teeth with cemental resorption which suggests that it may represent a form of
abnormal repair.
It may also develop after chronic inflammatory diseases, chronic periapical inflammation,
tooth implantation, and occlusal trauma and around embedded teeth.
Clinically, ankylosed tooth sounds dull / woody on percussion.
EXTERNAL FORCES & PDL:
• Within physiologic limits, the PDL can accommodate increased function with - an increase in
width,
- a thickening of its fiber bundles
- an increase in diameter & number of Sharpey’s fibers.
Forces that exceed the adaptive capacity of the periodontium produce “TRAUMA FROM
OCCLUSION”.
28. IMPLANTS & PDL:
Although dental implants typically enjoy a high survival rate, the literature is filled with a
variety of well-documented problems associated with implants in the biological and
mechanical spheres.
i. Periodontal sulcus versus peri-implant sulcus:
Peri-mucosa is composed of keratinized oral epithelium, sulcular epithelium, and junctional
epithelium, as well as the underlying connective tissue.
This soft-tissue interface is made up of the epithelium and the underlying connective tissue,
which includes a biologic zone known as the “biologic width” (the height of the attachment
apparatus).
The average dimension of 2.04 mm is comprised of supra-alveolar connective tissue and
junctional epithelial attachment.
But there is a difference between the implant surface and the epithelial cells with
hemidesmosomes and basal lamina present, leading to deeper sulcus, compared to that found
around natural teeth in a healthy situation.
Normal physiologic probing depths can be more than 4–5 mm around dental implants, whereas
with teeth, increased pocket depths usually are diagnosed as pathologic.
In addition, bleeding upon probing with dental implants may not always indicate disease,
whereas bleeding upon probing around teeth usually indicates an increased inflammatory state.
ii) Periodontal attachment versus peri-implant attachment:
With natural teeth, the gingival fibers run perpendicular to the tooth's long axis attaching to the
tooth's surface, whereas with implants, the fibers run parallel to the implant's long axis and do
not attach to the implant's surface.
The connective tissue adhesion with implants has poor mechanical resistance compared with
natural teeth.
when faced with bacterial challenge, attachment breakdown is greater with implants.
Once the "implant seal" around the implant-attachment complex breaks down, exacerbation
of tissue loss increases when compared with teeth.
29. It becomes imperative that supportive periodontal treatment and home hygiene are reinforced
to ensure long-term restoration.
iii. Inflammatory response:
The fibers on natural teeth provide a physical barrier to bacterial invasion.
This physical barrier is not present with implants, as the parallel orientation of the fibers allows
the apical progression of bacteria ... leading to the potential for a more rapid spread
of inflammation ... leading to peri-implantitis.
iv. Healing response of tissue:
Implants exhibit a poor gingival vascular supply compared with teeth.
Small, clean, closed wounds heal more quickly than large wounds, which heal slowly and with
significant scarring.
Flapless surgery has an added benefit of providing a better vascular supply and retaining
vitality of the supra-crestal connective tissue around the implant compared with raised soft-
tissue flaps, which inadvertently may lead to cutting and damaging of supra-periosteal vessels.
30. Due to the decreased vascularity around implants compared with teeth, the healing after
nonsurgical and/or surgical therapy is slower.
Tissue regeneration around diseased implants is not as predictable as it is around teeth and thus
may require additional growth factors, proteins, and/or stem cells added to conventional
regenerative biomaterials.
v. Tooth root versus implant body:
Implants do not have periodontal ligaments; therefore, occlusal loads are directly transferred
to the bone.
Bone loss may result when overload presents over time, especially in off-axis directions.
Crestal bone loss
Dislodged restorations
Screw loosening
Screw Fracture
Peri implantitis
Implant failure
In addition, because of the porous, rough surface of most implants, bacterial contamination of
the implant body versus the root surface is higher.
31. PDL - STEM CELLS: Current status & Future prospects:
The aim of periodontal regenerative treatment is to restore the physiological function of teeth.
With tissue regeneration, damaged periodontal tissues can be repaired via application of stem
cells, growth factors, or an extracellular matrix scaffold.
Mesenchymal stem cells (MSCs)
Embryonic stem cells (ESCs)
Induced pluripotent stem cells (iPSCs).
MSCs were initially discovered in bone marrow, and bone marrow mesenchymal stem cells
(BMMSCs) were found to promote periodontal regeneration when transplanted into
periodontal osseous defects.
In 2004 Seo et al. surgically created periodontal defects on the buccal cortex of
the mandibular molar of immunodeficient rats. Carrier used was hydroxyapatite / β-tricalcium
phosphate particles-isolated multipotent periodontal ligament stem cells(PDLSCs) from
human impacted third molars-
After 6-8 weeks, implanted PDLSC’s demonstrated the ability to form
cementum / PDL-like structures an aid in periodontal tissue repair.
32. FUTURE TRENDS:
• Despite of numerous clinical techniques for regeneration- no predictable outcomes..
• The knowledge of the presence of PDL stem cell and their inherent potential to regenerate
various desired tissues at site of destruction is of great importance.
• The plausibility of a stem cell-based tissue engineering approach to achieving periodontal
regeneration is supported by animal studies demonstrating that PDL cells cultured in vitro can
be successfully reimplanted into periodontal defects in order to promote periodontal
regeneration.
33. PDL – TISSUE ENGINEERING – LIGAPLANTS:
A new approach to the replacement of tooth loss is introduced, i.e., tissue engineering of the
PDL.
In this, tissue-engineered PDL cells are formed on the dental implants thus acting as a natural
tooth.
This new dimension in the field of implant dentistry is known as “Ligaplants”.
TISSUE ENGINEERING – FOUNDATION OF LIGAPLANTS:
• Tissue engineering utilizes biodegradable polymers to make scaffolds into the cells to produce
tissues in the presence of growth factors.
• “Langer” and “Vacanti” stated this as an interdisciplinary field that applies the principle of
engineering and life sciences for the evolution of biological substitutes that restore, maintain
or improve tissue function.
34. • Regeneration proceeds with a new layer of cementum, attached to original cementum of the
tooth root, into which new transverse fibers are integrated.
• Then, if a new cementum layer were to be laid down on the surface of the engineered-device,
this would accommodate the integration of a properly attached PDL with the potential to
stimulate the regeneration of adjacent alveolar bone.
• This hypothesis was supported by Sonoyama et al. who demonstrated the possibility of
constructing the entire root/periodontal complex by inserting a hydroxyapatite/ tricalcium
phosphate block coated with PDL-derived mesenchymal stromal cells into the tooth sockets of
mini- pigs.
• In 1990, “Buser” et al. showed that PDL of the roots served as a source of cells which could
populate the implant surface during healing when titanium dental implants were placed in
contact with retained root tips.
• Lin et al. reported the use of autologous rat PDL cells derived from molar tooth root surfaces
to regenerate PDL tissues of titanium.
• They used matrigel, a three-dimensional matrix scaffold to facilitate organized rat PDL
regeneration at the titanium-implant alveolar bone interface.
35. PREPARATION OF LIGAPLANTS:
• To harvest the cell sheet, human PDL cells are plated on temperature- responsive culture dishes at
a cell density of 1x105 and cultured at 37°C.
ADVANTAGES OF LIGAPLANTS:
1. It alleviates problems like gingival recession and bone defects of missing tooth.
2. Mimics insertion of natural tooth roots in alveolar process.
3. Ligaplants become firmly integrated without interlocking and without direct bone contact,
despite the initial fitting being loose in order to spare PDL cell cushion.
4. Bone formation was induced - intact communication between bone and implant surface.
DISADVANTAGES OF LIGAPLANTS:
1. The culturing of ligaplants should be done with caution i.e the temperature, the cells that are
used for culturing, the duration of the culturing and others.
36. 2. If some difficulty evokes during the culturing, the ligaplants may fail as other nonperiodontal
cells may develop.
3. With limited facilities and members to perform this research, the cost of this type of implant
is high.
4. The factors affecting the host to accept the implant or the growth of PDL in the socket is
unpredictable, which may result in failure of implant.
Nyman et al. 1982 suggested that the cells of the periodontal ligament possess the
ability to reestablish connective tissue attachment.
Nunez et al. 2012 further validated the regenerative potential of periodontal ligament
derived cells in a proof of principle study.
Several in vivo experiments have demonstrated the formation of cementum-like tissue with an
intervening periodontal ligament, when the dental implants were placed in proximity to tooth
roots.
This appeared to be due to migration of cementoblast and PDL fibroblast precursor cells
towards dental implants due to contact or proximity of the tooth-related cell populations to
those implants.
Gault P et al. 2010 stated that new tissue consistent with PDL developed on the surface
of dental implants after implantation. This evidence demonstrates the application of
ligament-anchored implants, which have potential advantages over osseointegrated oral implants.
Kiong AL et al. 2014 stated that ligaplants as tooth replacement has decisive
advantages as compared with osseosintegration devices, due to their periodontal tissue
regeneration.
The ligaplants surgery is moderately simple, because the implant is not tightly fitted to its site.
Besides that, patient may not have to undergo bone grafting, inconvenience and discomfort
with the ligaplants placement.
37. CONCLUSION:
PDL is a fibrous CT forming important part of the periodontium. Without it, the tooth is support
less.
Cells of the PDL are pleuripotent and helps in the regeneration of all the components of
periodontium lost in the periodontal disease.
A better understanding of the cell and molecular biology of developing and regenerating
periodontium offers newer avenues to regenerate PDL.
Newer options of treatment are made available from time to time yet safeguarding the integrity
of PDL and alveolar bone is still one of the most important challenge.
38. BIBLIOGRAPHY:
Carranza’s clinical periodontology-11th
ed.
Jan Lindhe, Niklaus P. Lang -6 th; Clinical periodontology and Implant Dentistry.
Orban’s Oral Histology & Embryology-13th
ed.
Thomas G. Wilson, Kenneth S. Kornman, Fundamentals of Periodontics- 2nd
ed.
Garg H, Deepa D. Bioengineered periodontal ligament: Ligaplants, a new dimension in the
field of implant dentistry – Mini review. J Oral Res Rev 2018;10:92-5.
Froum S et al, Top 5 anatomical differences between dental implants and teeth that influence
treatment outcomes : Perio – Implant advisory.com
Jain A, Agarwal A, Gokhale ST, Manjunath RGS, Mishra N. Periodontal ligament stem cell:
An update. J Adv Clin Res Insights 2014;3:120-122.
Zhu W, Liang M. Periodontal Ligament Stem Cells: Current Status, Concerns, and Future
Prospects -Review article: Hindawi Publishing Corporation Stem Cells International Volume
2015, Article ID 972313.