The periodontal ligament is a specialized connective tissue that connects the cementum of teeth to the alveolar bone. It develops from the dental follicle during root formation and tooth eruption. The periodontal ligament is composed of collagen fibers, fibroblasts, blood vessels and nerves. The principal collagen fibers are arranged in bundles and attach to the cementum and bone. The periodontal ligament helps maintain homeostasis between the teeth and surrounding tissues and allows for tooth mobility.

1. 1

2. PRESENTER
DR.PUNIT
(I YEAR PG)
2

3. CONTENTS
 Introduction
 Synonyms
 Shape of pdl
 Development
 Composition
 PDL as specialized connective tissue
 Blood supply
 Nerve supply
 Function
 Clinical considerations
 Conclusion
 References
3

4. INTRODUCTION
 Periodontium/Attachment
apparatus/Supporting tissues of
teeth):
 gingiva
 attachment apparatus (alveolar bone,
periodontal ligament and cementum)
• Main function –It attaches the tooth to
the bone of jaws.
 Maintains the integrity of the surface
of masticatory mucosa of the oral
cavity 4

5.  A ligament is defined as a band of fibrous tissue binding
together skeletal elements.
 The root of tooth connected to the socket in alveolar bone by
dense fibrous connective tissue which can be regarded as a
ligament.
 PDL is very unique from all other ligaments in the body
connects and restricts the hard tissues-tooth cementum and
alveolar bone.
5

6. The periodontal ligament is a soft, fibrous specialized
connective tissue which is present in the periodontal space,
which is situated between the cementum of root of the tooth
and the bone forming the socket wall.
The periodontal ligament extends coronally up to the most
apical part of connective tissue of gingiva
6

7. DEFINITIONS
 Periodontal ligament is composed of soft complex vascular and
highly cellular connective tissue that surrounds the tooth root and
connects to the inner wall of the alveolar bone (Mc Culloch CA,
Lekic P, Mc Kee MD Periodontol 2000 24:56,2000)
 ACCORDING TO BERKOVITZ:
“it is the dense fibrous connective tissue that occupies the
periodontal ligament space between the roots of teeth and
alveolus. It is derived from the dental follicle above alveolar
crest and is continuous with connective tissue of gingiva and
the apical foramen which is further continuation with dental
pulp.
7

8.  It is a narrow and highly cellular CT that forms the
interface between alveolar bone and cementum.
(Periodontol 2000,vol.3,1993)
 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)
8

9. COMPOSITION
 53 – 74 % of periodontal ligament volume consists of
collagen and oxytalan fibers.
 1 – 2 % consist of vascular elements.
 Remainder consists of cells and neural elements.
 The connective tissue of periodontal ligament
comprises collagen
 Proteoglycan, glycoprotein and small amount of
glycogen.
 Major component is Type – I collagen with Type III
collagen accounting for 15 – 20 % of total collagen
9

10. SHAPE OF PERIODONTAL LIGAMENT
 HOUR GLASS SHAPE
 Thinnest around the middle third of the root & widens both
apically and near the crest.
10

11.  It is neither a typical membrane nor typical ligament .
However , because it is a complex, soft connective tissue
providing continuity between two mineralized tissue
(cementum and bone).
 Width variable = average 0.15 mm– 0.38mm.
11

12. Age in
years
Width
11-16 0.21mm
32-52 0.18mm
51-67 0.15mm
PERIODONTAL LIGAMENT DECREASES WITH AGE
(TENCATE 6TH EDITION)
12

13. SYNONYMS OF PERIODONTAL LIGAMENT
1. Desmondont
2. Pericementum
3. Dental Periosteum
4. Alveolodental ligament
5. Periodontal membrane
 (PERIO 2000 volume 3)
13

14. EVOLUTION
 Reptiles have ankylosed teeth.
 During the period of transition following changes
takes place :
a. Size of jaw decreased
b. Change in articulation of jaw
c. Change in size and shape of the teeth
(ORBANS TEXTBOOK 13TH EDITION)
14

15. DEVELOPMENT
15

16. DEVELOPMENT OF PERIODONTAL LIGAMENT
16

17.  Development of periodontal ligament begins with root
formation ,prior to the tooth eruption. Continuous proliferation
of internal and external epithelium forms cervical cusp of tooth
bud. Sheath of epithelial cells grows apically in form of
HERTWIG’S ROOT SHEATH.
(Jan Lindhe 5th edition and Berkovitz 2nd edition)
17

18.  Sheath forms a circumferential structure enclosing dental
papilla separating it from the dental follicle cells. Dental follicle
cells located between alveolar bone and epithelial root sheath
composed of two cells:
 A. mesenchymal cells of dental follicle proper
 B. proliferative mesenchyme
18

19.  Mesenchymal cells of perifollicular mesenchyme bounded by
dental follicle proper & developing alveolar bone is stellate
shaped. Cells are widely separated & contain euchromatic
nucleus, very little cytoplasm, short cisternae of rough
endoplasmic reticulum, mitochondria, free ribosomes.
 As the root formation continues cells in perifollicular area gain
their polarity and cellular volume & synthetic activity increases.
These cells become elongated & contain increased amount of
ROUGH ENDOPLASMIC RETICULUM, mitochondria &
active Golgi complex. As a result actively synthesize collagen
fibrils
19

20. DEVELOPMENT OF PRINCIPAL FIBERS
 Immediately before tooth eruption active fibroblasts adjacent to
cementum of coronal third of root aligned in oblique direction to
long axis of the tooth. Soon thereafter the First collagen fiber
bundles of ligament become discernible and these are the
precursor of alveolar crest fiber bundles.
 Further apically organized fibers are not seen but examination of
root surface at higher magnification reveals fine brush like fibers
extending from cementum.
20

21.  Similar fibers are observed on the adjacent osseous surfaces of
the developing alveolar process . Both set of fibers cemental
and alveolar continue to elongate towards each other ultimately
to meet intertwine and fuse.
 By the time first occlusal contact of the tooth with its
antagonist the principal fibers around the coronal third of root
the horizontal group are almost completely developed.
21

22.  Oblique fibers in the middle of the root still being formed as
eruption continues & definite occlusion is established there is
progressive apical migration of oblique fiber bundles. With the
formation of apical fiber group definite periodontal architecture
is established.
22

23. Development….
Fig 2Fig 1 Fig 3

24. DEVELOPMENT OF CELLS
 Prior to the root formation cells of follicle show very few
organelles. With onset of root formation organelles in cells
increase, collagen & ground substance formation begins &
fills in extracellular space.
 Stem cells which give rise to cementoblasts, osteoblasts &
fibroblasts in perivascular location. Osteoclasts appear at
the alveolar bone surface allowing remodeling of bone in
association with tooth eruption.
24

25. PERIODONTAL LIGAMENT
HOMEOSTASIS
 Studies have indicated that population of the cells of
periodontal ligament both during development and
regeneration secrete molecules that can regulate the extent
of mineralization and prevent the fusion of the tooth root
with surrounding bone (ankylosis).
 Various molecules have been proposed which play a role in
maintaining an unmineralized periodontal ligament.
 MSX2 prevents osteogenic differentiation of periodontal
ligament fibroblasts by repressing RUNX2(RUNT RELATED
TRANSCRIPTION FACTOR 2)also known as cbfa1(core
binding factor alpha1)
25

26.  Balance between activities of bone sialoprotein and osteopontin
also contributes towards maintaining an unmineralized
periodontal ligament region.
 MATRIX ‘GLA’ protein an inhibitor of mineralization is also
present in periodontal ligament. It plays a role preserving
periodontal ligament region.
26

27.  RGD-CEMENTUM ATTACHMENT PROTEIN a collagen
associated protein play a role in maintaining the unmineralized
state of periodontal ligament.
 TGF-BETA isoforms synthesized by periodontal ligament cells
can induce mitogenic effects and also downregulate osteoblastic
differentiation of periodontal ligament cells.
 Prostaglandins which are also produced by the periodontal
ligament cells can inhibit mineralized bone nodule formation and
prevent mineralization by periodontal ligament cells in vitro
27

28.  The periodontal ligament has the capacity to adapt to functional
changes, when functional changes increase width of periodontal
ligament increases as much as by 50% and fiber bundles also
increases its thickness.
 A reduction in function leads to narrowing of the ligament and
decrease in number and thickness of fiber bundles.
28

29. PERIODONTAL LIGAMENT:
EXTRACELLULAR
CELLULAR
29

30. EXTRACELLULAR STRUCTURES
 Collagen Proteoglycans
Elastic Glycoproteins
RETICULAR Glycosaminoglycan's
INDIFFERENT FIBER PLEXUS
OXYTALAN
FIBERS
GROUND
SUBSTANCE
30

31. PERIODONTAL FIBERS
 Most important elements of periodontal ligament are
the principal fibers which are collagenous & arranged
in bundles & follow a wavy course when viewed in
longitudinal section.
 Terminal portions of principal fibers are inserted into
cementum called SHARPEY’S FIBERS. It forms a
continuous anastomosing network b/w tooth and
bone.
31

32.  Sharpey’s fibers are abundant non collagenous proteins found in
bone and cementum among these are OSTEOPONTIN AND
SIALOPROTEIN(regulators of mineralization).
 Collagen is protein of different amino acids most important are
GLYCINE,
PROLINE,HYDROXYPROLINE,HYDROXYLYSINE.
32

33. 33
1.Mesenchymal Cells & Their Derivatives
FIBROBLASTS ( major cells )
Chondrocytes
Osteoblasts
Odontoblasts
CEMENTOBLASTS

34. COLLAGEN
 It is a protein – most abundant protein in animal
kingdom.
 Derived from – Greek – kolla(glue) and gene.
- French – glue producing constituents.
 Rigid, rod-like structure-resists stretching and fibers made
of collagen have high tensile strength.
 Also participates in biologic functions-cell shape,
differentiation.
 It is an important constituent of PDL where mechanical
forces must be transmitted without loss
34

35. SEQUENCE OF EVENTS
A. Sequence of intracellular collagen biosynthesis
Assembly pro-alfa chains (directed by specific mRNAs)

Proline hydroxylation

Lysine hydroxylation

Hydroxylysine glycosylation

Disulphide bond formation/incorporation of C Terminal
Propeptides.
Secretion
35

36.  several enzymes are involved in the destruction of matrix
components collage breakdown is mediated primarily by
the COLLAGENASES ( Type of MMP) These are
specialized enzymes that have evolved specifically to
hydrolyze collagens ,because their triple helical collagen
structure is resistant to most common proteinases.
36

37. 38
Fibroblasts are responsible for the
production of the extracellular matrix
components.
They reside in close proximity to the
collagen fibers.
The nucleus appears as an elongated or disk
like structure in H & E preparations. The
thin, pale staining, flattened processes that
form the bulk of the cytoplasm are usually
not visible.
Myofibroblast is an elongate, spindle
connective tissue cell that displays typical
characteristics of the fibroblast along with
characteristics of smooth muscle cells

38.  Sequence of extracellular collagen biosynthesis
Amino terminal extension cleavage (procollagen aminopeptidase)

Carboxyl terminal extension cleavage ( procollagen carboxypeptidase)

formation of collagen fibrils and spontaneous arrangement of fibrils
cross link formation by the action of lysyl oxidase enzyme,deamination of lysyl
residues and maturation of cross-links. Growth and reorganization of fibers.
39

39. CHARACTERISTIC FEATURES OF COLLAGEN
1)Triple helical structure- alfa chains-left handed helices.
The triple helix may be continuous/interrupted by non-
collagenous segments.
2)Within triple helical domain, glycine –every 3rd
position in the amino acid sequence Gly-X-Y,where X , Y –
amino acids other than glycine.(Proline)
3) Contains 2 unique amino acids- Hydroxyproline and
Hydroxylysine.
4)Collagen is stabilized through formation of Lysine-derived
intra- and intermolecular cross-links.
42

40. COLLAGEN TYPES
So far 19 types of collagen have been discovered.
Collagen classes
a. Interstitial collagens ---- Type I,II,III
b. Basement membrane type ---- Type IV,VI,VII
c. Short chain collagens ---- Type IX,X
43

41. Based on their ability to form fibrils, collagens are of 3 groups:
-FIBRIL-FORMING : triple helix has uninterrupted stretch of Gly-X-Y
residues. Includes types 1,2,3,5,11.
-FACIT : (Fibril Associated Collagens with Interrupted Triple helices)-
collagenous domains interrupted by non-
collagenous sequences. Includes Types 9,12,14(contains GAG) and may be
16
-NON-FIBRILLAR: Forms sheets/membranes enclosing tissues and
organisms.
Types 4,8,10- Network forming
Type 6-Beaded
Type 7-Anchoring fibrils
44

42.  Collagen is responsible for maintenance of framework
and tone of tissue biosynthesis of collagen inside
fibroblasts to form procollagen molecules. It has a
transverse striations with characteristic periodicity of
64nm. These striations are caused by overlapping
arrangement of tropocollagen molecules.
45

43.  Collagen is gathered to form bundles approximately 5
micrometers in diameter. These bundles are called
PRINCIPAL FIBERS. within each bundle subunits are
present called COLLAGEN FIBRILS.
46

44.  Type I, III, V, XII – Periodontal Ligament
 Type VI, II – cartilage
 Type IV - Basement membrane
 Type VI – Ligaments, skin, bone
 Type VII - Anchoring fibrils of basement
membrane
 Type IX - Cartilage
 Type X, XI - Cartilage, Bone
 Type XIII - Epidermis Cartilage
 Collagen is synthesized by fibroblasts , chondroblasts ,
osteoblasts, odontoblasts and other cells.
47

45.  Principal fibers composed of mainly TYPE I
 RETICULAR FIBERS COMPOSED OF TYPE III
 BASAL LAMINA COMPOSED OF TYPE IV
48

46. TYPES OF COLLAGEN FIBERS
 TYPE I – SKIN,TENDON, VASCULAR
LIGATURE,ORGANS,BONE
 TYPE II – CARTILAGE
 TYPE III – RETICULAR
 TYPE IV – FORMS BASAL LAMINA
49

47.  TYPE V – CELL SURFACES , HAIR AND PLACENTA
 TYPE VI – SUBSTANCE FOR CELL ATTACHMENT &
AS AN ANCHORING MESHWORK THAT
CONNECTS COLLAGEN FIBERS , NERVES & BLOOD
VESSELS TO SURROUNDING MATRIX.
50

48.  TYPE VII – ACTS AS AN ANCHORING FIBRILS.
 TYPE XII – ASSOCIATED WITH TOOTH
DEVELOPMENT,ALIGNMENT, ORGANIZATION OF
PERIODONTAL FIBERS.
51

49. NON-COLLAGENOUS PROTEINS
FIBRONECTIN:
-2 forms-soluble plasma form(pFN) & cross-linked fibrillar
form in most tissues (cellular/cFN) .
-Functions: -Within matrix, bridge between cells & collagen-
(cell adhesion, migration)
-Has specific domains to bind to Heparin, fibrin,
collagen hence role in matrix
assembly & stabilization
-Reservoir for cytokines, growth factors.
-In wounds, it’s a chemotactic, helps to clear fibrin
from inflamed sites.
52

50. LAMININ
In embryonic tissues-the first extracellular protein detected &
in mature tissues –universally found as the major
noncollagen component in basement membranes.
-Involved in cell attachment, cell proliferation and cell
differentiation .
-Has domains for the attachment of cells, heparin ,elastin,
type IV collagen , nidogen,entactin and galactoside-binding
lectins.
- Associated with cell rests of Malassez of PDL.
53

51. OSTEOCALCIN / BONE Gla Protein
Osteocalcin is a small protein –odontoblasts & osteoblasts .
-Osteocalcin is highly specific for calcified tissues.
-The post-translational vitamin K dependent carboxylation of
glutamic acid residues allows the osteocalcin molecule to
bind calcium .
- The molecule undergoes a conformational shift
when associated with hydroxyapatite.
-Serum osteocalcin levels correlates with histomorphometric
analysis of new bone.
54

52. BONE SIALOPROTEIN
(BSP II)
Major structural protein of bone matrix, expressed by
fully differentiated osteoblasts.
-15% of non-collagenous proteins.
-Found in reversal lines of rapidly remodeling bone
-Expressed by cementoblasts during cementogenesis &
also during early formation of dentin
55

53. OSTEOPONTIN
High content –serine,asparagine,glutamate.
-Found primarily in bone & several nonskeletal tissues (the
central nervous system, kidney and placenta).
-In bone, the synthesis and release of Osteopontin by osteoblasts -
endocrine (calcitriol, corticosteroids, and parathyroid hormone)
and paracrine(TGF) control.
-Functions not clear-proposed that Osteopontin is involved in
both the attachment and movement of osteoblasts and
osteoclasts in bone via integrin mediated cell binding.
- implicated in calcium regulation
56

54. HOW OSTEOPONTIN HELPS IN
MINERALIZATION??
 In native bone tissue 10-30% of the tissue mass is proteinaceous and the
remaining 70-90% is comprised of calcium phosphate mineral, which is
primarily hydroxyapatite (HA).
 The protein component of bone has been shown to be ∼90% collagenous,
while the remaining 10% of the protein content is believed to play a role in
bone formation, growth, repair, and cellular adhesion to the matrix.
 The primary group of non-collagenous proteins found in bone are the
SIBLING (small integrin-binding ligand, N-linked glycoprotein) family
of proteins and they are believed to play a key role in these processes.
57

55. Continuation…….
 The SIBLING family of proteins consists of five members: osteopontin (OPN),
matrix extracellular phosphoglycoprotein (MEPE), bone sialoprotein (BSP),
dentin matrix protein 1 (DMP1), and dentin sialophosphoprotein (DSPP).
 The SIBLING proteins have a number of shared characteristics including a
collagen binding domain, a HA binding domain, and a cell binding arganine-
glycine-aspartic acid (RGD) sequence. Additionally, they are all located on the
same human chromosome (4q21)
 all of the proteins are post-translationally phosphorylated and have been
immunolocalized in mineralized tissues.Together, these characteristics
suggest that the SIBLING family of proteins play an important role in bone
development by facilitating cellular adhesion, mineral nucleation, and
mineral maturation.
58

56.  MEPE has been shown to be a potent inhibitor of mineralization both in
vitro and in vivo and therefore is not expected to play a role in the induction of
biomineralization.
 DMP1 is believed to regulate the mineralization process, possibly mediating
the transformation of amorphous calcium phosphate to crystalline HA.
 OPN has been shown to either inhibit or induce mineralization based on its
phosphorylation state, but most likely regulates the mineralization process in
bone.
59

57. SPARC / OSTEONECTIN
-SPARC: Secreted protein acidic and rich in cysteine.
-Found in greatest abundance in osseous tissue, tissues
characterized by high turnover ,basement membranes .
-Osteonectin is expressed -chondrocytes,fibroblasts, platelets,
endothelial cells, epithelial cells, Leydig cells, Sertoli cells,
adrenal cortical cells and numerous neoplastic cell lines.
-Functions- mineralization of bone and cartilage
-inhibiting mineralization.
-modulation of cell proliferation.
-anti adhesive, disrupts focal adhesion in fibroblasts.
60

58. TENASCIN/CYTOTACTIN
-Star shaped structure with central knot.
-Binds to fibronectin, chondrointin sulphate.
-Mediates both adhesive & repulsive interactions.
-Detected in attachment zone of periodontal ligament at
interface between mineralized & non mineralized tissues.
-Role in wound healing, tumourogenesis and cell migration.
61

59. NIDOGEN/ ENTACTIN
-Dumb bell shaped with 2 globular domains.
-Crucial role in basement membrane organization &
stabilization.
-Interacts with both cell surface proteins & extra cellular
matrix proteins.
-Binds to laminin & type 4 collagen
62

60. PERIODONTAL LIGAMENT FIBERS
63

61. ARRANGED IN 6 GROUPS
 TRANSSEPTAL
 OBLIQUE
 INTERRADICULAR
 APICAL
 ALVEOLAR CREST
 HORIZONTAL
64

62.  TRANSSEPTAL FIBERS:
Extend interproximally over alveolar crest and are
embedded in cementum of adjacent tissue.
Reconstructed even after destruction of alveolar bone
resulting from periodontal disease.
65

63.  ALVEOLAR CREST GROUP:
Extend obliquely from cementum just beneath
cementoenamel junctional epithelium to alveolar crest.
Fibers also run from cementum over the alveolar crest &
to the fibrous layer of periosteum covering the alveolar
bone.
66

64.  These fibers RESIST TILTING, INTRUSIVE,
EXTRUSIVE, ROTATIONAL FORCES.
 It is often confused with the dentoperiosteal groups of
fibers.
 Any collagenous fibers located apical to the line
joining the height of the each interdental bony septum
termed as periodontal and those coronal to the line is
gingival.
67

65.  HORIZONTAL GROUP:
These fibers run at right angles to the long axis of the
tooth from cementum to alveolar bone and parallel to
the occlusal plane of the arch.
Found immediately apical to the alveolar crest group.
These fibers pass from their cemental attachment
directly across the periodontal ligament space to
become inserted in alveolar process as sharpey’s fibers .
68

66.  Limited to the coronal one- fourth of periodontal
ligament space.
 These fibers RESIST HORIZONTAL AND TIPPING
FORCES.
69

67.  OBLIQUE GROUP:
These are the most numerous and occupy nearly 2/3rd of
the ligament.
Inserted into the alveolar bone at a position coronal to
their attachment to cementum resulting in their oblique
orientation within periodontal space. RESIST VERTICAL
AND INTRUSIVE FORCES
70

68.  APICAL GROUP :
From cementum at the root tip , fibers of the apical
bundles radiate through the periodontal space to
become anchored into the fundus of bony socket.
RESIST FORCES OF LUXATION, PREVENT TOOTH
TIPPING & PROTECT DELICATE BLOOD AND LYMPH
VESSELS AND NERVES TRAVERSING PERIODONTAL
LIGAMENT SPACE AT ROOT APEX.NOT SEEN IN
INCOMPLETE FORMED ROOTS.
71

69. INTERRADICULAR GROUP:
Principal fibers of this group are inserted into the
cementum from crest of interradicular septum in
multirooted tooth.
RESIST TOOTH TIPPING , TORQUING AND
LUXATION.
72

70.  These fibers are lost if age related gingival recession
proceeds to the extent that the furcation area is
exposed. Total loss of these fibers occur in chronic
inflammatory periodontal disease.
73

71.  Some author consider GINGIVAL FIBER GROUP to be
part of the principal fibers of the periodontal
ligament.
 The gingival fiber groups are found within the lamina
propria of marginal gingiva. These gingival fibers are
separate but adjacent fiber groups which support the
marginal gingival tissues to maintain the relationship
of the teeth.
74

72.  SHARPEYS’ FIBERS ;
Collagen fibers are embedded into the cementum on one
side of the periodontal space & into the alveolar bone on
the other.
The embedded fibers are called SHARPEY’S FIBERS.
75

73. 76

74.  These are the most numerous but smaller at their
attachment into cementum than alveolar bone. The
mineralized parts of the sharpey’s fibers in alveolar
bone proper appear as projecting stubs covered with
mineral clusters.
 The mineralization is at right angles to long axis of
fibers, indicating that fibers are subjected to tensional
forces.
77

75.  Sharpey’s fibers in primary acellular cementum are
mineralized fully those in cellular cementum and bone
are mineralized partially at their periphery.
 Few Sharpey's fibers pass uninterruptedly through the
bone of alveolar process termed (TRANSALVEOLAR
FIBERS)to continue as principal fibers of adjacent
periodontal ligament or mingle buccally or lingually
with fibers of periosteum that cover the outer plates of
alveolar process.
78

76.  These fibers pass through the alveolar process only
when process consists entirely of compact bone and
contains no haversian system.
 Once embedded in either the wall of alveolus or the
tooth Sharpey’s fibers calcify to certain degree & are
associated with abundance of non collagenous
proteins namely OSTEOPONTIN AND BONE
SIALOPROTEIN.
79

77.  INTERMEDIATE PLEXUSES :
It was believed that principal fibers frequently followed
a wavy course from cementum to alveolar bone and are
joined in the mid region of periodontal space giving rise
to a zone of distinct appearance called INTERMEDIATE
PLEXUSES
80

78.  The plexuses was considered to be an area of high
metabolic activity in which splicing and unsplicing of
fibers might occur. Studies have indicated that once
cemental fibers meet and fuse with the bone no such
plexuses remains.
81

79.  ELASTIC FIBERS :
There are three types of elastic fibers which are
histochemically and ultrastructurally different.
They are :
MATURE ELASTIC FIBERS
ELASTIN FIBERS
ELAUNIN FIBERS
OXYTALAN FIBERS
(BERKOVITZ 2ND edition)
82

80.  MATURE ELASTIC FIBERS:
Consist of microfibrillar component surrounding an
amorphous core of elastin protein. Elastin protein
contains high percentage of GLYCINE,PROLINE ,
HYDROPHOBIC RESIDUES with LITTLE
HYDROXYPROLINE & NO HYDROXYLYSINE.
83

81.  Microfibrillar component is located around the
periphery & scattered throughout the amorphous
component.
 These fibers are observed only in walls of different
blood vessels where they constitute the elastic laminae
of larger arterioles and arteries of greater caliber.
84

82.  ELAUNIN FIBERS :
These are seen as bundles of microfibrils embedded in a
relatively small amount of amorphous elastin.
These fibers found within the fibers of gingival
ligament. An elastic meshwork has been described in
pdl as being composed of many elastin lamellae with
peripheral oxytalan fibers and elaunin fibers .
85

83.  OXYTALAN FIBERS:
It is a type of immature elastic fibers, consist of
microfibrillar component only.
It forms a three dimensional meshwork that extends
from cementum to peripheral periodontal blood
vessels. The meshwork is largely oriented in apico-
occlusal plane & interconnected with fine lateral
fibrils.
86

84. 87

85.  Depending on site & species oxytalan fibers measures
between 0.2 -1.5 micrometer in diameter in electron
microscope and occupy 3% pdl in humans.
 In contrast in light microscopy they measure 0.5 – 2.5
micrometer in diameter.
 These fibers are not susceptible to acid hydrolysis .
88

86.  Orientation of oxytalan fibers is completely different
when compared to the other collagen fibers.
 Instead of running from bone to cementum they run
in axial direction. One end being embedded in
cementum or bone and other end in wall of blood
vessel.
89

87.  In the cervical region they follow the course of gingival
and trans septal fibers. Within the periodontal
ligament proper, these fibers are longitudinally
arranged, crossing the oblique fibers perpendicularly.
In the vicinity of the apex they form a complex
network.
90

88.  Function of oxytalan fibers is unknown but it has been
suggested that they may a play a pivotal role in
supporting the blood vessels of periodontal ligament.
 They are thicker and more numerous in teeth
subjected to high loads as in orthodontic tooth
movement. Thus, these fibers play a role in tooth
support.
91

89.  RETICULAR FIBERS:
These are fine immature collagen fibers with
argyrophilic staining properties and are related to
basement membrane of blood vessels and epithelial cells
which lie within the periodontal ligament. These fibers
are composed of TYPE III collagen.
92

90.  SECONDARY FIBERS:
 These are located between and among the principal
fibers.
These fibers are relatively non directional and
randomly oriented.
Represent newly formed collagenous elements that
have not yet incorporated into principal fiber bundles.
93

91.  These fibers traverse the periodontal ligament space
corono-apically and are often associated with paths of
vasculature and nervous elements.
94

92. INDIFFERENT INTERMEDIATE PLEXUSES :
 Small Collagen fibers in association with the larger
principal collagen fiber
 Run in all directions forming a plexus
 Described by Shackleford, 1971
 Once the tooth has erupted into clinical occlusion
such an intermediate plexus is no longer demonstrable
 Intermediate plexus has been reinterpreted by Sloan as
representing merely an optical effect explained
entirely by the arrangement of middle layer collagen
into sheets rather than bundles.
95

93. Small collagen fibers associated with large principal
collagen fibers have been described.
These fibers run in all directions forming a plexus
called INDIFFERENT FIBER PLEXUSES.
Some studies reported this plexuses seen in ground
section examined under scanning electron microscope
but not under transmission electron microscope.
Hence, some authors consider it to be an artifact.
96
continuation of indifferent fiber plexuses:

94. CELLS OF PERIODONTAL LIGAMENT
 The principal cells of healthy, functioning periodontal
ligament are concerned with the synthesis and
resorption of alveolar bone and fibrous connective of
the ligament and cementum . The cells of the PDL
may be divided as -
 Synthetic cells
 Resorptive cells
 Cells rests of malassez
97

95.  FIBROBLASTS:
 The fibroblasts is the predominant cell in the pdl . These
fibroblasts origin in part of from the ectomesenchyme of
investing layer of dental papilla and from the dental follicle .
Pdl contains a fibroblasts cell populations with different
functional characteristics .
98

96.  These fibroblasts are regularly distributed throughout the
ligament and are oriented with their long axis parallel to
the direction of collagen fibrils .
 Fibroblasts of pdl generate an organizational pattern as
they have ability to both synthesize and shape the proteins
of the extracellular matrix in which collagen fibrils form
bundles that insert into tooth and bone as SHARPEY’S
fibers .
 Once embedded in the wall of alveolus or tooth ,
these fibers calcify to a certain degree and are associated
with an abundance of non collagenous proteins found in
the bone i.e. osteopontin and bone sialoprotein .
99

97. Difference b/w periodontal and gingival
fibroblasts
 Periodontal ligament fibroblasts are ectomesenchymal
in origin whereas gingival fibroblasts are mesodermal
in origin.
 Expression of alkaline phosphatase & cyclic AMP is
more in periodontal ligament fibroblasts. Gingival
fibroblasts are less proliferative.
 Periodontal ligament fibroblasts can generate force for
tooth eruption as they are motile and contractile
 Fibroblasts of pdl are capable of collagen degradation.
(Orban’s textbook of histology 13 th edition)
100

98. OSTEOCLASTS
• These cells covering the periodontal surface of the alveolar
bone constitute a modified endosteum and not a periosteum .
• A cellular layer but not an fibrous layer is present on the
periodontal surface of the alveolar bone . The surface of the
bone is covered largely by osteoblasts as well as by occasional
osteoclasts .
• These are the cells lining the tooth socket and are cuboidal in
shape with a prominent round nucleus at the basal end of the
cell .
• These cells appear basophilic due to the presence of abundant
rough endoplasmic reticulum . The cells contact one another
through desmosomes and tight junctions .
101

99. CEMENTOBLASTS
 Its distribution is similar to that of osteoblasts on the
bone surface . These cells line the surface of cementum
. They are cuboidal with a large vesicular nucleus ,
with one ore more nucleoli and abundant cytoplasm.
 All the organelles are required for protein synthesis
and secretion are present . Cells actively depositing
cellular cementum exhibit abundant basophilic
cytoplasm and cytoplasmic processes
102

100. 103

101. RESORPTIVE CELLS
 OSTEOCLASTS : - These resorb bone and tend to
be large and multinucleated but can also be small and
mononuclear . Multinucleated osteoclasts are formed
by fusion of precursor cells similar to circulating
monocytes.
 These when viewed in light microscope are cells
occupy bays in bone or surround end of bone spicule .
 The part of plasma membrane lying adjacent to bone
that is being resorbed is raised in characteristic folds
and is termed the ruffled or striated border.
104

102. 105

103.  The ruffled border is separated from the rest of
plasma membrane by a zone of specialized membrane
that is closely applied to the bone the underlying
cytoplasm of which tends to be devoid of organelles
and has been called the clear zone .
 The area of bone that is sealed off by virtue of active
pumping of protons by the osteoclast into this
environment .
106

104.  FIBROBLASTS: - These cells show rapid degradation of
collagen by fibroblast phagocytosis and is the basis for fast turnover in
periodontal ligament . Collagen degradation was an extracellular event
involving the activity of the enzyme collagenase .

 Intracellular collagen profiles are organelles present . These are
associated with the degradation of collagen that has been ingested
from extracellular environment . Some studies suggested that collagen
degradation is intracellular .
 The extracellular elements in degradation of collagenase involve
Collagenase which cleaves the triple helical portion of molecules
within the fibrils .
107

105.  INTRACELLULAR DEGRADATION - Fibroblasts are
capable of phagocytosing collagen fibrils from extracellular
environment and degrading them inside phagolysomal
bodies . Collagenase is not involved in the intracellular
phase of degradation of collagen fibrils .
 CEMENTOCLASTS: - These resemble osteoclasts and
sometimes found in normally functioning periodontal
ligament . Cementum is not remodeled in the fashion of
alveolar bone and periodontal ligament . Its origin is
unknown bit it is conceivable that they arise in the same
manner as osteoclasts .
108

106.  PROGENITOR CELLS : - All connective tissues including
periodontal ligament contain progenitors for synthetic cells that
have the capacity to undergo mitotic division .
 If they were not present there would be no cells available to replace
differentiated cells lying at the end of their life span or as a result of
trauma.
 These cell populations within the ligament appear to be in highest
concentrations in locations adjacent to blood vessel and exhibit
some of the classical cytological features .
109

107. Epithelial rests of malassez
 The ligament contains epithelial cells that are found close
to the cementum . At the time of cementum formation the
continuous layer of epithelium that covers the surface of
newly formed dentin breaks into lacelike stands . The
epithelial rests persist as a network stands islands or
tubelike structures near and parallel to the surface of the
root .
 Their function is not clear but they could be involved in
periodontal repair and generation .
 These cells rests can be distinguished from fibroblasts in
pdl by the close packing of their cuboidal cells and their
nucleus stains more deeply . They are more numerous in
older individuals and more numerous in children . These
cells may proliferate to form cysts and tumors. These cells
may undergo calcification to become CEMENTICLES.
110

108. 111

109. DEFENCE CELLS
 MAST CELLS – These are relatively small round or
oval cell having a diameter of about 12 to 15 um . Mast
cells are often associated with blood vessels . These
cells are characterized by numerous cytoplasmic
granules which frequently obscure the small , round
nucleus .
112

110.  Mast cells histamine plays a role in the inflammatory
reaction and have been shown to de granulate in response to
antigen – antibody reaction on their surface .
 The release of histamine into the extracellular environment
causes proliferation of endothelial cells and mesenchymal
cells .
113

111.  MACROPHAGES- These are found in the ligament
and are predominantly located adjacent to blood
vessels . The wandering type are derived from blood
monocytes has a characteristic ultrastructure that
permits it to be readily distinguished from fibroblasts .
114

112.  EOSINOPHILLS – These are seen in the periodontal
ligament . They posses granules that consist of one or
more crystalloid structures . These are capable of
phagocytosis
115

113. GROUND SUBSTANCE
 Ground substance composed of glycoproteins and
proteoglycans . Ground substance has been estimated to
contain 70 % water and is thought to have a significant
effect on the tooth ‘s ability to withstand stress loads .
 Ground substance is a gel like matrix in which are
embedded the cellular components such as collagen .
Berkovitz et al estimated that ground substance accounted
for 65 % of the volume in the pdl
116

114.  All anabolites reaching the cells from the
microcirculation in the ligament and all catabolites
passing in the opposite direction must pass
through the ground substance . Its integrity is
essential if the cells of ligament are to function
properly
117

115.  The ground substance consists of mainly of
hyaluronate , glycosaminoglycans , proteoglycans and
glycoproteins . All components are presumed to be
secreted by fibroblasts .
 Proteoglycans are compounds containing anionic
polysaccharides covalently attached to a protein .
 Glycosaminoglycans are linear polymers of
disaccharide repeat sequence which contains a
hexosamine,,heparin sulfate and hexuronic acid .
118

116.  Substrate adhesion molecules such as tenascin ,
osteonectin , laminin , undulin , and fibronectin have been
identified in pdl .
INTERSTITIAL TISSUE
 Some of blood vessels , lymphatics , and nerves of the pdl
are surrounded by loose connective tissue and can be readily
recognized in light microscope .
119

117. STRUCTURES PRESENT IN CONNECTIVE TISSUE
 The following discrete structures are present in connective
tissue of pdl
 Blood vessels
 Lymphatics
 Nerves
 Cementicles
120

118. The blood supply to the periodontal
ligament are derived from three
sources:
-Branches from apical vessels
supplying the dental pulp.
-Branches from intra-alveolar
vessel, runs horizontally through
nutrient canals.
-Branches from gingival vessels,
enter the PDL from the coronal
direction.
BLOOD SUPPLY OF
PERIODONTAL LIGAMENT
121

119. -Vessels form basket-like network.
-Runs parallel to long axis of tooth between the principle fibres.
-Main supply: SUPERIOR & INFERIOR ALVEOLAR artery- intraosteal
course – gives alveolar branches ascending within the bone.
-Branches then run horizontally, penetrating alveolar bone and then PDL.
Hence called PERFORATING ARTERIES.
-Maximum in mandible & maximum in posterior teeth.
-Single rooted teeth-more in the gingival third followed by apical
third.( Significant in wound healing).
122

120.  The interradicular arteries branch into vessels of lesser
caliber to emerge from the cribiform plate as perforating
arteries and supply the pdl along most of the coronoapical
extent including the bifurcation and trifurcation arteries .
 The interdental artery also exit the bone to supply the
middle three fifth of the pdl though most of the interdental
arteries emerge from the crest of the alveolar process and
supply the coronal aspect of pdl .
 The pdl has some specialized features in the vasculature
namely the presence of large number of fenestrations in the
capillaries and a cervical plexus of capillary loops .
123

121. 124
Alignment of alpha chains by formation of disulphide bonds at C-
terminal ends
Formation of collagen alpha chains
Hydroxylysine residues are glycosylated by addition of galactose
in the presence of galactosyltransferase
Hydroxylation of proline and lysine residues by vitamin C-
dependent enzyme prolylhydroxylase and lysylhydroxylase
Translocated into lumen of RER for post-translational modifications
Initial polypeptides formed (one and a half times longer than final
collagen molecule as they have N- and C- terminal extensions)
m-RNA directs specific amino acids into polypeptide chains on ribosomes
associated with RER

122.  VENOUS DRAINAGE- The venous channels
accompanying their arterial counterparts . The
channels are larger in diameter with mean average
of 28 um . These channels receive blood from the
capillary network and also specialized shunts
called glomera in the pdl . These shunts provides
an arteriovenous anastomosis .
125

123. 126

124.  LYMPHATIC DRAINAGE - A network of lymphatic
vessels following the path of the blood vessels , provides
the lymph drainage of the pdl . The flow is from the
ligament toward and into the adjacent alveolar bone .
 It may course apically through the substance of pdl to arise
and pass through the fundus of the socket or may through
the cribiform plate . They finally enter into larger channels
after pursuing intraosseous path .
 The flow is via the alveolar lymph channels which are
joined by the dental and interrradicular lymph channels
127

125.  NERVES – The pdl has functionally two types of nerve fibers
sensory and autonomic . The sensory fibers are associated
with nociception and of mechanoception , with touch ,
pressure , pain and proprioceptive sensations . The
autonomic fibers are associated with pdl vessels .
 All pdl innervations are mediated by the dental branches
of alveolar nerves which enter through apical perforation
of the tooth socket and perforating branches of
interalveolar nerves traversing the bone .

128

126. INNERVATION OF LIGAMENT
According to Tencate:
There are 3 patterns of nerve innervation
i)general anatomic configuration
ii)regional variation in termination of neural elements
iii)types of neural terminations.
129

127. ANATOMIC CONFIGURATION
-Nerve fibres run from apical region towards gingival
margin.
-They are joined by fibers entering laterally through the
foramina of the socket wall.
-They divide into branches -one extending apically
-the other gingivally .
130

128. -Nerve bundles divide into single myelinated fibers-
then lose their myelin sheaths and end in one of the
4 neural terminations:
 Free endings-tree like configuration: pain sensation
 Ruffini-like mechanoreceptors: primarily in apical area
 coiled Meissner’s corpuscles: mechanoreceptors
found in mid-root
region
 Spindle-like pressure and vibration endings:
surrounded by fibrous capsule, located
mainly in apex.
131

129. 132

130. REGIONAL VARIATION
Apical region –more nerve endings.
-Maxillary incisors-more innervated than molars.
-Dense distribution also seen in coronal half of
labial PDL and also apically
133

131. TYPES OF NEURAL TRANSMISSION
 4 types- BYERS,1985
a)Tree –like pattern:
-most frequent type
-along root length
-free nerve endings in tree like pattern.
-originate mostly from unmyelinated nerve fibres
- they carry Schwann cell envelope & processes
projecting into surrounding CT.
- Endings carry-mechanoreceptors & noci receptors
134

132. RUFFINI CORPUSCLES
Found at the root apex.
-Appears dendritic .
-Ends in terminal expansions among fiber
bundles.
-Electron microscopic study -
i) simple receptors – single neurite
ii) compound receptors- several terminations.
-Both have ensheathing schwann cells that are especially close to collagen fiber
bundles
-Mechanoreceptors.
135

133. COILED MEISSENER’S CORPUSCLES
• -Nerve terminal in coiled form
• -Found in the mid region of the PDL.
• -Function and the ultra structure- not yet
determined.
136

134. SPINDLE LIKE ENDINGS
 Lowest frequency.
 -Found associated with the root apex
 -Consists of the spindle like endings surrounded by
fibrous capsule.
 -Said to sense pressure & vibration.
137

135.  Nerves which usually are associated with blood vessels pass
through foramina in the alveolar bone including the apical
foramen to enter the pdl . In the region of apex apex they run
toward the cervix whereas along the length of root they branch
and run both coronally and apically .
 Nerve fibers are either of large diameter and myelinated or
small diameter in which case they may or not be myelinated .
138

136.  The pdl is abundantly supplied with sensory nerve fibers capable of
transmitting tactile pressure and pain sensations by the trigeminal
pathways . Nerve bundles pass into pdl from the periapical area and
through channels from the alveolar bone that follow the course of the
blood vessels .
 The bundles divide into single myelinated fibers which ultimately loose
their myelin sheath and end in one of four types of neural termination
139

137.  CEMENTICLES - Calcified bodies called cementicles ,
sometimes found in the pdl . These bodies are seen in older
individuals and they may remain free in the connective
tissue and may fuse into large calcified masses or they may
be joined with the cementum . As the cementum thickens
with advancing age it may envelop these bodies . When they
are adherent to the cementum they form excementoses. The
origin of these calcified bodies is not established . It is
possible that degenerated epithelial cells form the nidus for
their calcification .
140

138. MECHANISM OF SHOCK ABSORPTION
 TENSIONAL THEORY
Principal fibers of the PDL are the major factor in supporting the
tooth and transmitting forces to the bone.
When forces are applied to tooth, principal fibers unfold and
straighten and then transmit the forces to alveolar bone, causing
elastic deformation of socket.
141

139. Force applied to crown
Principles fibres first unfold and straighten
Transmit forces to alveolar bone(causing elastic deformation
of the bony socket)
Once alveolar bone reaches its limit , load is transmitted to
basal bone
142

140. A. Tooth in a resting state
B. The periodontal ligament fibers are
compressed in areas of pressure and
stretched in area of tension.
143

141. VISCOELASTIC THEORY
• According to it, the fluid movement largely controls the
displacement of the tooth, with fibers playing a secondary role.
• When forces are transmitted to the tooth, the extracellular fluid
is pushed from periodontal ligament into marrow spaces
through the cribriform plate.
• After depletion of tissue fluids, the bundle fibers absorb the
shock and tighten.
• This leads to blood vessel stenosis  arterial lack pressure 
ballooning of vessels tissue replenishes with fluids.
144

142. THIXOTROPIC GEL THEORY
PDL fluid acts as a gel.
-When pdl fibers are disturbed the gel which is present
between pdl fibers becomes fluid
-Forces on tooth gel to fluid.
-Removal of forces fluid to gel.
-Helps in shock absorption.
(perio 2000 volume 13,1997)
145

143. TRANSMISSION OF OCCLUSAL FORCES TO BONE
Arrangement of principle fibres is similar to a suspension
bridge/hammock
Axial force when applied
Root displaces into the alveolus
Oblique fibres alter their wavy course, assume full
length and sustain major part of the axial force.
146

144. When horizontal forces are applied- 2 phases of movements
occur.
i)within confines of ligament.
ii)displacement of facial & lingual bony plates.
-Force - tension & pressure areas.
-Tension side - fibres taut.
- Pressure side - fibres are compressed, tooth displaced,
distortion of bone in direction of root movement.
147

145. AXIS OF ROTATION
Single rooted teeth: Between
the apical and middle third
-In multirooted teeth: Bone
between roots
-Compression resorbs
-Tension deposition
148

146. FUNCTIONS OF PERIODONTAL LIGAMENT
 Periodontal ligament has following functions:
1.Supportive
2.Sensory
3.Nutritive
4.Homeostatic
5.Eruptive
6.Physical
149

147. SUPPORTIVE
 When a force is applied on tooth either by mastication or orthodontic tooth
movement there is compression of pdl and other areas widening of pdl.
 The compressed pdl fibers will act as support for the loaded tooth, water
molecules and other molecules bound to collagen act as cushion for
displaced tooth. The pressure of blood vessels also provides a hydraulic
cushion for the support of the teeth.
 Load is dissipated to alveolar bone through oblique fibers of pdl when
placed in tension and on release elastic recoil of tissue enables the tooth in
original position.
150

148. SENSORY
 Nerve supply of pdl provides most efficient proprioceptive mechanism and
allows to detect the application of the most delicate forces of teeth.
 Mechanoprotection protects both supporting structures of the tooth and the
substances of the crown from excessive masticatory forces.
 Cortin actin assembly regulates the activity of stretch activated calcium
permeable channels since forces desensitizes channels to force applications.
151

149. continuation
 ACTIN BINDING PROTEIN – 280 plays a pivotal role in
mechanoreception by :
a. Reinforcing the membrane cortex and preventing force induced membrane
disruption.
b. Increasing the strength of cytoskeletal links to extracellular matrix
c. Desensitizing stretch activated ion channel activity
152

150. NUTRITIVE:
 Ligament contains blood vessels provide anabolites required by the cells of
pdl.
 Any extirpation of ligament results in necrosis of underlying cells.
 Occlusion of blood vessels leads to necrosis of cells in affected parts of
ligament- when too heavy forces is applied to teeth in orthodontic therapy.
153

151. HOMEOSTATIC:
 The cells of pdl have the ability to resorb and synthesize the extracellular
substance of the connective tissue of the ligament , alveolar bone and
cementum .
 Alveolar bone appears to be resorbed and replaced at a rate higher than
other tissue in jaws . Furthermore the collagen of pdl is turned over at a
rate that may be the fastest of all connective tissues in the body and the cells
in the bone half of ligament may be more active than those on the
cementum side
154

152. ERUPTIVE
 The cells of vascular elements and extracellular matrix proteins
of pdl function collectively enable the teeth to limited eruption
and adjust the position while remaining fibers attach the teeth
firmly to the alveolar bone.
 It provides a space and acts as a medium for cellular
remodeling and hence continued eruption and approximal shift
occurs.
155

153. PHYSICAL :
1. Provision of a soft tissue “casing” to protect the vessels &
nerves from injury by mechanical forces.
2. Transmission of occlusal forces to the bone.
3. Attachment of the teeth to the bone.
4. Maintenance of the gingival tissues in their proper
relationship to the teeth.
5. Resistance to the impact of occlusal forces (shock
absorption
156

154. HOMEOSTATIC MECHANISM
• The resorption and synthesis are controlled procedures.
• If there is a long term damage of periodontal ligament, which is
not repaired, the bone is deposited in the periodontal space.
• This results in obliteration of space and ankylosis between
bone and the tooth.
• The quality of tissue changes if balance between synthesis and
resorption is disturbed.
157

155. • If there is deprivation of Vit. C which are essential for
collagen synthesis, resorption of collagen will continue.
• So there is progressive destruction and loss of extra
cellular substance of ligament.
• This occurs more on bone side of ligament.
• Hence, loss of attachment between bone and tooth and at
last, loss of tooth.
158

156. NORMAL CELL BIOLOGY
 The production and destruction of tissue matix ( turnover ) in a
healthy state , involves interaction among a myriad of effector
molecules that are synthesized and secreted by resident cell of
periodontal ligament .
 Cytokines are a series of multifunctional polypeptides and
glycoproteins that are secreted by one or several cell types and act
locally or systemically . These includes Interleukins , cytotoxic
factors , interferons , growth factors , colony stimulating factors.
 Growth factors have been defined as substances capable of re –
initiating proliferation of cells that are in a quiescent state .
159

157.  In vivo cytokines play an important role in
numerous biological events , including
development , homeostasis , regeneration , repair ,
inflammation and neoplasia
160

158.  1 . Fibroblast growth factors (FGF) - Two of seven isoforms of
fibroblast growth factors have been described in particular one is
acidic and other basic .
 Acidic fibroblast growth factors has effects on endothelial cell
replication and neovascularisation . It stimulates dna synthesis
and cell replication , in bone tissue cultures which results in
increased protein synthesis especially type 1 collagen .
161

159.  Basic fibroblast growth factors has angiogenic
properties has highly chemotactic and mitogenic
for a variety of cell types . It stimulates bone cell
replication and increases the number of cells of
osteoblastic lineage .
162

160. 2 . Platelet derived growth factor ( PGDF ) This factor is
potent growth factor for various connective tissue
cells and is released from the a – granules in platelets
in conjunction with blood coagulation .
 PGDF is a promoter of cell migration and a potent
mitogen for cells bearing PGDF receptors . It acts
synergistically with other growth factors as a
competence factor .
 PGDF stimulated type v collagen formation and a
drop in type III production in gingival fibroblasts .
163

161.  Transforming Growth factor ( TGF ) : - These
factors are polypeptides from normal and
neoplastic tissues which are known to cause a
change in normal cell growth . TGF is of 2 types α
and b according to relationship to EGF .
 TGF – α similar isolated biological effects acting
through EGF receptor .
 TGF – β was originally purified from human
placenta , platelets and bovine kidney . It
stimulates the synthesis of connective tissue matrix
components such as collagen , fibronectin
proteoglycan and glycosaminoglycans .
164

162.  . Interleukin- 1 ( IL – 1 ) : - Interleukin – 1 is a
polypeptide with a great number of roles in
immunity , inflammation , tissue breakdown and
tissue homeostasis . It is synthesized by various cell
types including macrophages , monocytes ,
lymphocytes vascular cells brain cells skin cells and
fibroblasts following cellular activation . 2 types of
IL are known interleukin – 1 α and 1β .
165

163.  Interferon – ɤ : - It posses important
immunomodulatory effect and thus is a
lymphokine as much as an interferon . Its
production is modulated by other cytokines such
as interleukin – 1 . Many biological activities have
been ascribed to interferon like action on B and T
lymphocytes , antibody production , natural killer
cells , macrophages and tumour cells .
166

164.  Matrix metalloproteinases and their
tissue inhibitors : - Connective tissue cells
participate in both the formation and breakdown of
connective tissue matrix . Such cells are found to
synthesize and secrete a family of enzymes known
as MMP’s .
 MMP gene family encodes a total 24
homologous proteinases classified into collagenases
, gelatinases , stromeolysins , membrane type MMP
depending on their susbstrate specificity and
molecular structures .

167

165. COLLAGEN TURN OVER RATE
 Sodek ,1977 found collagen synthesis in PDL of adult rat to be
- two fold greater than that of gingiva,
- four fold greater than that of skin, &
- six fold greater than that of bone.
 Almost all the newly synthesized collagen in the ligament was converted to
mature cross linked collagen, whereas much less was converted in the
gingiva & skin.
168

166. Continuation….
 Half-life for collagen turnover: in ligament – 1 day,
in bone – 6 days
in gingiva - 5 days,
in skin - 15 days
 According to Rippin: half life
in the apical areas 2.45 days,
in the crestal areas 6.42days,
fibers in mid-root region 5.7 days,
transseptal fibers 8.4 days
for dentogingival fibers 25 days.
169

167. EXTERNAL FORCES & PDL
 Within physiologic limits, the pdl can accommodate increased function with
an increase in width,
a thickening of its fiber bundles, and
an increase in diameter & number of
Sharpey’s fibers.
 Forces that exceed the adaptive capacity of the periodontium produce injury
called trauma from occlusion.
 Slight excessive pressure: resorption of bone, widening of PDL space
 Slight excessive tension: elongation of PDL fibers & apposition of bone
170

168. Replantation & transplantation
 To have any chance of success , it is essential to maintain the
viability of PDL .
 Avoid dehydration of PDL.
 Avoid loss of viability of its cell rests.
Transplantation
 Best results when unerupted tooth with partially formed roots
as there is less damage to PDL.
171

169. AGE CHANGES IN PERIODONTAL LIGAMENT
-Rate of collagen synthesis decreases.
-Rate of maturation of the synthesized collagen changes.
-Decrease in the number of fibers.
-Collagen fibril diameter – decreases by 50%
-Degenerative vascular changes seen.
-Sharpey's fiber insertion – the alveolar bone surface jagged
and uneven with irregular fiber insertions
172

170. CLINICAL CONSIDERATIONS
• The primary role of periodontal ligament is to support the tooth
in the bony socket.
• The width of periodontal ligament varies from 0.15 to
0.38mm. The average width is:
- 0.21mm at 11 to 16 years of age.
- 0.18mm at 32 to 50 years of age.
- 0.15mm at 51 to 67 years of age.
• So, the width of periodontal ligament decreases as age
advances.
173

171. WIDTH OF PERIODONTAL LIGAMENT
 Conflicting results have been obtained
 Klein & Tozat concluded – width increases with age
 Tonna et al (1972) – width decreases with age
 Why the width of periodontal ligament in hour glass shape??
Root convexity
Acts as fulcrum
Width of cementum is more at center
174

172. With age
Less teeth present
Forces acting on remaining teeth increases
INCREASE WIDTH OF PDL SPACE WITH AGE
175
Masticatory forces decreases
with age
DECREASE WIDTH OF
PDL SPACE WITH AGE
Tonna et al (1972)
Klein & Tozat

173. • In the periodontal ligament, aging results in more number of
elastic fibers and decrease in vascularity, mitotic activity, fibroplasia
and in the number of collagen fibers and mucopolysaccharides.
• If gingivitis is not cured and supporting structure become involved,
the disease is termed as periodontitis.
• There are few coccal cells and more motile rods and spirochetes in
the diseased site than in the healthy site. The bacteria consists of
gram-positive facultative rods and cocci in healthy site while in
diseased site, gram-negative rods and anaerobes are more in
number.
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174. • Resorption and formation of both bone and periodontal
ligament play an important role in orthodontic tooth
movement. If tooth movement takes place, the compression of
PDL is compensated by bone resorption whereas on tension
side, apposition takes place.
• Periapical area of the tooth is the main pathologic site.
Inflammation of the pulp reached to the apical periodontal
ligament and replaces its fiber bundles with granulation tissue
called as granuloma, which then progresses into apical cyst.
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175. • Chronic periodontal disease can lead to infusion of
microorganisms into the blood stream.
• The pressure receptors in ligament have a protective
role. Apical blood vessels are protected from excessive
compression by sensory apparatus of the teeth.
• The rate of mesial drift of tooth is related to health,
dietary factor and age. It varies from 0.05 to 0.7mm per
year.
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176. Effect of hyper & hypo glycaemia on PDL
 Nishimura et al, 1998 - PDL cells - susceptible to hyper &
hypoglycemia & effects - mediated via the integrin system.
 Hyperglycemia – increased expression of fibronectin receptor
→ results in reduced cellular adhesion & motility → probable
tissue impairment.
 Hypoglycemia – decreased expression of fibronectin receptor
→ lowers the viability & ultimately results in cell death &
hence tissue impairment
179

177. PDL space Radiographic appearance
 Thin radiolucent line interposed between the root & lamina
dura.
 Occlusal Trauma → widened PDL space or funneling of
coronal aspect of PDL space.
 It can also widened in case of vertical fractures & progressive
systemic sclerosis (Scleroderma).
180

178. EMD & PDL
 Gestrelium et al, 1997 studied effects of EMD on periodontal ligament cell
migration, attachment, proliferation, biosynthetic activity mineral nodule
formation & ability to absorb a large range of polypeptide growth factors &
cytokine.
 In culture, EMD formed protein aggregates which appeared to provide ideal
conditions for cell-matrix interactions.
 Under these conditions EMD enhanced the proliferation of PDL cells,
increased protein & collagen production of PDL cells & promoted mineral
nodule formation by these cells.
 However, no effect on migration, attachment & spreading of these cells nor
did they absorb any of the growth factor or cytokine that were tested.
181

179. NEOPLASTIC INVOLVEMENT OF PDL
 Mostly reactive rather than neoplastic.
 Oxytalan fibers are found in peripheral odontogenic
fibromas & Adenomatoid odontogenic tumors
 Epithelial rests of malassez --- neoplastic change
 Infiltration of PDL by 1º or 2° malignant tumors --- widening
of PDL space--- mobility –malignant loosening of teeth.
182

180. BLOOD & LYMPHO RETICULAR DISORDERS
 Changes due to reduced host response to plaque.
 Destruction of PDL follows neutrophil defeciencies or
functional defects such as defeciency of leucocyte adhesion
receptors
183

181. PERIODONTAL CYSTS
 Inflammatory ---- Radicular cyst
 Developmental ---- Lateral periodontal cyst
184

182. SOFT C.T.DISORDERS & PDL
a. PROGRESSIVE SYSTEMIC SCLEROSIS
 Radiographically ---- PDL widening upto 3mm
thickening
 Collagen ---- dense, mature & more hyalinised than
normal
 Oxytalan fibers increased.
185

183. . LATHYRISM
 Condition caused by drugs that inhibit cross linking in collagen
& elastin (cystamine)
 Fragile collagen fibers
 Retard eruption
c. DISUSE ATROPHY
 Narrowing of PDL & reduction in no. of principal fibers.
 Fibers oriented parallel to the long. Axis of root & PDL shows
reduced rate of collagen turn over.
186

184. NUTRITION & PDL
a. FOOD TEXTURE
 Little correlation between the advent of soft, fiber deficient
diet & dental health.
 Significant factor in chronic inflammatory periodontal
disease is loss of natural masticatory function, leading to
accumulation of dental plaque.
 Influences pattern of mastication & hence the mode of
support offered by the PDL.
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185. CARBOHYDRATES
 Refined carbohydrates in the diet influence the severity of PDL
disease in humans (Holloway et. Al 1963)
 No direct evidence showing the direct effect of carbohydrates
per se on PDL , though in some circumstances there could be
an influence as a result of modifying the diet consistency.
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186. PROTEINS
 Deficiency of protein might be expected to produce changes
within it.
 Reduction in PDL transseptal fibers ( Stien & Ziskin 1949; Ten
Cate et..al.1976)
 Reduction in cementoblasts, fibroblasts
 Occlusal trauma exacerbates these effects (Chawla & Glickman
1951)
 Healing is delayed in rats fed on protein deficient diet.
189

187. PERIODONTITIS
 CHRONIC PERIODONTITIS
 AGGRESSIVE PERIODONTITIS
 PERIODONTITIS AS A MANIFESTATIONS OF
SYSTEMIC DISEASES
190

188. CHRONIC PERIODONTITIS
 The most prevalent form in adults
 Amount of destruction consistent
with local factors
 Associated with a variable microbial pattern
 Subgingival calculus frequently found
 Slow to moderate rate of progression
 Possibly modified by or associated
with the following:
- Systemic diseases
- Local factors predisposing
factors
- Environmental factors
191

189. CLASSIFICATION OF CHRONIC
PERIODONTITIS
I. Localized form: <30% of sites
involved
Generalized form: >30% of sites
involved
II. Slight: 1-2 mm of clinical
attachment loss
Moderate: 3-4 mm of clinical
attachment loss
Severe: ≥5 mm of clinical
attachment loss
192

190. AGGRESSIVE PERIODONTITIS
Primary Features
1. Except for the presence of periodontitis, patients are
otherwise clinically healthy
2. Rapid attachment loss and bone destruction
3. Familial aggregation
193

191. Secondary Features
1. Amounts of microbial deposits are inconsistent with the severity of
periodontal tissue destruction
2. Elevated proportions of Aggregatebacter actinomycetemcomitans and,
in some populations, Porphyromonas gingivalis may be elevated
3. Phagocyte abnormalities
4. Hyper-responsive macrophage phenotype, including elevated levels of
PGE2 and IL-1β
5. Progression of attachment loss and bone loss may be self-arresting
194

192. HEALING AFTER PERIODONTAL THERAPY
REGENERATION is the reproduction or reconstitution of a lost
or injured part.
REPAIR is the healing of a wound by tissue that does not fully
restore the architecture or the function of the part.
PERIODONTAL REGENERATION is defined histologically
as regeneration of the tooth’s supporting tissues, including
alveolar bone, periodontal ligament, and cementum over a
previously diseased root surface.
195

193.  NEW ATTACHMENT is defined as the union of connective
tissue or epithelium with a root surface that has been deprived
of its original attachment apparatus. This new attachment may
be epithelial adhesion and/or connective tissue adaptation or
attachment and may include new cementum.
196

194. TO SUMMARIZE:PERIODONTAL LIGAMENT
 The PDL is the means of attaching the tooth to the bone for
mastication. As a labile connective tissue, it:
 Adapts to varying load
 senses loads for proprioceptive feedback controlling
muscle actions
 helps to move the teeth for better occlusion
 supplies & nourishes cementum & alveolar bone
 defends against microbes
 prevents damage to cementum
197

195. REFERENCES
 Carranza’s Clinical Periodontology, 10th Edition
 Clinical Periodontology and Implantology by Jan Lindhe, 5th edition
 Oral Histology and Embryology by Orban, 13th edition
 Tencate oral histology, 5th edition
 Textbook of biochemistry – HARPER’S 2nd edition
 Xiong J, Gronthos S, Bartold PM. Role of the epithelial cell rests of
Malassez in the development, maintenance and regeneration of periodontal
ligament tissues. Periodontol 2000, Vol. 63, 2013, 217–233.
 Bosshardt DD, Selvig KA.Dental cementum: the dynamic tissue covering of
the root. Periodontol 2000 1997;13:41-75
198

196.  Fundamentals of Periodontics, 2nd Edition, by Thomas G. Wilson, Kennath
S. Kornman
 Textbook of oral pathology by Shafer, 5th edition.
 The periodontal ligament in health and disease: 2nd edition, Barry K B
Berkovitz
 Bartold PM, Walsh LJ, Sampath Narayan A. Molecular and cell biology of
gingiva. Periodontol 2000, Vol. 24, 2000, 28–55
 Ertsenc W, Mcculloc HG , Sodek HJ. The periodontal ligament: a unique,
multifunctional connective tissue. Periodontol 2000. Vol. 13, 1997, 20-40.
 Wright JM. Reactive, dysplastic and neoplastic conditions of periodontal
ligament origin. Periodontol 2000, Vol. 21, 1999, 7-15.
 Cho MI, Garant PR. Development and general structure of the
periodontium, Periodontol 2000, Vol. 24, 2000, 9–27
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