Complete dentures

Bone resorption and prosthodontics

Aaron H. Fenton, D.D.S.*

Eastman Dental Center, Rochester, N. Y.

R esorption is defined as the loss of substance through physiologic

means, such as loss of dentin and cementum
or pathologic
of a tooth or of the alveolar process of
the mandible or maxi1la.l This places notable dental emphasis on the subject.
Koelliker,2 in 1873, discussed aspects of bone resorption and suggested hypotheses
for the mechanisms involved. He felt that bone mineral and matrix were resorbed
simultaneously, and he concluded that osteoclasts resorb bone by chemical means.
Since then, there has been much progressive research, but few definite answers have
been produced.
Research on bone resorption and its mechanism has importance in four areas:
the regulation of calcium homeostasis in the body, the integrity of the skeleton as a
structural unit, the treatment of metabolic diseases, and the understanding of local-
ized bone resorption.

DENTAL SIGNIFICANCE
It is in this fourth area that dentists are most interested. Orthodontists wish to
understand and control resorption so that they can position individual teeth within
alveolar bone with the least possible trauma. Oral surgeons have an interest in bone
diseases, as well as a need to understand the mechanisms of bone metabolism, to
successfully provide treatment of trauma and developmental defects. Periodontists
are concerned with attempting to maintain the maximum amount of alveolar support
about the roots of teeth in the presence of inflammatory and infectious processes.
The more alveolar bone that is retained about the teeth, the more surface area avail-
able for attachment of the teeth to bone via the periodontal membrane.
Prosthodontists wish to maintain and preserve the alveolar bone in edentulous
and dentulous areas to provide support for dental prostheses.
In 1962, an estimated 20.1 million Americans were edentulous.3 Approximately
15.8 million persons, or four out of five, possessed satisfactory sets of dentures. At
present, approximately 100 million man-hours are expended in rendering prostho-

Prize winning paper presented to the Rochester Academy of Medicine for the Sybron
Frank Ritter Memorial Award for Dentistry, May 8, 1972.
*Assistant Professor, Prosthodontic Department, The University of Toronto.

477
478 Fenton J. Prosthet. Dent.
May, 1973

dontic service. Assuming that complete dentures are remade every five to ten years
and new complete dentures are constructed every 15 years for all patients who re-
quire them, this prosthodontic need will rise to 250 million man-hours by 1990.4 This
constitutes a considerable expenditure in time and manpower to adequately care for
the dental needs of edentulous people.
Much of this need is due to the fact that the edentulous residual alveolar ridge
diminishes in size. As a result, tissue-borne prostheses need to be altered. Atwood’
has termed this phenomenon “the reduction of residual ridges” (RRR) and discusses
it as a major oral disease entity. J
It is generally agreed that residual edentulous alveolar ridges resorb; however,
there remains some controversy regarding the effect of dentures on the process.
Some authorities discussed the concept of disuse atrophy and recommended that
dentures be constructed and worn to preserve the alveolar ridge.6, 7 In contrast to
this idea, others have emphasized the mechanical trauma that is associated with
the wearing of complete dentures .8-10 Longitudinal studies have been reported to
determine the effect of wearing complete dentures upon the remaining bone. There
does not seem to be any geographic or dental constant in the results.
Campbellll measured casts of 38 denture and 31 non-denture wearers. All had
been in the conditions noted on examination for five to 21 years. He found that
there was a significantly smaller ridge dimension recorded for denture wearers in
three of four analyses. The labiolingual dimension of the maxilla and mandible and
vertical dimension of the mandible were reduced for denture wearers. Denture wear-
ing did not significantly affect the vertical height of the maxillary alveolar ridge in
this study.
Conversely, JozefowicP made plaster impressions of the maxillary labial sulcus
of 1,012 patients ranging in age from 40 to 79 years. He found that wearing dentures
produced a statistically significant decrease in ridge height, except in women over
60 years of age. Whether or not the dentures were worn at night did not appear to
be significant.
It must be realized that investigations such as these in which casts or tissue con-
tours are measured do not truly reflect the amount of bone resorption which may
have occurred. Instead, they only record the shape and size of the residual alveolar
ridge.
Atwood and CoyI used lateral cephalometric radiographs to determine the
status of the remaining alveolar bone. Anterior alveolar vertical bone loss was their
criterion in a study of 76 patients covering an average period of 31 months. All
dentures were constructed with a standardized technique. The mean vertical rate of
alveolar ridge resorption was found to be 0.5 mm. per year, with a wide range of
0 to 2.2 mm. per year. It was noted that the anterior vertical bone loss was four
times greater in the mandible than in the maxilla.
Tallgren14 used the occlusal and rest vertical face heights as her criteria in ana-
lyzing the results of edentulousness and denture wearing. In a cross-section study
of 302 subjects with and without dentures, she noted that patients wearing dentures
had extremely reduced face height and increased interocclusal clearance when com-
pared to dentulous control subjects of the same age and sex. Then, in a longitudinal
 Bone resorption and prosthodontics 479

study of 23 patients over seven years, she followed the reduction of facial height in
complete and partial denture wearers. l5 This reduction amounted to almost 7 mm.
in 7 years for complete denture wearers.
Other studies have been reported in the literature which confirm these investiga-
tions.‘“, Iti These observations suggest that the removal of teeth from the alveoli and
the wearing of prosthetic dentures increase the amount of alveolar bone resorption
that occurs-irrespective of the health of the total skeleton.

BONE RESORPTION AND CALCIUM HOMEOSTASIS

lIespite the dental profession’s concern with local problems of alveolar bone loss,
resorption is part of a much larger picture.
Calcium is a component of the body that has wide ranging effects. The proper
concentration of calcium ions is necessary for (1’) all nerve and muscle functioll,
( 2) every excitation and response process that occurs, (3) function of all endocrine
glands, and (1) intercellular bridging which is necessary for nutrition and communi-
cation.
The only sources of calcium for the body are the diet and the bone reservoir.
Calcium homeostasis is maintained by controlling calcium obtained from these two
sources. This can occur by altering intestinal absorption mechanisms (income’ or
tubular reabsorption (recycling) or by liberation of calcium from the skeleton via
resorption (savings’).
There is a reciprocal relationship between calcium concentration and bone rcl-
sorption to maintain calcium homeostasis. I7 As the level of serum calcium increases.
this depresses agents that would stimulate bone resorption and also stimulates agents
that inhibit bone resorption. The converse is true: As the level of serum calcium
drops, resorption is stimulated, and factors that would inhibit resorption are dc-
pressed.
Nicholsl’ makes the point that calcium homeostasis is a distinct entity with
separate control and that bone resorption is only one mechanism involved in calcium
metabolism.

PHYSIOLOGIC REGULATION OF BONE RESORPTION

Physiologic regulators of bone resorption are factors which act directly on bone
resorbing cells, maintain homeostasis in the presence of a deficiency or excess of
calcium, and are essential for bone growth and remodeling.
Kais?” has presented the following hypothesis: The maintenance of a constant
extracellular calcium concentration depends on the dual reciprocal control of bone
resorption by parathyroid hormone (PTH) and thyrocalcitonin (TCT) .
Bone resorption is stimulated by PTH and the active form of vitamin I>, 25
hydroxycholecalciferol (HCC) . It is inhibited by the action of thyrocalcitonin (TCT 1
and phosphate (P04) (Fig. 1)
PTH acts at the cell membrane to increase production of cyclic 3’,5’-adenosine
monophosphate (CAMP) from adenosine triphosphate (ATP) : CAMP controls
the entry of extracellular calcium (Ca”) into the cell.
The level of Ca++ in the nucleus is controlled by HCC. As the nuclear level of
 J. Prosthet. Dent.
480 Fenton May, 1973

OSTEOLYTIC CELL
BONE

* COLLAGENOLYSIS R

Fig. 1. Model of an osteolytic cell indicating the following possible mechanisms and sites of
action of physiologic regulators: Passive entry of Ca++ from extracellular fluid, with active
extrusion of Ca++ from cell to blood; PTH binding to the cell membrane and activating adenyl
cyclase; increased membrane permeability to calcium mediated by CAMP; vitamin D binding
to the nuclear membrane and altering Cat’ permeability; binding of Cat+ to specific nuclear
proteins that control the DNA-dependent RNA synthesis required for differentiation to osteo-
lytic activity; RNA formation controlling the synthesis of proteins involved in calcium trans-
location and matrix removal; TCT blocking the calcium extrusion pump; phosphate inhibiting
calcium removal by causing deposition of calcium either intracellularly or in bone matrix.
(From Raisz, L. G.: N. Engl. J. Med. 282: 909-916, 1970.)

Ca++ increases, it is bound to specific nuclear proteins which affect the deoxyribo-
nucleic acid (DNA) to control ribonucleic acid (RNA) synthesis of resorption
proteins.
These proteins act extracellularly on bone to cause collagenolysis and mineral
removal. Several investigators believe that the mineral component is removed first,
and the collagen is subsequently digested by lysosomal enzymes.20-23
TCT acts at the cell membrane to inhibit an active calcium pump. As the intra-
cellular level of Ca increases, this could inhibit calcium removal from bone. This
would explain the action of TCT inhibiting resorption without inhibiting the effect
of PTH on cells to differentiate for synthesis and secretion of enzymes.
Changes in PO., concentration could affect many sites, such as intracellular energy
metabolism, CAMP production, or calcium ion activity. A simpler explanation would
be that PO, stimulates Ca++ precipitation in bone, thereby inhibiting resorption of
the calcified elements.

MODE OF ACTION
Vae? has performed tissue culture experiments to produce a hypothesis explain-
ing the action of the osteolytic cell upon bone. In his model system, he added para-
thyroid extract (PTE) to cultures of embryonic mouse calvaria and monitored
changes in the lacunae close to osteoclasts.
He observed that the following increases in solution: ( 1) hydroxyproline, bone
mineral, and hexosamine and (2) lysosomal hydrolases, such as P-glucuronidase,
N-acetyl+glucosaminidase, P-galactosidase, acid protease, and acid deoxyribonucle-
ase. Non-lysosomal enzymes, such as alkaline phosphatese and catalase, decreased in
concentration.
 Bone resorption and prosthodontics 481

He concluded that parathyroid extract (PTE) acts to cause a release of lyso-

somes from osteolytic cells. Lysosomal enzymes would resorb the organic matris of
bone, and acids from glycolysis could act to dissolve bone mineral. These would be
the resorptive proteins of Raisz.
He also thought that lysosomes may contain pyrophosphateses which could act
to remove the pyrophosphate outer layer of hydroxyapatite crystals.
The preceding outlined concepts of bone resorption relative to the total skeleton
and calcium.

LOCALIZED BONE RESORPTION

There is ample clinical evidence available in the fields of orthopedics and ortho-
dontics to indicate that mechanical stimulus can cause changes in bone structurr
an d surface contour. The exact mechanism of this local control and influence is
unknown. Two theories have been advanced.
Electrical eflects in bone. Piezoelectric behavior is an inherent property of bone
as well as other mineralized structures such as dentin and hydroxyapatite.“‘-“’ The
term “piezoelectric” implies that a material generates an electric current when it
is mechanically deformed. The origin of this effect in bone is not clear. A piczo-
electric effect occurs in hyaluronate of the ground substance, dry collagen, demin-
eralized bone, moist bone, and apatite. Also, collagen and apatite together have
been considered as a source of piezoelectricity in the form of a solid-state phenom-
enon. Collagen is produced as an n-type material and apatite, a p-type material;
together the two would function as a p-n junction diode.
The electrical current produced in bone when it is deformed has been advanced
by RassetV7 as a force of sufficient magnitude to exert a wide range of effects in
living systems. He has demonstrated that osteogenesis is associated with negative
electrodes embedded in bone, while osteoclastic activity is associated with regions
known to be positive.2S
How this occurs is not known, but the following speculation exists. Mechanical
strain and stress on a piezoelectric substance (i.e., bone) are converted into an elec-
trical stimulus. This stimulus, through its effect on cellular and extracellular eie-
ments, produces a change in osseous structure. This change will be appropriate
to resist the deforming mechanical force and stop the initial piezoelectric signal.“”
Epker and Frost3” applied this reasoning to physical analogues of teeth in sockets
and bending long bones, They theorized that the effect of strain on the surface of
bone is a major influence on the behavior of cells in the bone. Under deformation
or strain, as a bone surface becomes more concave, bone formation occurs: as thr
bone surface becomes less concave, bone resorption occurs.
To consider these hypotheses in a more dental application, Cochran and others”
stressed intact, moist bovine mandibles containing teeth and periodontal membrane
with 5 Kg. loads, and they observed generated potentials of 1 to 5 mv. Presumably
when teeth are not present, this magnitude of electrical potential cannot be grn-
erated.
Mechanochemical hypothesis for bone remodeling. Justus and Luft3’ have pre-
sented another explanation for the translation of mechanical stress into osteoclastic
or osteoblastic activity. They stressed hydroxyapatite crystals and observed that solu-
bility of the crystals in solution or the resultant calcium ion activity varied with thr
mechanical loading. Bone responds to mechanical stress by alteration of shape IO
resist the applied stress. Presumably, this is regulated by a negative feedback svstenl.
Their hypothesis is that strain would give the “signal” for bone remodelin,g in ;u-t’:lq
01” mechanical stress.
Strain on the bone would alter the solubility of the hydroxyapatite crystals. This,
in turn, produces an altered extracellular calcium activity in that local area. As it
is known that cells are very sensitive to calcium activity, it is possible that the bonr
cells will react by either producing or removing bone until their extracellular cnlciuln
environment returns to an optimum level.

SUMMARY

The phenomenon of bone resorption and its importance to dentistry, specificall\

prosthodontics, have been briefly reviewed.
At a skeletal level, bone resorption is thought to be controlled by the opposincr
actions of parathyroid hormone and thyrocalcitonin. The importance of vitamin I)
and phosphate in this mechanism was discussed.
Bone resorption is thought to occur as a result of the release of lysosomes frorrl
osteolytic cells. The enzymes contained in the lysosomes cause a removal of thtb
mineral portion of bone followed by a dissolution of the organic matrix.
Local control of bone resorption in response to mechanical stimulus requires ‘I
biologic transducer to translate pressure into a tissue reaction. In bone, it is thought
that this message may be transmitted by either a piezoelectric effect or by alteration
of solubility of hydroxyapatite crystals when stressed.

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FACULTY OF DENTISTRY
THE UNIVERSITY OF TORONTO
124 EDWAKD ST.
TORONTO, ONTARIO, CANADA